Dear Editor,Idiopathic orbital inflammation(IOI),also known as orbital inflammatory pseudotumor,is a relatively common orbital disorder[1].Its pathogenesis remains unclear,often regarded as a nonspecific immune-mediat...Dear Editor,Idiopathic orbital inflammation(IOI),also known as orbital inflammatory pseudotumor,is a relatively common orbital disorder[1].Its pathogenesis remains unclear,often regarded as a nonspecific immune-mediated response[2].IOI presents with symptoms such as pain,photophobia,proptosis,eyelid swelling,edema,conjunctival congestion,and diplopia,with possible vision loss occurring in some cases.Based on the soft tissue structures involved,IOI can be classified into subtypes such as myositis,optic neuritis,dacryoadenitis,diffuse orbital inflammation,and orbital inflammatory masses[2].展开更多
Neuroinflammation,the inflammatory response of the central nervous system(CNS),is a common feature of many neurological disorders such as sepsis-associated encephalopathy(SAE),multiple sclerosis(MS),and Parkinson'...Neuroinflammation,the inflammatory response of the central nervous system(CNS),is a common feature of many neurological disorders such as sepsis-associated encephalopathy(SAE),multiple sclerosis(MS),and Parkinson's disease(PD).Prior studies identified cytokines(e.g.,tumor necrosis factor[TNF],interleukin[IL]-1,and IL-6)delivered by resident glial cells and brain-invading peripheral immune cells as the major contributor to neuroinflammation(Becher et al.,2017).In addition to pro-inflammatory cytokines,elevated levels of extracellular purine molecules such as adenosine triphosphate(ATP)and adenosine can be detected upon any pathological insults(e.g.,injury,ischemia,and hypoxia),contributing to the progression of neurological disorders(Borea et al.,2017).展开更多
Stroke is a major cause of death and disability worldwide.It is characterized by a highly interconnected and multiphasic neuropathological cascade of events,in which an intense and protracted inflammatory response pla...Stroke is a major cause of death and disability worldwide.It is characterized by a highly interconnected and multiphasic neuropathological cascade of events,in which an intense and protracted inflammatory response plays a crucial role in worsening brain injury.Neuroinflammation,a key player in the pathophysiology of stroke,has a dual role.In the acute phase of stroke,neuroinflammation exacerbates brain injury,contributing to neuronal damage and blood–brain barrier disruption.This aspect of neuroinflammation is associated with poor neurological outcomes.Conversely,in the recovery phase following stroke,neuroinflammation facilitates brain repair processes,including neurogenesis,angiogenesis,and synaptic plasticity.The transition of neuroinflammation from a harmful to a reparative role is not well understood.Therefore,this review seeks to explore the mechanisms underlying this transition,with the goal of informing the development of therapeutic interventions that are both time-and context-specific.This review aims to elucidate the complex and dual role of neuroinflammation in stroke,highlighting the main actors,biomarkers of the disease,and potential therapeutic approaches.展开更多
Neuroinflammation is an inflammatory response in the central nervous system associated with various neurological conditions.The inflammatory process is typically treated with non-steroidal and steroidal anti-inflammat...Neuroinflammation is an inflammatory response in the central nervous system associated with various neurological conditions.The inflammatory process is typically treated with non-steroidal and steroidal anti-inflammatory drugs,which have a range of serious adverse effects.As an alternative,naturally derived molecules such as quercetin and its derivatives show promising anti-inflammatory properties and beneficial effects on various physiological functions.Our objective was to synthesize the evidence on the anti-inflammatory effect of quercetin and its derivatives in in vivo models,in the face of neuroinflammatory insults induced by lipopolysaccharide,through a systematic review and meta-analysis.A search of the preclinical literature was conducted across four databases(Pub Med,Web of Science,Scielo,and Google Scholar).Studies were selected based on inclusion and exclusion criteria,assessed for methodological quality using CAMARADES,and risk of bias using the SYRCLE tool,and data were extracted from the studies.The quantitative assessment of quercetin effects on the expression of pro-inflammatory cytokines and microgliosis was performed through a meta-analysis.A total of 384 potentially relevant articles were identified,of which 11 studies were included in the analysis.The methodological quality was assessed,resulting in an average score of 5.8/10,and the overall risk of bias analysis revealed a lack of methodological clarity in most studies.Furthermore,through the meta-analysis,it was observed that treatment with quercetin statistically reduces pro-inflammatory cytokines,such as tumor necrosis factor alpha,interleukin 6,interleukin 1β(n=89;SMD=–2.00;95%CI:–3.29 to–0.71),and microgliosis(n=33;SMD=–2.56;95%CI:–4.07 to–1.10).In terms of underlying mechanisms,quercetin and its derivatives exhibit antioxidant and anti-apoptotic properties,possibly through the nuclear factor erythroid 2-related factor 2(Nrf2)/HO-1 pathways,increasing the expression of antioxidant enzymes and reducing reactive species,and modulating the caspase pathway,increasing levels of anti-apoptotic proteins and decreasing proapoptotic proteins.Quercetin and its derivatives exhibit highly pleiotropic actions that simultaneously contribute to preventing neuroinflammation.However,despite promising results in animal models,future directions should focus on well-designed clinical studies to assess the safety,bioavailability,and efficacy of quercetin and its derivatives in humans.Additionally,standardization of methods and dosages in studies is crucial to ensure consistency of findings and optimize their application in clinical settings.展开更多
Gastric ulcer(GU)represents a clinically significant manifestation of peptic ulcer disease,driven by a complex interplay of microbial,environmental,and immuneinflammatory factors.A recent cross-sectional study by Shen...Gastric ulcer(GU)represents a clinically significant manifestation of peptic ulcer disease,driven by a complex interplay of microbial,environmental,and immuneinflammatory factors.A recent cross-sectional study by Shen et al systematically evaluated six complete blood count-derived inflammatory indices:Neutrophil-tolymphocyte ratio,monocyte-to-lymphocyte ratio,platelet-to-lymphocyte ratio,systemic immune-inflammation index,systemic inflammatory response index(SIRI),and aggregate index of systemic inflammation and demonstrated their positive associations with GU prevalence,identifying SIRI as the strongest predictor.This editorial contextualizes these findings within the broader literature,clarifies that these indices reflect systemic rather than GU-specific inflammation,highlights methodological strengths and major limitations,and proposes a conceptual clinical algorithm for integrating SIRI into GU risk assessment.Future multicenter studies incorporating Helicobacter pylori infection,non-steroidal antiinflammatory drug exposure,and prospective design are essential to validate and translate these findings into clinical practice.展开更多
Neuroinflammation is a key process in the pathogenesis of various neurodegenerative diseases,such as multiple sclerosis(MS),Alzheimer's disease,and traumatic brain injury.Even for disorders historically unrelated ...Neuroinflammation is a key process in the pathogenesis of various neurodegenerative diseases,such as multiple sclerosis(MS),Alzheimer's disease,and traumatic brain injury.Even for disorders historically unrelated to neuroinflammation,such as Alzheimer's disease,it is now shown to precede pathological protein aggregations.展开更多
