BACKGROUND Cumulative evidence suggests that the aberrant immune responses in acquired aplastic anemia(AA) are sustained by active chronic infections in genetically susceptible individuals. Recently, the constant sour...BACKGROUND Cumulative evidence suggests that the aberrant immune responses in acquired aplastic anemia(AA) are sustained by active chronic infections in genetically susceptible individuals. Recently, the constant source to trigger and sustain the pathophysiology has been proposed to come from the altered gut microbiota and chronic intestinal inflammation. In this case, our serendipitous finding provides convincing evidence that the persistently dysregulated autoimmunity may be generated, at least in a significant proposition of AA patients, by the altered gut microbiota and compromised intestinal epithelium.CASE SUMMARY A 30-year-old Chinese male patient with refractory severe AA experienced a 3-month-long febrile episode, and his fever was refractory to many kinds of injected broad-spectrum antibiotics. When presenting with abdominal cramps, he was prescribed oral mannitol and gentamycin to get rid of the gut infection. This treatment resulted in a quick resolution of the fever. Unanticipatedly, it also produced an excellent hematological response. He had undergone three episodes of recurrence within the one-year treatment, with each recurrence occurring 7-8 wk from the gastrointestinal inflammation eliminating preparations. However,subsequent treatments were able to produce subsequent remissions and consecutive treatments were successful in achieving durative hematological improvements, strongly indicating an etiological association between chronic gut inflammation and the development of AA. Interestingly, comorbid diseases superimposed on this patient(namely, psychiatric disorders, hypertension,insulin resistance, and renal dysfunction) were ameliorated together with the hematological improvements.CONCLUSION Chronic gut inflammation may be responsible for AA pathogenesis. The comorbidities and AA may share a common etiological association.展开更多
Gut inflammation is a challenging concern in humans and animals,which disturbs normal growth and leads to severe bowel diseases.Short chain fatty acids(SCFA)are the gut microbiota metabolites produced from fermentatio...Gut inflammation is a challenging concern in humans and animals,which disturbs normal growth and leads to severe bowel diseases.Short chain fatty acids(SCFA)are the gut microbiota metabolites produced from fermentation of non-digestible carbohydrates,and have been reported to modulate gut inflammation.SCFA have been implicated as the potential therapeutic bioactive molecules for gut inflammatory diseases,and could be an alternative to antibiotic growth promoters(AGP).In this review,the existing knowledge about the types of SCFA,the related gut microbes producing SCFA,the roles of SCFA in maintaining gut homeostasis,and how SCFA modulate gut inflammation is summarized.The therapeutic application of SCFA in the treatment of inflammatory bowel disease(IBD)is also highlighted展开更多
Parkinson's disease has long been considered a disorder that primarily affects the brain,as it is defined by the dopaminergic neurodegeneration in the substantia nigra and the brain accumulation of Lewy bodies con...Parkinson's disease has long been considered a disorder that primarily affects the brain,as it is defined by the dopaminergic neurodegeneration in the substantia nigra and the brain accumulation of Lewy bodies containingα-synuclein protein.In recent decades,however,accumulating research has revealed that Parkinson's disease also involves the gut and uncovered an intimate and important bidirectional link between the brain and the gut,called the“gut–brain axis.”Numerous clinical studies demonstrate that gut dysfunction frequently precedes motor symptoms in Parkinson's disease patients,with findings including impaired intestinal permeability,heightened inflammation,and distinct gut microbiome profiles and metabolites.Furthermore,α-synuclein deposition has been consistently observed in the gut of Parkinson's disease patients,suggesting a potential role in disease initiation.Importantly,individuals with vagotomy have a reduced Parkinson's disease risk.From these observations,researchers have hypothesized thatα-synuclein accumulation may initiate in the gut and subsequently propagate to the central dopaminergic neurons through the gut–brain axis,leading to Parkinson's disease.This review comprehensively examines the gut's involvement in Parkinson's disease,focusing on the concept of a gut-origin for the disease.We also examine the interplay between altered gut-related factors and the accumulation of pathologicalα-synuclein in the gut of Parkinson's disease patients.Given the accessibility of the gut to both dietary and pharmacological interventions,targeting gut-localizedα-synuclein represents a promising avenue for developing effective Parkinson's disease therapies.展开更多
