Helicobacter pylori(H.pylori)is generally regarded as a human pathogen and a class 1 carcinogen,etiologically related to gastric and duodenal ulcers,gastric cancer,and mucosa-associated lymphoid tissue lymphoma.Howeve...Helicobacter pylori(H.pylori)is generally regarded as a human pathogen and a class 1 carcinogen,etiologically related to gastric and duodenal ulcers,gastric cancer,and mucosa-associated lymphoid tissue lymphoma.However,H.pylori can also be regarded as a commensal symbiont.Unlike other pathogenic/opportunistic bacteria,H.pylori colonization in infancy is facilitated by T helper type 2 immunity and leads to the development of immune tolerance.Fucosylated gastric mucin glycans,which are an important part of the innate and adaptive immune system,mediate the adhesion of H.pylori to the surface of the gastric epithelium,contributing to successful colonization.H.pylori may have beneficial effects on the host by regulating gastrointestinal(GI)microbiota and protecting against some allergic and autoimmune disorders and inflammatory bowel disease.The potential protective role against inflammatory bowel disease may be related to both modulation of the gut microbiota and the immunomodulatory properties of H.pylori.The inverse association between H.pylori and some potentially proinflammatory and/or procarcinogenic bacteria may suggest it regulates the GI microbiota.Eradication of H.pylori can cause various adverse effects and alter the GI microbiota,leading to short-term or long-term dysbiosis.Overall,studies have shown that gastric Actinobacteria decrease after H.pylori eradication,Proteobacteria increase during short-term follow-up and then return to baseline levels,and Enterobacteriaceae and Enterococcus increase in the short-term and interim follow-up.Various gastric mucosal bacteria(Actinomyces,Granulicatella,Parvimonas,Peptostreptococcus,Prevotella,Rothia,Streptococcus,Rhodococcus,and Lactobacillus)may contribute to precancerous gastric lesions and cancer itself after H.pylori eradication.H.pylori eradication can also lead to dysbiosis of the gut microbiota,with increased Proteobacteria and decreased Bacteroidetes and Actinobacteria.The increase in gut Proteobacteria may contribute to adverse effects during and after eradication.The decrease in Actinobacteria,which are pivotal in the maintenance of gut homeostasis,can persist for>6 mo after H.pylori eradication.Furthermore,H.pylori eradication can alter the metabolism of gastric and intestinal bacteria.Given the available data,eradication cannot be an unconditional recommendation in every case of H.pylori infection,and the decision to eradicate H.pylori should be based on an assessment of the benefit-risk ratio for the individual patient.Thus,the current guidelines based on the unconditional"test-and-treat"strategy should be revised.The most cautious and careful approach should be taken in elderly patients with multiple eradication failures since repeated eradication can cause antibiotic-associated diarrhea,including severe Clostridioides difficile-associated diarrhea and colitis and antibiotic-associated hemorrhagic colitis due to Klebsiella oxytoca.Furthermore,since eradication therapy with antibiotics and proton pump inhibitors can lead to serious adverse effects and/or dysbiosis of the GI microbiota,supplementation of probiotics,prebiotics,and microbial metabolites(e.g.,butyrate+inulin)should be considered to decrease the negative effects of eradication.展开更多
BACKGROUND Necrotizing enterocolitis(NEC)is a multifactorial disease that predominantly affects premature neonates.Intestinal dysbiosis plays a critical role in NEC pathogenesis in premature neonates.The main risk fac...BACKGROUND Necrotizing enterocolitis(NEC)is a multifactorial disease that predominantly affects premature neonates.Intestinal dysbiosis plays a critical role in NEC pathogenesis in premature neonates.The main risk factor for NEC in term infants is mesenteric hypoperfusion associated with ductaldependent congenital heart disease(CHD)that eventually leads to intestinal ischemia.The incidence of NEC in neonates with critical CHD is 6.8%-13%.However,the role of the intestinal microbiome in NEC pathogenesis in infants with ductal-dependent CHD remains unclear.CASE SUMMARY A male term neonate with right atrial isomerism underwent modified Blalock-Taussig shunt placement on the 14^(th)day of life and had persistent mesenteric hypoperfusion after surgery.The patient had episodes of NEC stageⅡA on the 1^(st)and 28^(th)days after cardiac surgery.Fecal microbial composition was analyzed before and after cardiac