The shared links between Alzheimer’s disease and type 2 diabetes mellitus:Alzheimer’s disease(AD)and type 2 diabetes mellitus(T2DM)are two prevalent conditions that come with substantial daily struggles.Emerging evi...The shared links between Alzheimer’s disease and type 2 diabetes mellitus:Alzheimer’s disease(AD)and type 2 diabetes mellitus(T2DM)are two prevalent conditions that come with substantial daily struggles.Emerging evidence highlights that these diseases share similar pathophysiological features,including insulin resistance and chronic inflammation,which contribute to their rapid progression(Chen et al.,2022).Insulin resistance,a hallmark of T2DM,has been suggested to exacerbate neurodegeneration in AD.Similarly,chronic low-grade inflammation in T2DM parallels with neuroinflammation,which is observed in AD,suggesting overlapping pathophysiological mechanisms in T2DM and AD.展开更多
AIM:To report and analyze cases of sterile intraocular inflammation(IOI)following intravitreal faricimab injections in patients treated for neovascular age-related macular degeneration(nAMD)and diabetic macular edema(...AIM:To report and analyze cases of sterile intraocular inflammation(IOI)following intravitreal faricimab injections in patients treated for neovascular age-related macular degeneration(nAMD)and diabetic macular edema(DME).METHODS:This double-center case series included nine eyes of six patients who developed uveitis after faricimab therapy.Comprehensive clinical evaluation was performed,including slit-lamp examination,intraocular pressure(IOP)measurement,fluorescein and indocyanine green angiography(ICGA),and laboratory tests.Inflammatory responses were treated with topical or systemic corticosteroids,and patients were monitored for visual acuity and inflammatory activity.RESULTS:The incidence of IOI was 0.8%per patient(Innsbruck)and 0.23%(Czechia),with inflammation typically occurring between the third and sixth injection(mean interval:10d post-injection).Inflammator y presentations ranged from anterior uveitis to posterior segment involvement.One notable case demonstrated novel choroidal hypofluorescent lesions on angiography,suggesting deeper ocular involvement.The mean patient age was 76y;five of six affected patients were female.All cases responded to local and systemic corticosteroids,with full recovery of initial visual acuity.CONCLUSION:Sterile IOI after faricimab appears to be a rare but relevant adverse event.Although the incidence falls within expected ranges for anti-vascular endothelial growth factor(anti-VEGF)agents,the observed choroidal involvement represents a potentially new safety signal.Prompt diagnosis and corticosteroid therapy are effective in all cases.Our findings support the need for vigilant post-marketing surveillance and further studies to better understand the underlying mechanisms and risk factors of faricimab-associated inflammation.展开更多
AIM:To define the prevalence and anatomical patterns of paranasal sinus abnormalities(PSA)in thyroid-associated ophthalmopathy(TAO)and to test the hypothesis that TAO is partially driven by contiguous orbital inflamma...AIM:To define the prevalence and anatomical patterns of paranasal sinus abnormalities(PSA)in thyroid-associated ophthalmopathy(TAO)and to test the hypothesis that TAO is partially driven by contiguous orbital inflammation rather than systemic autoimmunity or generalized orbital pressure.METHODS:Data included ophthalmic assessments and a panel of thyroid function and autoimmune biomarkers.Blinded radiological analysis of orbital computed tomography(CT)scans was performed to quantify sinus abnormalities and extraocular muscles(EOMs)involvement.Patients were categorized into two groups based on CT findings,those with no radiological evidence of sinus abnormalities(non-PSA control group)and those with identifiable PSA.Furthermore,ethmoid sinus mucosal biopsies from a subset of TAO patients and noninflammatory controls were subjected to histopathological analysis.RESULTS:Totally 121 TAO patients(mean age 42.4±12.8y,range 10-78y),male:female=42:79,were included.PSA was identified in 44.6%(n=54)of patients,with a distribution anatomically restricted to the maxillary(50.0%isolated)and ethmoid sinuses(18.5%isolated;29.6%combined).Compared to the non-PSA group(n=67),patients with PSA were significantly older(45.1±11.8 vs 40.3±13.2y;P=0.040)and were more likely to be male(55.6%vs 17.9%;P<0.001).They also had significantly higher proptosis(22.1±3.2 vs 20.7±2.9 mm;P<0.001).Medial/inferior rectus involvement was most frequent(88.4%vs 89.3%).Histopathological analysis of sinus mucosa from PSA patients provided direct evidence of pathology,revealing a dense,chronic lymphoplasmacytic infiltrate and submucosal edema,validating the radiological findings as a true inflammatory process.No significant correlation was found with systemic autoimmune markers,including thyroid-stimulating hormone(TSH)receptor antibodies(TRAb,median 4.86 vs 2.71 IU/L,P=0.104).CONCLUSION:TAO is associated with a high prevalence of PSA in a pattern consistent with the orbital anatomy.The correlation with ipsilateral muscle thickening combined with the lack of association with proptosis laterality or systemic biomarkers lend strong support to a model of contiguous inflammation over systemic autoimmunity,a hypothesis that warrants further validation through longitudinal and mechanistic studies.展开更多
Obesity is widely recognized as a global epidemic,primarily driven by an imbalance between energy expenditure and caloric intake associated with a sedentary lifestyle.Diets high in carbohydrates and saturated fats,par...Obesity is widely recognized as a global epidemic,primarily driven by an imbalance between energy expenditure and caloric intake associated with a sedentary lifestyle.Diets high in carbohydrates and saturated fats,particularly palmitic acid,are potent inducers of chronic low-grade inflammation,largely due to disruptions in glucose metabolism and the onset of insulin resistance(Qiu et al.,2022).While many organs are affected,the brain,specifically the hypothalamus,is among the first to exhibit inflammation in response to an unhealthy diet,suggesting that obesity may,in fact,be a brain-centered disease with neuroinflammation as a central factor(Thaler et al., 2012).展开更多
Studies have shown that chitosan protects against neurodegenerative diseases. However, the precise mechanism remains poorly understood. In this study, we administered chitosan intragastrically to an MPTP-induced mouse...Studies have shown that chitosan protects against neurodegenerative diseases. However, the precise mechanism remains poorly understood. In this study, we administered chitosan intragastrically to an MPTP-induced mouse model of Parkinson's disease and found that it effectively reduced dopamine neuron injury, neurotransmitter dopamine release, and motor symptoms. These neuroprotective effects of chitosan were related to bacterial metabolites, specifically shortchain fatty acids, and chitosan administration altered intestinal microbial diversity and decreased short-chain fatty acid production in the gut. Furthermore, chitosan effectively reduced damage to the intestinal barrier and the blood–brain barrier. Finally, we demonstrated that chitosan improved intestinal barrier function and alleviated inflammation in both the peripheral nervous system and the central nervous system by reducing acetate levels. Based on these findings, we suggest a molecular mechanism by which chitosan decreases inflammation through reducing acetate levels and repairing the intestinal and blood–brain barriers, thereby alleviating symptoms of Parkinson's disease.展开更多