Growing evidence suggests the implication of the gut microbiota in various facets of health and disease. In this review, the focus is put on microbiota-host molecular cross-talk at the gut epithelial level with specia...Growing evidence suggests the implication of the gut microbiota in various facets of health and disease. In this review, the focus is put on microbiota-host molecular cross-talk at the gut epithelial level with special emphasis on two defense systems： intestinal alkaline phosphatase（IAP） and inducible heat shock proteins（iHSPs）. Both IAP and iHSPs are induced by various microbial structural components（e.g. lipopolysaccharide, flagellin, CpG DNA motifs）,metabolites（e.g. n-butyrate） or secreted signal molecules（e.g., toxins, various peptides, polyphosphate）. IAP is produced in the small intestine and secreted into the lumen and in the interior milieu. It detoxifies microbial components by dephosphorylation and, therefore, down-regulates microbe-induced inflammation mainly by inhibiting NF-κB pro-inflammatory pathway in enterocytes. IAP gene expression and enzyme activity are influenced by the gut microbiota. Conversely, IAP controls gut microbiota composition both directly, and indirectly though the detoxification of pro-inflammatory free luminal adenosine triphosphate and inflammation inhibition. Inducible HSPs are expressed by gut epithelial cells in proportion to the microbial load along the gastro-intestinal tract. They are also induced by various microbial components, metabolites and secreted molecules. Whether iHSPs contribute to shape the gut microbiota is presently unknown. Both systems display strong anti-inflammatory and anti-oxidant properties that are protective to the gut and the host. Importantly, epithelial gene expressions and protein concentrations of IAP and iHSPs can be stimulated by probiotics, prebiotics and a large variety of dietary components, including macronutrients（protein and amino acids, especially L-glutamine, fat, fiber）, and specific minerals（e.g. calcium）and vitamins（e.g. vitamins K1 and K2）. Some food components（e.g. lectins, soybean proteins, various polyphenols） may inhibit or disturb these systems. The general cel ular and molecular mechanisms involved in the microbiota-host epithelial crosstalk and subsequent gut protection through IAP and iHSPs are reviewed along with their nutritional modulation.Special emphasis is also given to the pig, an economically important species and valuable biomedical model.展开更多
We previously reported a serendipitous finding from a patient with refractory severe aplastic anemia who had gotten an unexpected hematological response to treatment with gut-cleansing preparations(GCPs).This patient ...We previously reported a serendipitous finding from a patient with refractory severe aplastic anemia who had gotten an unexpected hematological response to treatment with gut-cleansing preparations(GCPs).This patient experienced three recurrences over the ensuing one year of intermittent GCP treatments,with each recurrence occurring 7-8 wk from a GCP.After his third recurrence,he was prescribed successive treatment with rifampicin,berberine,and monthly administered GCP for 4 mo,and he developed an erythroid proliferative neoplasma and an overwhelming enteropathy,and eventually died of septic shock.Laboratory investigations had validated the resolution of myelosuppression and the appearance of malignant clonal hematopoiesis.From the treatment process and laboratory investigations,it is reasonably inferred that the engagement of gut inflammation is critically required in sustaining the overall pathophysiology of acquired aplastic anemia probably by creating a chronic inflammatory state.Incorporation of rifampicin,berberine,and monthly GCP into cyclosporine can enhance the immunosuppressive effect.In a subgroup of acquired aplastic anemia patients whose pathogenesis is associated with genotoxic exposure,the suppressed normal hematopoiesis may result from the bystander insult that is mediated by the soluble inflammatory cytokines generated in response to the immunogenic products of damaged hematopoietic cells in the context of chronic inflammatory state and may offer a protective antineoplastic mechanism against malignant proliferation.展开更多
Background Zinc glycine chelate(Zn-Gly)has anti-inflammation and growth-promoting properties;however,the mechanism of Zn-Gly contribution to gut barrier function in Cherry Valley ducks during intestinal inflammation i...Background Zinc glycine chelate(Zn-Gly)has anti-inflammation and growth-promoting properties;however,the mechanism of Zn-Gly contribution to gut barrier function in Cherry Valley ducks during intestinal inflammation is unknown.Three-hundred 1-day-old ducks were divided into 5 groups(6 replicates and 10 ducks per replicate)in a completely randomized design:the control and dextran sulfate sodium(DSS)groups were fed a corn-soybean meal basal diet,and experimental groups received supplements of 70,120 or 170 mg/kg Zn in form of Zn-Gly.The DSS and treatment groups were given 2 mL of 0.45 g/mL DSS daily during d 15–21,and the control group received normal saline.The experiment lasted 21 d.Results Compared with DSS group,70,120 and 170 mg/kg Zn significantly increased body weight(BW),villus height and the ratio of villus to crypt,and significantly decreased the crypt depth of jejunum at 21 d.The number of goblet cells in jejunal villi in the Zn-Gly group was significantly increased by periodic acid-Schiff staining.Compared with control,the content of intestinal permeability marker D-lactic acid(D-LA)and fluxes of fluorescein isothiocyanate(FITC-D)in plasma of DSS group significantly increased,and 170 mg/kg Zn supplementation significantly decreased the D-LA content and FITC-D fluxes.Compared with control,contents of plasma,jejunum endotoxin and jejunum pro-inflammatory factors IL-1β,IL-6 and TNF-αwere significantly increased in DSS group,and were significantly decreased by 170 mg/kg Zn supplementation.Dietary Zn significantly increased the contents of anti-inflammatory factors IL-10,IL-22 and sIgA and IgG in jejunum.Real-time PCR and Western blot results showed that 170 mg/kg Zn supplementation significantly increased mRNA expression levels of CLDN-1 and expression of OCLN protein in jejunum,and decreased gene and protein expression of CLDN-2 compared with DSS group.The 120 mg/kg Zn significantly promoted the expressions of IL-22 and IgA.Dietary Zn-Gly supplementation significantly decreased pro-inflammatory genes IL-8 and TNF-αexpression levels and TNF-αprotein expression in jejunum.Additionally,Zn significantly reduced the gene and protein expression of TLR4,MYD88 and NF-κB p65.Conclusions Zn-Gly improved duck BW and alleviated intestinal injury by regulating intestinal morphology,barrier function and gut inflammation-related signal pathways TLR4/MYD88/NF-κB p65.展开更多
The gut microbiome plays a key role in the pathogenesis and disease activity of inflammatory bowel disease(IBD).While research has focused on the bacterial microbiome,recent studies have shifted towards host genetics ...The gut microbiome plays a key role in the pathogenesis and disease activity of inflammatory bowel disease(IBD).While research has focused on the bacterial microbiome,recent studies have shifted towards host genetics and host-fungal interactions.The mycobiota is a vital component of the gastrointestinal microbial community and plays a significant role in immune regulation.Among fungi,Candida species,particularly Candida albicans(C.albicans),have been extensively studied due to their dual role as gut commensals and invasive pathogens.Recent findings indicate that various strains of C.albicans exhibit consid-erable differences in virulence factors,impacting IBD's pathophysiology.Intestinal fungal dysbiosis and antifungal mucosal immunity may be associated to IBD,especially Crohn's disease(CD).This article discusses intestinal fungal dysbiosis and antifungal immunity in healthy individuals and CD patients.It discusses factors influencing the mycobiome's role in IBD pathogenesis and highlights significant contributions from the scientific community aimed at enhancing understanding of the mycobiome and encouraging further research and targeted intervention studies on specific fungal populations.Our article also provided insights into a recent study by Wu et al in the World Journal of Gastroenterology regarding the role of the gut microbiota in the pathogenesis of CD.展开更多