BACKGROUND Gastric ulcer(GU),a common gastrointestinal condition,is influenced by multiple factors,particularly inflammatory and immune responses.Complete blood count(CBC)-derived inflammatory biomarkers represent a n...BACKGROUND Gastric ulcer(GU),a common gastrointestinal condition,is influenced by multiple factors,particularly inflammatory and immune responses.Complete blood count(CBC)-derived inflammatory biomarkers represent a novel indicator of systemic inflammation and immune status;however,their association with GU remains unclear.AIM To investigate the association between CBC-derived inflammatory markers and GU.METHODS The study sample included individuals admitted to the Gastroenterology Unit of the Second Affiliated Hospital of Nanchang University from 2023 to 2024.We explored how each CBC-based inflammation indicator correlated with GU occurrence through logistic models,and assessed their predictive ability using receiver operating characteristic curve analysis.Additionally,we applied the least absolute shrinkage and selection operator method along with stepwise regression techniques to determine which inflammatory indicators were most significantly linked to GU.RESULTS Higher levels of log2 neutrophil-to-lymphocyte ratio,log2 monocyte-to-lymphocyte ratio,log2 systemic immuneinflammation index,log2 systemic inflammatory response index(SIRI),and log2 aggregate index of systemic inflammation were significantly associated with increased GU prevalence across all models,while log2 platelet-tolymphocyte ratio was significant only in the fully adjusted model.SIRI demonstrated the highest discriminative ability,with an area under the curve of 0.868.CONCLUSION Hematological indicators derived from CBC tests show a significant correlation with the prevalence of GU.Among them,SIRI demonstrated the most prominent association.These markers could act as practical tools in recognizing individuals more likely to develop GU.展开更多
BACKGROUND Inflammatory bowel diseases(IBD),including ulcerative colitis(UC)and Crohn’s disease(CD),are chronic gastrointestinal disorders with an increasing global prevalence and significant healthcare impact.The ex...BACKGROUND Inflammatory bowel diseases(IBD),including ulcerative colitis(UC)and Crohn’s disease(CD),are chronic gastrointestinal disorders with an increasing global prevalence and significant healthcare impact.The exact etiology of this condition remains unclear.Neutrophils play a critical role in IBD pathogenesis.Translocator protein(TSPO),a mitochondrial protein linked to immune responses,has demonstrated potential as an inflammatory marker.However,its role in IBD remains underexplored.AIM To investigate the role of TSPO in IBD pathogenesis,particularly in neutrophils.METHODS Bioinformatics analyses of Gene Expression Omnibus datasets(GE75214,GSE94648,GSE156776)assessed TSPO expression in IBD patients.TSPO expression was evaluated in human IBD samples,neutrophiles and a chronic colitis mouse model.Neutrophil function was examined in 18 samples using reactive oxygen species(ROS)production and neutrophil extracellular trap(NET)formation assays.Positron emission tomography-computed tomography(PET-CT)imaging and histology from 12 mice revealed TSPO expression in colitis.PET-CT and immunofluorescence staining assessed TSPO expression in brain under neuroinflammation condition.RESULTS Bioinformatics analysis revealed elevated TSPO expression in the intestinal mucosa and peripheral blood of patients with IBD,especially in neutrophils.This was confirmed by quantitative real-time polymerase chain reaction and immunohistochemical staining,which showed a significant upregulation of TSPO in active IBD.Neutrophils from patients with UC and CD exhibited higher TSPO expression,which correlated with increased ROS production and NET formation.In a mouse model of dextran sodium sulfate-induced chronic colitis,TSPO was upregulated in the colonic neutrophils and brain tissues,indicating its systemic involvement.PET-CT imaging showed enhanced TSPO uptake in the inflamed colon and brain regions,particularly in the microglia,highlighting neuroinflammation.CONCLUSION TSPO is significantly upregulated in neutrophils in IBD and contributes to intestinal inflammation.Its elevated expression in gut highlights its potential as a promising therapeutic target for IBD.展开更多
Neurotoxic astrocytes are a promising therapeutic target for the attenuation of cerebral ischemia/reperfusion injury.Low-density lipoprotein receptor,a classic cholesterol regulatory receptor,has been found to inhibit...Neurotoxic astrocytes are a promising therapeutic target for the attenuation of cerebral ischemia/reperfusion injury.Low-density lipoprotein receptor,a classic cholesterol regulatory receptor,has been found to inhibit NLR family pyrin domain containing protein 3(NLRP3)inflammasome activation in neurons following ischemic stroke and to suppress the activation of microglia and astrocytes in individuals with Alzheimer’s disease.However,little is known about the effects of low-density lipoprotein receptor on astrocytic activation in ischemic stroke.To address this issue in the present study,we examined the mechanisms by which low-density lipoprotein receptor regulates astrocytic polarization in ischemic stroke models.First,we examined low-density lipoprotein receptor expression in astrocytes via immunofluorescence staining and western blotting analysis.We observed significant downregulation of low-density lipoprotein receptor following middle cerebral artery occlusion reperfusion and oxygen-glucose deprivation/reoxygenation.Second,we induced the astrocyte-specific overexpression of low-density lipoprotein receptor using astrocyte-specific adeno-associated virus.Low-density lipoprotein receptor overexpression in astrocytes improved neurological outcomes in middle cerebral artery occlusion mice and reversed neurotoxic astrocytes to create a neuroprotective phenotype.Finally,we found that the overexpression of low-density lipoprotein receptor inhibited NLRP3 inflammasome activation in oxygen-glucose deprivation/reoxygenation injured astrocytes and that the addition of nigericin,an NLRP3 agonist,restored the neurotoxic astrocyte phenotype.These findings suggest that low-density lipoprotein receptor could inhibit the NLRP3-meidiated neurotoxic polarization of astrocytes and that increasing low-density lipoprotein receptor in astrocytes might represent a novel strategy for treating cerebral ischemic stroke.展开更多
Sirtuin 2 is a member of the sirtuin family nicotinamide adenine dinucleotide(NAD~+)-dependent deacetylases, known for its regulatory role in different processes, including inflammation. In this context, sirtuin 2 has...Sirtuin 2 is a member of the sirtuin family nicotinamide adenine dinucleotide(NAD~+)-dependent deacetylases, known for its regulatory role in different processes, including inflammation. In this context, sirtuin 2 has been involved in the modulation of key inflammatory signaling pathways and transcription factors by deacetylating specific targets, such as nuclear factor κB and nucleotide-binding oligomerization domain-leucine-rich-repeat and pyrin domain-containing protein 3(NLRP3). However, whether sirtuin 2-mediated pathways induce a pro-or an anti-inflammatory response remains controversial. Sirtuin 2 has been implicated in promoting inflammation in conditions such as asthma and neurodegenerative diseases, suggesting that its inhibition in these conditions could be a potential therapeutic strategy. Conversely, arthritis and type 2 diabetes mellitus studies suggest that sirtuin 2 is essential at the peripheral level and, thus, its inhibition in these pathologies would not be recommended. Overall, the precise role of sirtuin 2 in inflammation appears to be context-dependent, and further investigation is needed to determine the specific molecular mechanisms and downstream targets through which sirtuin 2 influences inflammatory processes in various tissues and pathological conditions. The present review explores the involvement of sirtuin 2 in the inflammation associated with different pathologies to elucidate whether its pharmacological modulation could serve as an effective strategy for treating this prevalent symptom across various diseases.展开更多
Atrial fibrillation(Afib)is a common arrhythmia with significant public health implications,affecting millions of individuals worldwide.Catheter ablation(CA)is an established treatment for drug-resistant Afib,yet recu...Atrial fibrillation(Afib)is a common arrhythmia with significant public health implications,affecting millions of individuals worldwide.Catheter ablation(CA)is an established treatment for drug-resistant Afib,yet recurrence remains a major concern,impacting quality of life in a significant portion of patients.Inflammation plays a critical role in the recurrence of Afib after ablation,with systemic inflammatory markers such as C-reactive protein being linked to higher recurrence rates.In this editorial,we discuss the study by Wang et al,published in the latest issue,which investigates the predictive role of the systemic immune inflammation index(SII)in Afib recurrence following radiofrequency CA.Elevated pre-ablation SII levels are identified as an independent predictor of recurrence,significantly enhancing the predictive power of the APPLE score.Integration of SII improved the APPLE score’s predictive performance,as shown by enhanced area under the curve,net reclassification improvement,and integrated discrimination improvement.This combined model highlights the importance of both structural and inflammatory factors in Afib recurrence,offering a more personalized approach to patient management.Additionally,the affordability and accessibility of SII enhance its practicality in clinical workflows.The study by Wang et al underscores the potential of integrating SII with existing scoring systems to refine risk stratification and optimize treatment strategies.Future research should validate these findings across diverse populations,explore limitations such as the potential influence of comorbidities on SII reliability,and investigate additional biomarkers to enhance predictive accuracy.展开更多
Atrial fibrillation(AF)is the most common arrhythmia in humans,affecting more than 40 million people worldwide.Radiofrequency catheter ablation(RFCA)was first introduced as a treatment for AF by Haïssaguerre M in...Atrial fibrillation(AF)is the most common arrhythmia in humans,affecting more than 40 million people worldwide.Radiofrequency catheter ablation(RFCA)was first introduced as a treatment for AF by Haïssaguerre M in the late 1990s.This procedure quickly became the treatment of choice,especially for symptomatic patients with AF refractory to medication.However,up to 45%of patients may experience AF recurrence within 12 months after RFCA.In this setting,AF recurrence is likely multifactorial,including atrial remodeling,local fibrosis or incomplete ablation due to failure in locating the trigger.Additionally,patients with obesity,sleep apnea,hypertension,or diabetes are at an increased risk of AF recurrence after RFCA.Inflammation is increasingly recognized as a potential key factor in AF recurrence and may arise both from the healing response of heart tissue post-ablation or from chronic low-grade inflammation,as observed in many risk factors.Here,we present an original study by Wang et al,which investigated the combination of the systemic immune-inflammation index-a marker developed to assess overall inflammatory status-and the APPLE score,designed to predict AF recurrence following RFCA.The study found that using both indicators together improved the accuracy of AF recurrence prediction.These findings underscore the significant role of inflammation in cardiovascular disease and demonstrated its impact on AF recurrence after RFCA.Further research is warranted to validate the combined use of these two scores in clinical settings for predicting AF recurrence following catheter ablation.展开更多
Gastric carcinoma is a leading cause of cancer-related mortality worldwide,yet reliable noninvasive biomarkers for its early detection remain limited.As research continues to elucidate the inflammatory underpinnings o...Gastric carcinoma is a leading cause of cancer-related mortality worldwide,yet reliable noninvasive biomarkers for its early detection remain limited.As research continues to elucidate the inflammatory underpinnings of tumor initiation and progression,it has become increasingly clear that pro-inflammatory cytokines may hold promise as diagnostic adjuncts.Serum cytokines such as interleukin(IL)-1β,IL-6,IL-8,and interferon-gamma have been frequently reported as elevated in gastric cancer patients compared to healthy individuals.These molecules,known for their roles in modulating tumor-promoting inflammation,angiogenesis,and immune evasion,may serve as accessible indicators of disease presence or progression.Several studies have shown that individual cytokines,particularly IL-6 and IL-8,can achieve receiver operating characteristic curves and area under the curve values exceeding 0.70,suggesting reasonable diagnostic utility.We assess the comparative utility of individual cytokines versus multiplex panels,evaluate their roles in tumor biology and treatment resistance,and situate these findings within the broader inflammatory biomarker landscape.Limitations of the current literature,including small sample sizes,heterogeneity in study design,and lack of specificity,are critically discussed.We advocate for prospective,multicenter validation studies and highlight the promise of integrating inflammatory cytokine profiling into diagnostic algorithms.Composite cytokine panels may better reflect the complex immunobiology of tumor progression and offer a scalable,accessible adjunct to current gastric cancer screening strategies.展开更多
Deep phenotyping and genetic characterization of individuals are fundamental to assessing the metabolic status and determining nutrition-specific requirements.This study aimed to ascertain the utmost effectiveness of ...Deep phenotyping and genetic characterization of individuals are fundamental to assessing the metabolic status and determining nutrition-specific requirements.This study aimed to ascertain the utmost effectiveness of personalized interventions by aligning dietary adjustments with both the genotype and metabolotype of individuals.Therefore,we assessed here the usefulness of a polygenic score(PGS)characterizing a potential pro-inflammatory profile(PGSi)as a nutrigenetic tool to discern individuals from the Danish PREVENTOMICS cohort that could better respond to precision nutrition(PN)plans,specifically targeted at counteracting the low-grade inflammatory profile typically found in obesity.The cohort followed a PN plan to counteract the pro-inflammatory profile(PNi group)or generic dietary recommendations(Control)for 10 weeks.PGSi was applied for genetic stratification(Low/High).The effects of the intervention on anthropometrics and biomarkers related to inflammatory profile and carbohydrate metabolism were assessed.Around 30%of subjects had a high genetic predisposition to pro-inflammatory status(high-PGSi).These individuals demonstrated the most effective response to the dietary plan,experiencing improved body composition,with significant decreases in body weight(∆:-4.84%;P=0.039)and body fat(∆:-4.86%;P=0.007),and beneficial changes in pro-and anti-inflammatory biomarkers,with significant increases in IL-10(∆:71.3%;P=0.025)and decreases in TNF-α(∆:-3.0%;P=0.048),CRP(∆:-31.1%),ICAM1(∆:-5.8%),and MCP1(∆:-4.2%)circulating levels,compared to low-PGSi individuals.Both phenotypic and genetic stratification contributed to a better understanding of metabolic heterogeneity in response to diet.This approach allows for refinement of the prediction of individual requirements and potentially for better management of obesity.展开更多
Inflammatory bone diseases constitute a category of chronic inflammatory disorders,with the primary pathological characteristic being the impact of chronic inflammation on bone metabolism and remodeling.It leads to pa...Inflammatory bone diseases constitute a category of chronic inflammatory disorders,with the primary pathological characteristic being the impact of chronic inflammation on bone metabolism and remodeling.It leads to pain,spinal joint deformities,and functional impairments.Common clinical types of inflammatory bone diseases include rheumatoid arthritis,ankylosing spondylitis,and osteoarthritis.However,there is a paucity of effective clinical treatments for inflammatory bone diseases,and pharmacological interventions are frequently associated with intolerable side effects.Traditional Chinese medicine(TCM)has a long-standing history and proven efficacy in managing inflammatory bone diseases.In recent years,an increasing number of studies have highlighted the potential of TCM in this context.This article systematically evaluates the application of TCM in treating inflammatory bone diseases,emphasizing the underlying molecular mechanisms of its anti-inflammatory effects.By elucidating the specific targets of TCM in the treatment of rheumatoid arthritis,ankylosing spondylitis,and osteoarthritis,we aim to provide novel insights into the further exploration of TCM’s role in clinical application for inflammatory bone diseases.展开更多
基金Supported by the National Natural Science Foundation of China(No.82388101,No.81930024)the Science and Technology Commission of Shanghai(No.22YS1400400,No.20DZ2270800).