Recently, the increasing number of patients worldwide who are sensitive to dietary gluten without evidence of celiac disease or wheat allergy has contributed to the identification of a new gluten-related syndrome defi...Recently, the increasing number of patients worldwide who are sensitive to dietary gluten without evidence of celiac disease or wheat allergy has contributed to the identification of a new gluten-related syndrome defined as non-celiac gluten sensitivity. Our knowledge regarding this syndrome is still lacking, and many aspects of this syndrome remain unknown. Its pathogenesis is heterogeneous, with a recognized pivotal role for innate immunity; many other factors also contribute, inctuding tow-grade intestinal inflammation, increased intestinal barrier function and changes in the intestinal microbiota. Gluten and other wheat proteins, such as amylase trypsin inhibitors, are the primary triggers of this syndrome, but it has also been hypothesized that a diet rich in fermentable monosaccharides and polyols may elicit its functional gastrointestinal symptoms. The epidemiology of this condition is far from established; its prevalence in the general population is highly variable, ranging from 0.63% to 6%. From a clinical point of view, non-celiac gluten sensitivity is characterized by a wide array of gastrointestinal and extraintestinal symptoms that occur shortly after the ingestion of gluten and improve or disappear when gluten is withdrawn from the diet. These symptoms recur when gluten is reintroduced. Because diagnostic biomarkers have not yet been identified, a double-blind placebo-controlled gluten challenge is currently the diagnostic method with the highest accuracy. Future research is needed to generate more knowledge regarding non-celiac gluten sensitivity, a condition that has global acceptance but has only a few certainties and many unresolved issues.展开更多
Importance:The cause of the hepatic dysfunction that commonly accompanies Kawasaki disease(KD)remains unclear.Objective:We tried to clarify the cause of the hepatic dysfunction.Methods:A total of 381 consecutive patie...Importance:The cause of the hepatic dysfunction that commonly accompanies Kawasaki disease(KD)remains unclear.Objective:We tried to clarify the cause of the hepatic dysfunction.Methods:A total of 381 consecutive patients with acute KD,who had undergone inpatient treatment with intravenous immunoglobulin until the 7th day of illness,were divided into a group of 199 patients with an alanine aminotransferase(ALT)level≥40 IU/L on admission(group I),a group of 52 patients with an ALT level≥40 IU/L at some point after admission(group II),and a group of 130 patients with ALT levels consistently<40 IU/L throughout hospitalization(group III).Aspartate aminotransferase(AST),ALT,total bilirubin(T-Bil),and C-reactive protein(CRP)levels were analyzed over time,and time-courses were compared.results:In the initial stage of illness,in group I,AST,ALT,T-Bil peaked on days 1-3,and AST tended to improve significantly on the 4th day(P<0.001).T-Bil improved on day 5(P<0.01),and ALT improved significantly on day 6(P<0.001).CRP increased every day up to day 6(P<0.001).In group II,AST and ALT increased after admission,and thereafter CRP increased,then decreased.The frequency of use of aspirin and aspirin doses did not differ significantly in the three groups.Interpretation:Recovery from liver dysfunction occurred in the initial stage of illness in group I-within the period of CRP exacerbation,which is an indicator of systemic inflammation.展开更多
文摘BACKGROUND Cumulative evidence suggests that the aberrant immune responses in acquired aplastic anemia(AA) are sustained by active chronic infections in genetically susceptible individuals. Recently, the constant source to trigger and sustain the pathophysiology has been proposed to come from the altered gut microbiota and chronic intestinal inflammation. In this case, our serendipitous finding provides convincing evidence that the persistently dysregulated autoimmunity may be generated, at least in a significant proposition of AA patients, by the altered gut microbiota and compromised intestinal epithelium.CASE SUMMARY A 30-year-old Chinese male patient with refractory severe AA experienced a 3-month-long febrile episode, and his fever was refractory to many kinds of injected broad-spectrum antibiotics. When presenting with abdominal cramps, he was prescribed oral mannitol and gentamycin to get rid of the gut infection. This treatment resulted in a quick resolution of the fever. Unanticipatedly, it also produced an excellent hematological response. He had undergone three episodes of recurrence within the one-year treatment, with each recurrence occurring 7-8 wk from the gastrointestinal inflammation eliminating preparations. However,subsequent treatments were able to produce subsequent remissions and consecutive treatments were successful in achieving durative hematological improvements, strongly indicating an etiological association between chronic gut inflammation and the development of AA. Interestingly, comorbid diseases superimposed on this patient(namely, psychiatric disorders, hypertension,insulin resistance, and renal dysfunction) were ameliorated together with the hematological improvements.CONCLUSION Chronic gut inflammation may be responsible for AA pathogenesis. The comorbidities and AA may share a common etiological association.