文摘Dear Editor,Idiopathic orbital inflammation(IOI),also known as orbital inflammatory pseudotumor,is a relatively common orbital disorder[1].Its pathogenesis remains unclear,often regarded as a nonspecific immune-mediated response[2].IOI presents with symptoms such as pain,photophobia,proptosis,eyelid swelling,edema,conjunctival congestion,and diplopia,with possible vision loss occurring in some cases.Based on the soft tissue structures involved,IOI can be classified into subtypes such as myositis,optic neuritis,dacryoadenitis,diffuse orbital inflammation,and orbital inflammatory masses[2].
基金supported by grants from the Deutsche Forschungsgemeinschaft(HU 2614/1-1(Project No.462650276))the Fritz Thyssen Foundation(10.21.1.021MN)the Medical faculty of the University of Saarland(HOMFOR2016,HOMFORexzellent2017,HOMFOR2024 Anschubfinanzierung)to WH。
文摘Neuroinflammation,the inflammatory response of the central nervous system(CNS),is a common feature of many neurological disorders such as sepsis-associated encephalopathy(SAE),multiple sclerosis(MS),and Parkinson's disease(PD).Prior studies identified cytokines(e.g.,tumor necrosis factor[TNF],interleukin[IL]-1,and IL-6)delivered by resident glial cells and brain-invading peripheral immune cells as the major contributor to neuroinflammation(Becher et al.,2017).In addition to pro-inflammatory cytokines,elevated levels of extracellular purine molecules such as adenosine triphosphate(ATP)and adenosine can be detected upon any pathological insults(e.g.,injury,ischemia,and hypoxia),contributing to the progression of neurological disorders(Borea et al.,2017).
基金supported by European Union-NextGeneration EU under the Italian University and Research(MUR)National Innovation Ecosystem grant ECS00000041-VITALITY-CUP E13C22001060006(to MdA)。
文摘Stroke is a major cause of death and disability worldwide.It is characterized by a highly interconnected and multiphasic neuropathological cascade of events,in which an intense and protracted inflammatory response plays a crucial role in worsening brain injury.Neuroinflammation,a key player in the pathophysiology of stroke,has a dual role.In the acute phase of stroke,neuroinflammation exacerbates brain injury,contributing to neuronal damage and blood–brain barrier disruption.This aspect of neuroinflammation is associated with poor neurological outcomes.Conversely,in the recovery phase following stroke,neuroinflammation facilitates brain repair processes,including neurogenesis,angiogenesis,and synaptic plasticity.The transition of neuroinflammation from a harmful to a reparative role is not well understood.Therefore,this review seeks to explore the mechanisms underlying this transition,with the goal of informing the development of therapeutic interventions that are both time-and context-specific.This review aims to elucidate the complex and dual role of neuroinflammation in stroke,highlighting the main actors,biomarkers of the disease,and potential therapeutic approaches.
基金supported by the Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior-Brasil(CAPES)[Finance Code 001](to MGS)Conselho Nacional de Desenvolvimento Cientifico e Tecnologico(CNPq)fellowship[research grants 309840/2022-8]。
文摘Neuroinflammation is an inflammatory response in the central nervous system associated with various neurological conditions.The inflammatory process is typically treated with non-steroidal and steroidal anti-inflammatory drugs,which have a range of serious adverse effects.As an alternative,naturally derived molecules such as quercetin and its derivatives show promising anti-inflammatory properties and beneficial effects on various physiological functions.Our objective was to synthesize the evidence on the anti-inflammatory effect of quercetin and its derivatives in in vivo models,in the face of neuroinflammatory insults induced by lipopolysaccharide,through a systematic review and meta-analysis.A search of the preclinical literature was conducted across four databases(Pub Med,Web of Science,Scielo,and Google Scholar).Studies were selected based on inclusion and exclusion criteria,assessed for methodological quality using CAMARADES,and risk of bias using the SYRCLE tool,and data were extracted from the studies.The quantitative assessment of quercetin effects on the expression of pro-inflammatory cytokines and microgliosis was performed through a meta-analysis.A total of 384 potentially relevant articles were identified,of which 11 studies were included in the analysis.The methodological quality was assessed,resulting in an average score of 5.8/10,and the overall risk of bias analysis revealed a lack of methodological clarity in most studies.Furthermore,through the meta-analysis,it was observed that treatment with quercetin statistically reduces pro-inflammatory cytokines,such as tumor necrosis factor alpha,interleukin 6,interleukin 1β(n=89;SMD=–2.00;95%CI:–3.29 to–0.71),and microgliosis(n=33;SMD=–2.56;95%CI:–4.07 to–1.10).In terms of underlying mechanisms,quercetin and its derivatives exhibit antioxidant and anti-apoptotic properties,possibly through the nuclear factor erythroid 2-related factor 2(Nrf2)/HO-1 pathways,increasing the expression of antioxidant enzymes and reducing reactive species,and modulating the caspase pathway,increasing levels of anti-apoptotic proteins and decreasing proapoptotic proteins.Quercetin and its derivatives exhibit highly pleiotropic actions that simultaneously contribute to preventing neuroinflammation.However,despite promising results in animal models,future directions should focus on well-designed clinical studies to assess the safety,bioavailability,and efficacy of quercetin and its derivatives in humans.Additionally,standardization of methods and dosages in studies is crucial to ensure consistency of findings and optimize their application in clinical settings.
基金Supported by the National Natural Science Foundation of China,No.82170406 and No.81970238.
文摘Gastric ulcer(GU)represents a clinically significant manifestation of peptic ulcer disease,driven by a complex interplay of microbial,environmental,and immuneinflammatory factors.A recent cross-sectional study by Shen et al systematically evaluated six complete blood count-derived inflammatory indices:Neutrophil-tolymphocyte ratio,monocyte-to-lymphocyte ratio,platelet-to-lymphocyte ratio,systemic immune-inflammation index,systemic inflammatory response index(SIRI),and aggregate index of systemic inflammation and demonstrated their positive associations with GU prevalence,identifying SIRI as the strongest predictor.This editorial contextualizes these findings within the broader literature,clarifies that these indices reflect systemic rather than GU-specific inflammation,highlights methodological strengths and major limitations,and proposes a conceptual clinical algorithm for integrating SIRI into GU risk assessment.Future multicenter studies incorporating Helicobacter pylori infection,non-steroidal antiinflammatory drug exposure,and prospective design are essential to validate and translate these findings into clinical practice.
基金supported by FWO(Fonds voor Wetenschappelijk Onderzoek),grant number G07562NFWO(to BB)。
文摘Neuroinflammation is a key process in the pathogenesis of various neurodegenerative diseases,such as multiple sclerosis(MS),Alzheimer's disease,and traumatic brain injury.Even for disorders historically unrelated to neuroinflammation,such as Alzheimer's disease,it is now shown to precede pathological protein aggregations.
基金supported by grants from NIH T32(DK007260,to WC)the Steno North American Fellowship awarded by the Novo Nordisk Foundation(NNF23OC0087108,to WC).
文摘The shared links between Alzheimer’s disease and type 2 diabetes mellitus:Alzheimer’s disease(AD)and type 2 diabetes mellitus(T2DM)are two prevalent conditions that come with substantial daily struggles.Emerging evidence highlights that these diseases share similar pathophysiological features,including insulin resistance and chronic inflammation,which contribute to their rapid progression(Chen et al.,2022).Insulin resistance,a hallmark of T2DM,has been suggested to exacerbate neurodegeneration in AD.Similarly,chronic low-grade inflammation in T2DM parallels with neuroinflammation,which is observed in AD,suggesting overlapping pathophysiological mechanisms in T2DM and AD.
文摘AIM:To report and analyze cases of sterile intraocular inflammation(IOI)following intravitreal faricimab injections in patients treated for neovascular age-related macular degeneration(nAMD)and diabetic macular edema(DME).METHODS:This double-center case series included nine eyes of six patients who developed uveitis after faricimab therapy.Comprehensive clinical evaluation was performed,including slit-lamp examination,intraocular pressure(IOP)measurement,fluorescein and indocyanine green angiography(ICGA),and laboratory tests.Inflammatory responses were treated with topical or systemic corticosteroids,and patients were monitored for visual acuity and inflammatory activity.RESULTS:The incidence of IOI was 0.8%per patient(Innsbruck)and 0.23%(Czechia),with inflammation typically occurring between the third and sixth injection(mean interval:10d post-injection).Inflammator y presentations ranged from anterior uveitis to posterior segment involvement.One notable case demonstrated novel choroidal hypofluorescent lesions on angiography,suggesting deeper ocular involvement.The mean patient age was 76y;five of six affected patients were female.All cases responded to local and systemic corticosteroids,with full recovery of initial visual acuity.CONCLUSION:Sterile IOI after faricimab appears to be a rare but relevant adverse event.Although the incidence falls within expected ranges for anti-vascular endothelial growth factor(anti-VEGF)agents,the observed choroidal involvement represents a potentially new safety signal.Prompt diagnosis and corticosteroid therapy are effective in all cases.Our findings support the need for vigilant post-marketing surveillance and further studies to better understand the underlying mechanisms and risk factors of faricimab-associated inflammation.
基金Supported by The National Natural Science Foundation of China(No.82101180)the Fund for Beijing Science&Technology Development of TCM(No.BJZYYB-2023-17)the Beijing Municipal Natural Science Foundation grant(No.7252093).
文摘AIM:To define the prevalence and anatomical patterns of paranasal sinus abnormalities(PSA)in thyroid-associated ophthalmopathy(TAO)and to test the hypothesis that TAO is partially driven by contiguous orbital inflammation rather than systemic autoimmunity or generalized orbital pressure.METHODS:Data included ophthalmic assessments and a panel of thyroid function and autoimmune biomarkers.Blinded radiological analysis of orbital computed tomography(CT)scans was performed to quantify sinus abnormalities and extraocular muscles(EOMs)involvement.Patients were categorized into two groups based on CT findings,those with no radiological evidence of sinus abnormalities(non-PSA control group)and those with identifiable PSA.Furthermore,ethmoid sinus mucosal biopsies from a subset of TAO patients and noninflammatory controls were subjected to histopathological analysis.RESULTS:Totally 121 TAO patients(mean age 42.4±12.8y,range 10-78y),male:female=42:79,were included.PSA was identified in 44.6%(n=54)of patients,with a distribution anatomically restricted to the maxillary(50.0%isolated)and ethmoid sinuses(18.5%isolated;29.6%combined).Compared to the non-PSA group(n=67),patients with PSA were significantly older(45.1±11.8 vs 40.3±13.2y;P=0.040)and were more likely to be male(55.6%vs 17.9%;P<0.001).They also had significantly higher proptosis(22.1±3.2 vs 20.7±2.9 mm;P<0.001).Medial/inferior rectus involvement was most frequent(88.4%vs 89.3%).Histopathological analysis of sinus mucosa from PSA patients provided direct evidence of pathology,revealing a dense,chronic lymphoplasmacytic infiltrate and submucosal edema,validating the radiological findings as a true inflammatory process.No significant correlation was found with systemic autoimmune markers,including thyroid-stimulating hormone(TSH)receptor antibodies(TRAb,median 4.86 vs 2.71 IU/L,P=0.104).CONCLUSION:TAO is associated with a high prevalence of PSA in a pattern consistent with the orbital anatomy.The correlation with ipsilateral muscle thickening combined with the lack of association with proptosis laterality or systemic biomarkers lend strong support to a model of contiguous inflammation over systemic autoimmunity,a hypothesis that warrants further validation through longitudinal and mechanistic studies.
文摘Obesity is widely recognized as a global epidemic,primarily driven by an imbalance between energy expenditure and caloric intake associated with a sedentary lifestyle.Diets high in carbohydrates and saturated fats,particularly palmitic acid,are potent inducers of chronic low-grade inflammation,largely due to disruptions in glucose metabolism and the onset of insulin resistance(Qiu et al.,2022).While many organs are affected,the brain,specifically the hypothalamus,is among the first to exhibit inflammation in response to an unhealthy diet,suggesting that obesity may,in fact,be a brain-centered disease with neuroinflammation as a central factor(Thaler et al., 2012).
基金supported by the National Natural Science Foundation of China,Nos. 32260196 (to JY), 81860646 (to ZY) and 31860274 (to JY)a grant from Yunnan Department of Science and Technology,Nos. 202101AT070251 (to JY), 202201AS070084 (to ZY), 202301AY070001-239 (to JY), 202101AZ070001-012, and 2019FI016 (to ZY)。
文摘Studies have shown that chitosan protects against neurodegenerative diseases. However, the precise mechanism remains poorly understood. In this study, we administered chitosan intragastrically to an MPTP-induced mouse model of Parkinson's disease and found that it effectively reduced dopamine neuron injury, neurotransmitter dopamine release, and motor symptoms. These neuroprotective effects of chitosan were related to bacterial metabolites, specifically shortchain fatty acids, and chitosan administration altered intestinal microbial diversity and decreased short-chain fatty acid production in the gut. Furthermore, chitosan effectively reduced damage to the intestinal barrier and the blood–brain barrier. Finally, we demonstrated that chitosan improved intestinal barrier function and alleviated inflammation in both the peripheral nervous system and the central nervous system by reducing acetate levels. Based on these findings, we suggest a molecular mechanism by which chitosan decreases inflammation through reducing acetate levels and repairing the intestinal and blood–brain barriers, thereby alleviating symptoms of Parkinson's disease.