基金The National Key Research and Development Program of China(2017YFE0113700)the Hubei Provincial Natural Science Foundation of China(2017CFB514)the National Natural Science Foundation of China(30800808).
文摘Gut inflammation is a challenging concern in humans and animals,which disturbs normal growth and leads to severe bowel diseases.Short chain fatty acids(SCFA)are the gut microbiota metabolites produced from fermentation of non-digestible carbohydrates,and have been reported to modulate gut inflammation.SCFA have been implicated as the potential therapeutic bioactive molecules for gut inflammatory diseases,and could be an alternative to antibiotic growth promoters(AGP).In this review,the existing knowledge about the types of SCFA,the related gut microbes producing SCFA,the roles of SCFA in maintaining gut homeostasis,and how SCFA modulate gut inflammation is summarized.The therapeutic application of SCFA in the treatment of inflammatory bowel disease(IBD)is also highlighted
基金supported by the National Research Foundation(NRF)of Korea(2022R1C1C1005741 and RS-2023-00217595)。
文摘Parkinson's disease has long been considered a disorder that primarily affects the brain,as it is defined by the dopaminergic neurodegeneration in the substantia nigra and the brain accumulation of Lewy bodies containingα-synuclein protein.In recent decades,however,accumulating research has revealed that Parkinson's disease also involves the gut and uncovered an intimate and important bidirectional link between the brain and the gut,called the“gut–brain axis.”Numerous clinical studies demonstrate that gut dysfunction frequently precedes motor symptoms in Parkinson's disease patients,with findings including impaired intestinal permeability,heightened inflammation,and distinct gut microbiome profiles and metabolites.Furthermore,α-synuclein deposition has been consistently observed in the gut of Parkinson's disease patients,suggesting a potential role in disease initiation.Importantly,individuals with vagotomy have a reduced Parkinson's disease risk.From these observations,researchers have hypothesized thatα-synuclein accumulation may initiate in the gut and subsequently propagate to the central dopaminergic neurons through the gut–brain axis,leading to Parkinson's disease.This review comprehensively examines the gut's involvement in Parkinson's disease,focusing on the concept of a gut-origin for the disease.We also examine the interplay between altered gut-related factors and the accumulation of pathologicalα-synuclein in the gut of Parkinson's disease patients.Given the accessibility of the gut to both dietary and pharmacological interventions,targeting gut-localizedα-synuclein represents a promising avenue for developing effective Parkinson's disease therapies.
文摘Growing evidence suggests the implication of the gut microbiota in various facets of health and disease. In this review, the focus is put on microbiota-host molecular cross-talk at the gut epithelial level with special emphasis on two defense systems： intestinal alkaline phosphatase（IAP） and inducible heat shock proteins（iHSPs）. Both IAP and iHSPs are induced by various microbial structural components（e.g. lipopolysaccharide, flagellin, CpG DNA motifs）,metabolites（e.g. n-butyrate） or secreted signal molecules（e.g., toxins, various peptides, polyphosphate）. IAP is produced in the small intestine and secreted into the lumen and in the interior milieu. It detoxifies microbial components by dephosphorylation and, therefore, down-regulates microbe-induced inflammation mainly by inhibiting NF-κB pro-inflammatory pathway in enterocytes. IAP gene expression and enzyme activity are influenced by the gut microbiota. Conversely, IAP controls gut microbiota composition both directly, and indirectly though the detoxification of pro-inflammatory free luminal adenosine triphosphate and inflammation inhibition. Inducible HSPs are expressed by gut epithelial cells in proportion to the microbial load along the gastro-intestinal tract. They are also induced by various microbial components, metabolites and secreted molecules. Whether iHSPs contribute to shape the gut microbiota is presently unknown. Both systems display strong anti-inflammatory and anti-oxidant properties that are protective to the gut and the host. Importantly, epithelial gene expressions and protein concentrations of IAP and iHSPs can be stimulated by probiotics, prebiotics and a large variety of dietary components, including macronutrients（protein and amino acids, especially L-glutamine, fat, fiber）, and specific minerals（e.g. calcium）and vitamins（e.g. vitamins K1 and K2）. Some food components（e.g. lectins, soybean proteins, various polyphenols） may inhibit or disturb these systems. The general cel ular and molecular mechanisms involved in the microbiota-host epithelial crosstalk and subsequent gut protection through IAP and iHSPs are reviewed along with their nutritional modulation.Special emphasis is also given to the pig, an economically important species and valuable biomedical model.