文摘BACKGROUND Gastric ulcer(GU),a common gastrointestinal condition,is influenced by multiple factors,particularly inflammatory and immune responses.Complete blood count(CBC)-derived inflammatory biomarkers represent a novel indicator of systemic inflammation and immune status;however,their association with GU remains unclear.AIM To investigate the association between CBC-derived inflammatory markers and GU.METHODS The study sample included individuals admitted to the Gastroenterology Unit of the Second Affiliated Hospital of Nanchang University from 2023 to 2024.We explored how each CBC-based inflammation indicator correlated with GU occurrence through logistic models,and assessed their predictive ability using receiver operating characteristic curve analysis.Additionally,we applied the least absolute shrinkage and selection operator method along with stepwise regression techniques to determine which inflammatory indicators were most significantly linked to GU.RESULTS Higher levels of log2 neutrophil-to-lymphocyte ratio,log2 monocyte-to-lymphocyte ratio,log2 systemic immuneinflammation index,log2 systemic inflammatory response index(SIRI),and log2 aggregate index of systemic inflammation were significantly associated with increased GU prevalence across all models,while log2 platelet-tolymphocyte ratio was significant only in the fully adjusted model.SIRI demonstrated the highest discriminative ability,with an area under the curve of 0.868.CONCLUSION Hematological indicators derived from CBC tests show a significant correlation with the prevalence of GU.Among them,SIRI demonstrated the most prominent association.These markers could act as practical tools in recognizing individuals more likely to develop GU.
基金Supported by National Natural Science Foundation of China,No.82300604Science and Technology Innovation Action Plan Star Project Application Guide/Star Project Incubation(Yangfan Special Program)of Shanghai,No.24YF2727600.
文摘BACKGROUND Inflammatory bowel diseases(IBD),including ulcerative colitis(UC)and Crohn’s disease(CD),are chronic gastrointestinal disorders with an increasing global prevalence and significant healthcare impact.The exact etiology of this condition remains unclear.Neutrophils play a critical role in IBD pathogenesis.Translocator protein(TSPO),a mitochondrial protein linked to immune responses,has demonstrated potential as an inflammatory marker.However,its role in IBD remains underexplored.AIM To investigate the role of TSPO in IBD pathogenesis,particularly in neutrophils.METHODS Bioinformatics analyses of Gene Expression Omnibus datasets(GE75214,GSE94648,GSE156776)assessed TSPO expression in IBD patients.TSPO expression was evaluated in human IBD samples,neutrophiles and a chronic colitis mouse model.Neutrophil function was examined in 18 samples using reactive oxygen species(ROS)production and neutrophil extracellular trap(NET)formation assays.Positron emission tomography-computed tomography(PET-CT)imaging and histology from 12 mice revealed TSPO expression in colitis.PET-CT and immunofluorescence staining assessed TSPO expression in brain under neuroinflammation condition.RESULTS Bioinformatics analysis revealed elevated TSPO expression in the intestinal mucosa and peripheral blood of patients with IBD,especially in neutrophils.This was confirmed by quantitative real-time polymerase chain reaction and immunohistochemical staining,which showed a significant upregulation of TSPO in active IBD.Neutrophils from patients with UC and CD exhibited higher TSPO expression,which correlated with increased ROS production and NET formation.In a mouse model of dextran sodium sulfate-induced chronic colitis,TSPO was upregulated in the colonic neutrophils and brain tissues,indicating its systemic involvement.PET-CT imaging showed enhanced TSPO uptake in the inflamed colon and brain regions,particularly in the microglia,highlighting neuroinflammation.CONCLUSION TSPO is significantly upregulated in neutrophils in IBD and contributes to intestinal inflammation.Its elevated expression in gut highlights its potential as a promising therapeutic target for IBD.
基金supported by the National Natural Science Foundation of China,No.82201460(to YH)Nanjing Medical University Science and Technology Development Fund,No.NMUB20210202(to YH).
文摘Neurotoxic astrocytes are a promising therapeutic target for the attenuation of cerebral ischemia/reperfusion injury.Low-density lipoprotein receptor,a classic cholesterol regulatory receptor,has been found to inhibit NLR family pyrin domain containing protein 3(NLRP3)inflammasome activation in neurons following ischemic stroke and to suppress the activation of microglia and astrocytes in individuals with Alzheimer’s disease.However,little is known about the effects of low-density lipoprotein receptor on astrocytic activation in ischemic stroke.To address this issue in the present study,we examined the mechanisms by which low-density lipoprotein receptor regulates astrocytic polarization in ischemic stroke models.First,we examined low-density lipoprotein receptor expression in astrocytes via immunofluorescence staining and western blotting analysis.We observed significant downregulation of low-density lipoprotein receptor following middle cerebral artery occlusion reperfusion and oxygen-glucose deprivation/reoxygenation.Second,we induced the astrocyte-specific overexpression of low-density lipoprotein receptor using astrocyte-specific adeno-associated virus.Low-density lipoprotein receptor overexpression in astrocytes improved neurological outcomes in middle cerebral artery occlusion mice and reversed neurotoxic astrocytes to create a neuroprotective phenotype.Finally,we found that the overexpression of low-density lipoprotein receptor inhibited NLRP3 inflammasome activation in oxygen-glucose deprivation/reoxygenation injured astrocytes and that the addition of nigericin,an NLRP3 agonist,restored the neurotoxic astrocyte phenotype.These findings suggest that low-density lipoprotein receptor could inhibit the NLRP3-meidiated neurotoxic polarization of astrocytes and that increasing low-density lipoprotein receptor in astrocytes might represent a novel strategy for treating cerebral ischemic stroke.
基金funded by FEDER/Ministerio de Ciencia,Innovación y Universidades Agencia Estatal de Investigación/Project(PID2020-119729GB-100,REF/AEI/10.13039/501100011033)(to EP)a predoctoral fellowship from the Spanish Ministry of Universities(FPU)and Amigos de la Universidad de Navarra(to NSS)“Programa MRR Investigo 2023”(to MGB and MMD)。
文摘Sirtuin 2 is a member of the sirtuin family nicotinamide adenine dinucleotide(NAD~+)-dependent deacetylases, known for its regulatory role in different processes, including inflammation. In this context, sirtuin 2 has been involved in the modulation of key inflammatory signaling pathways and transcription factors by deacetylating specific targets, such as nuclear factor κB and nucleotide-binding oligomerization domain-leucine-rich-repeat and pyrin domain-containing protein 3(NLRP3). However, whether sirtuin 2-mediated pathways induce a pro-or an anti-inflammatory response remains controversial. Sirtuin 2 has been implicated in promoting inflammation in conditions such as asthma and neurodegenerative diseases, suggesting that its inhibition in these conditions could be a potential therapeutic strategy. Conversely, arthritis and type 2 diabetes mellitus studies suggest that sirtuin 2 is essential at the peripheral level and, thus, its inhibition in these pathologies would not be recommended. Overall, the precise role of sirtuin 2 in inflammation appears to be context-dependent, and further investigation is needed to determine the specific molecular mechanisms and downstream targets through which sirtuin 2 influences inflammatory processes in various tissues and pathological conditions. The present review explores the involvement of sirtuin 2 in the inflammation associated with different pathologies to elucidate whether its pharmacological modulation could serve as an effective strategy for treating this prevalent symptom across various diseases.