文摘We previously reported a serendipitous finding from a patient with refractory severe aplastic anemia who had gotten an unexpected hematological response to treatment with gut-cleansing preparations(GCPs).This patient experienced three recurrences over the ensuing one year of intermittent GCP treatments,with each recurrence occurring 7-8 wk from a GCP.After his third recurrence,he was prescribed successive treatment with rifampicin,berberine,and monthly administered GCP for 4 mo,and he developed an erythroid proliferative neoplasma and an overwhelming enteropathy,and eventually died of septic shock.Laboratory investigations had validated the resolution of myelosuppression and the appearance of malignant clonal hematopoiesis.From the treatment process and laboratory investigations,it is reasonably inferred that the engagement of gut inflammation is critically required in sustaining the overall pathophysiology of acquired aplastic anemia probably by creating a chronic inflammatory state.Incorporation of rifampicin,berberine,and monthly GCP into cyclosporine can enhance the immunosuppressive effect.In a subgroup of acquired aplastic anemia patients whose pathogenesis is associated with genotoxic exposure,the suppressed normal hematopoiesis may result from the bystander insult that is mediated by the soluble inflammatory cytokines generated in response to the immunogenic products of damaged hematopoietic cells in the context of chronic inflammatory state and may offer a protective antineoplastic mechanism against malignant proliferation.
基金supported by the Natural Science Foundation of Sichuan Province(No.2022NSFSC0060)。
文摘Background Zinc glycine chelate(Zn-Gly)has anti-inflammation and growth-promoting properties;however,the mechanism of Zn-Gly contribution to gut barrier function in Cherry Valley ducks during intestinal inflammation is unknown.Three-hundred 1-day-old ducks were divided into 5 groups(6 replicates and 10 ducks per replicate)in a completely randomized design:the control and dextran sulfate sodium(DSS)groups were fed a corn-soybean meal basal diet,and experimental groups received supplements of 70,120 or 170 mg/kg Zn in form of Zn-Gly.The DSS and treatment groups were given 2 mL of 0.45 g/mL DSS daily during d 15–21,and the control group received normal saline.The experiment lasted 21 d.Results Compared with DSS group,70,120 and 170 mg/kg Zn significantly increased body weight(BW),villus height and the ratio of villus to crypt,and significantly decreased the crypt depth of jejunum at 21 d.The number of goblet cells in jejunal villi in the Zn-Gly group was significantly increased by periodic acid-Schiff staining.Compared with control,the content of intestinal permeability marker D-lactic acid(D-LA)and fluxes of fluorescein isothiocyanate(FITC-D)in plasma of DSS group significantly increased,and 170 mg/kg Zn supplementation significantly decreased the D-LA content and FITC-D fluxes.Compared with control,contents of plasma,jejunum endotoxin and jejunum pro-inflammatory factors IL-1β,IL-6 and TNF-αwere significantly increased in DSS group,and were significantly decreased by 170 mg/kg Zn supplementation.Dietary Zn significantly increased the contents of anti-inflammatory factors IL-10,IL-22 and sIgA and IgG in jejunum.Real-time PCR and Western blot results showed that 170 mg/kg Zn supplementation significantly increased mRNA expression levels of CLDN-1 and expression of OCLN protein in jejunum,and decreased gene and protein expression of CLDN-2 compared with DSS group.The 120 mg/kg Zn significantly promoted the expressions of IL-22 and IgA.Dietary Zn-Gly supplementation significantly decreased pro-inflammatory genes IL-8 and TNF-αexpression levels and TNF-αprotein expression in jejunum.Additionally,Zn significantly reduced the gene and protein expression of TLR4,MYD88 and NF-κB p65.Conclusions Zn-Gly improved duck BW and alleviated intestinal injury by regulating intestinal morphology,barrier function and gut inflammation-related signal pathways TLR4/MYD88/NF-κB p65.