文摘Atrial fibrillation(Afib)is a common arrhythmia with significant public health implications,affecting millions of individuals worldwide.Catheter ablation(CA)is an established treatment for drug-resistant Afib,yet recurrence remains a major concern,impacting quality of life in a significant portion of patients.Inflammation plays a critical role in the recurrence of Afib after ablation,with systemic inflammatory markers such as C-reactive protein being linked to higher recurrence rates.In this editorial,we discuss the study by Wang et al,published in the latest issue,which investigates the predictive role of the systemic immune inflammation index(SII)in Afib recurrence following radiofrequency CA.Elevated pre-ablation SII levels are identified as an independent predictor of recurrence,significantly enhancing the predictive power of the APPLE score.Integration of SII improved the APPLE score’s predictive performance,as shown by enhanced area under the curve,net reclassification improvement,and integrated discrimination improvement.This combined model highlights the importance of both structural and inflammatory factors in Afib recurrence,offering a more personalized approach to patient management.Additionally,the affordability and accessibility of SII enhance its practicality in clinical workflows.The study by Wang et al underscores the potential of integrating SII with existing scoring systems to refine risk stratification and optimize treatment strategies.Future research should validate these findings across diverse populations,explore limitations such as the potential influence of comorbidities on SII reliability,and investigate additional biomarkers to enhance predictive accuracy.
文摘Atrial fibrillation(AF)is the most common arrhythmia in humans,affecting more than 40 million people worldwide.Radiofrequency catheter ablation(RFCA)was first introduced as a treatment for AF by Haïssaguerre M in the late 1990s.This procedure quickly became the treatment of choice,especially for symptomatic patients with AF refractory to medication.However,up to 45%of patients may experience AF recurrence within 12 months after RFCA.In this setting,AF recurrence is likely multifactorial,including atrial remodeling,local fibrosis or incomplete ablation due to failure in locating the trigger.Additionally,patients with obesity,sleep apnea,hypertension,or diabetes are at an increased risk of AF recurrence after RFCA.Inflammation is increasingly recognized as a potential key factor in AF recurrence and may arise both from the healing response of heart tissue post-ablation or from chronic low-grade inflammation,as observed in many risk factors.Here,we present an original study by Wang et al,which investigated the combination of the systemic immune-inflammation index-a marker developed to assess overall inflammatory status-and the APPLE score,designed to predict AF recurrence following RFCA.The study found that using both indicators together improved the accuracy of AF recurrence prediction.These findings underscore the significant role of inflammation in cardiovascular disease and demonstrated its impact on AF recurrence after RFCA.Further research is warranted to validate the combined use of these two scores in clinical settings for predicting AF recurrence following catheter ablation.
文摘Gastric carcinoma is a leading cause of cancer-related mortality worldwide,yet reliable noninvasive biomarkers for its early detection remain limited.As research continues to elucidate the inflammatory underpinnings of tumor initiation and progression,it has become increasingly clear that pro-inflammatory cytokines may hold promise as diagnostic adjuncts.Serum cytokines such as interleukin(IL)-1β,IL-6,IL-8,and interferon-gamma have been frequently reported as elevated in gastric cancer patients compared to healthy individuals.These molecules,known for their roles in modulating tumor-promoting inflammation,angiogenesis,and immune evasion,may serve as accessible indicators of disease presence or progression.Several studies have shown that individual cytokines,particularly IL-6 and IL-8,can achieve receiver operating characteristic curves and area under the curve values exceeding 0.70,suggesting reasonable diagnostic utility.We assess the comparative utility of individual cytokines versus multiplex panels,evaluate their roles in tumor biology and treatment resistance,and situate these findings within the broader inflammatory biomarker landscape.Limitations of the current literature,including small sample sizes,heterogeneity in study design,and lack of specificity,are critically discussed.We advocate for prospective,multicenter validation studies and highlight the promise of integrating inflammatory cytokine profiling into diagnostic algorithms.Composite cytokine panels may better reflect the complex immunobiology of tumor progression and offer a scalable,accessible adjunct to current gastric cancer screening strategies.
基金supported through the European Union’s Horizon 2020 Research and Innovation Program(818318)。
文摘Deep phenotyping and genetic characterization of individuals are fundamental to assessing the metabolic status and determining nutrition-specific requirements.This study aimed to ascertain the utmost effectiveness of personalized interventions by aligning dietary adjustments with both the genotype and metabolotype of individuals.Therefore,we assessed here the usefulness of a polygenic score(PGS)characterizing a potential pro-inflammatory profile(PGSi)as a nutrigenetic tool to discern individuals from the Danish PREVENTOMICS cohort that could better respond to precision nutrition(PN)plans,specifically targeted at counteracting the low-grade inflammatory profile typically found in obesity.The cohort followed a PN plan to counteract the pro-inflammatory profile(PNi group)or generic dietary recommendations(Control)for 10 weeks.PGSi was applied for genetic stratification(Low/High).The effects of the intervention on anthropometrics and biomarkers related to inflammatory profile and carbohydrate metabolism were assessed.Around 30%of subjects had a high genetic predisposition to pro-inflammatory status(high-PGSi).These individuals demonstrated the most effective response to the dietary plan,experiencing improved body composition,with significant decreases in body weight(∆:-4.84%;P=0.039)and body fat(∆:-4.86%;P=0.007),and beneficial changes in pro-and anti-inflammatory biomarkers,with significant increases in IL-10(∆:71.3%;P=0.025)and decreases in TNF-α(∆:-3.0%;P=0.048),CRP(∆:-31.1%),ICAM1(∆:-5.8%),and MCP1(∆:-4.2%)circulating levels,compared to low-PGSi individuals.Both phenotypic and genetic stratification contributed to a better understanding of metabolic heterogeneity in response to diet.This approach allows for refinement of the prediction of individual requirements and potentially for better management of obesity.
文摘Inflammatory bone diseases constitute a category of chronic inflammatory disorders,with the primary pathological characteristic being the impact of chronic inflammation on bone metabolism and remodeling.It leads to pain,spinal joint deformities,and functional impairments.Common clinical types of inflammatory bone diseases include rheumatoid arthritis,ankylosing spondylitis,and osteoarthritis.However,there is a paucity of effective clinical treatments for inflammatory bone diseases,and pharmacological interventions are frequently associated with intolerable side effects.Traditional Chinese medicine(TCM)has a long-standing history and proven efficacy in managing inflammatory bone diseases.In recent years,an increasing number of studies have highlighted the potential of TCM in this context.This article systematically evaluates the application of TCM in treating inflammatory bone diseases,emphasizing the underlying molecular mechanisms of its anti-inflammatory effects.By elucidating the specific targets of TCM in the treatment of rheumatoid arthritis,ankylosing spondylitis,and osteoarthritis,we aim to provide novel insights into the further exploration of TCM’s role in clinical application for inflammatory bone diseases.