文摘The gut microbiome plays a key role in the pathogenesis and disease activity of inflammatory bowel disease(IBD).While research has focused on the bacterial microbiome,recent studies have shifted towards host genetics and host-fungal interactions.The mycobiota is a vital component of the gastrointestinal microbial community and plays a significant role in immune regulation.Among fungi,Candida species,particularly Candida albicans(C.albicans),have been extensively studied due to their dual role as gut commensals and invasive pathogens.Recent findings indicate that various strains of C.albicans exhibit consid-erable differences in virulence factors,impacting IBD's pathophysiology.Intestinal fungal dysbiosis and antifungal mucosal immunity may be associated to IBD,especially Crohn's disease(CD).This article discusses intestinal fungal dysbiosis and antifungal immunity in healthy individuals and CD patients.It discusses factors influencing the mycobiome's role in IBD pathogenesis and highlights significant contributions from the scientific community aimed at enhancing understanding of the mycobiome and encouraging further research and targeted intervention studies on specific fungal populations.Our article also provided insights into a recent study by Wu et al in the World Journal of Gastroenterology regarding the role of the gut microbiota in the pathogenesis of CD.
文摘Recently, the increasing number of patients worldwide who are sensitive to dietary gluten without evidence of celiac disease or wheat allergy has contributed to the identification of a new gluten-related syndrome defined as non-celiac gluten sensitivity. Our knowledge regarding this syndrome is still lacking, and many aspects of this syndrome remain unknown. Its pathogenesis is heterogeneous, with a recognized pivotal role for innate immunity; many other factors also contribute, inctuding tow-grade intestinal inflammation, increased intestinal barrier function and changes in the intestinal microbiota. Gluten and other wheat proteins, such as amylase trypsin inhibitors, are the primary triggers of this syndrome, but it has also been hypothesized that a diet rich in fermentable monosaccharides and polyols may elicit its functional gastrointestinal symptoms. The epidemiology of this condition is far from established; its prevalence in the general population is highly variable, ranging from 0.63% to 6%. From a clinical point of view, non-celiac gluten sensitivity is characterized by a wide array of gastrointestinal and extraintestinal symptoms that occur shortly after the ingestion of gluten and improve or disappear when gluten is withdrawn from the diet. These symptoms recur when gluten is reintroduced. Because diagnostic biomarkers have not yet been identified, a double-blind placebo-controlled gluten challenge is currently the diagnostic method with the highest accuracy. Future research is needed to generate more knowledge regarding non-celiac gluten sensitivity, a condition that has global acceptance but has only a few certainties and many unresolved issues.
文摘Importance:The cause of the hepatic dysfunction that commonly accompanies Kawasaki disease(KD)remains unclear.Objective:We tried to clarify the cause of the hepatic dysfunction.Methods:A total of 381 consecutive patients with acute KD,who had undergone inpatient treatment with intravenous immunoglobulin until the 7th day of illness,were divided into a group of 199 patients with an alanine aminotransferase(ALT)level≥40 IU/L on admission(group I),a group of 52 patients with an ALT level≥40 IU/L at some point after admission(group II),and a group of 130 patients with ALT levels consistently<40 IU/L throughout hospitalization(group III).Aspartate aminotransferase(AST),ALT,total bilirubin(T-Bil),and C-reactive protein(CRP)levels were analyzed over time,and time-courses were compared.results:In the initial stage of illness,in group I,AST,ALT,T-Bil peaked on days 1-3,and AST tended to improve significantly on the 4th day(P<0.001).T-Bil improved on day 5(P<0.01),and ALT improved significantly on day 6(P<0.001).CRP increased every day up to day 6(P<0.001).In group II,AST and ALT increased after admission,and thereafter CRP increased,then decreased.The frequency of use of aspirin and aspirin doses did not differ significantly in the three groups.Interpretation:Recovery from liver dysfunction occurred in the initial stage of illness in group I-within the period of CRP exacerbation,which is an indicator of systemic inflammation.