surgery by sequencing region V4 of the 16S rRNA gene.Before surgery,species belonging to genera Veillonella and Clostridia and class Gammaproteobacteria were detected,Bifidobacteriaceae showed a low abundance.The first NEC episode was associated with postoperative hemodynamic instability,intestinal ischemiareperfusion injury during cardiopulmonary bypass,and a high abundance of Clostridium paraputrificum(Clostridium sensu stricto I)(56.1%).Antibacterial therapy after the first NEC episode resulted in increased abundance of Gammaproteobacteria,decreased abundance of Firmicutes,and low alpha diversity.These changes in the microbial composition promoted the growth of Clostridium sensu strictoⅠ(72.0%)before the second NEC episode.CONCLUSION A high abundance of Clostridium sensu strictoⅠand mesenteric hypoperfusion may have contributed to NEC in the present case.展开更多
基金Supported by the Russian Science Foundation,No.20-65-47026。
文摘Helicobacter pylori(H.pylori)is generally regarded as a human pathogen and a class 1 carcinogen,etiologically related to gastric and duodenal ulcers,gastric cancer,and mucosa-associated lymphoid tissue lymphoma.However,H.pylori can also be regarded as a commensal symbiont.Unlike other pathogenic/opportunistic bacteria,H.pylori colonization in infancy is facilitated by T helper type 2 immunity and leads to the development of immune tolerance.Fucosylated gastric mucin glycans,which are an important part of the innate and adaptive immune system,mediate the adhesion of H.pylori to the surface of the gastric epithelium,contributing to successful colonization.H.pylori may have beneficial effects on the host by regulating gastrointestinal(GI)microbiota and protecting against some allergic and autoimmune disorders and inflammatory bowel disease.The potential protective role against inflammatory bowel disease may be related to both modulation of the gut microbiota and the immunomodulatory properties of H.pylori.The inverse association between H.pylori and some potentially proinflammatory and/or procarcinogenic bacteria may suggest it regulates the GI microbiota.Eradication of H.pylori can cause various adverse effects and alter the GI microbiota,leading to short-term or long-term dysbiosis.Overall,studies have shown that gastric Actinobacteria decrease after H.pylori eradication,Proteobacteria increase during short-term follow-up and then return to baseline levels,and Enterobacteriaceae and Enterococcus increase in the short-term and interim follow-up.Various gastric mucosal bacteria(Actinomyces,Granulicatella,Parvimonas,Peptostreptococcus,Prevotella,Rothia,Streptococcus,Rhodococcus,and Lactobacillus)may contribute to precancerous gastric lesions and cancer itself after H.pylori eradication.H.pylori eradication can also lead to dysbiosis of the gut microbiota,with increased Proteobacteria and decreased Bacteroidetes and Actinobacteria.The increase in gut Proteobacteria may contribute to adverse effects during and after eradication.The decrease in Actinobacteria,which are pivotal in the maintenance of gut homeostasis,can persist for>6 mo after H.pylori eradication.Furthermore,H.pylori eradication can alter the metabolism of gastric and intestinal bacteria.Given the available data,eradication cannot be an unconditional recommendation in every case of H.pylori infection,and the decision to eradicate H.pylori should be based on an assessment of the benefit-risk ratio for the individual patient.Thus,the current guidelines based on the unconditional"test-and-treat"strategy should be revised.The most cautious and careful approach should be taken in elderly patients with multiple eradication failures since repeated eradication can cause antibiotic-associated diarrhea,including severe Clostridioides difficile-associated diarrhea and colitis and antibiotic-associated hemorrhagic colitis due to Klebsiella oxytoca.Furthermore,since eradication therapy with antibiotics and proton pump inhibitors can lead to serious adverse effects and/or dysbiosis of the GI microbiota,supplementation of probiotics,prebiotics,and microbial metabolites(e.g.,butyrate+inulin)should be considered to decrease the negative effects of eradication.
基金Supported by the Russian Science Foundation,No.22-25-00484。
文摘BACKGROUND Necrotizing enterocolitis(NEC)is a multifactorial disease that predominantly affects premature neonates.Intestinal dysbiosis plays a critical role in NEC pathogenesis in premature neonates.The main risk factor for NEC in term infants is mesenteric hypoperfusion associated with ductaldependent congenital heart disease(CHD)that eventually leads to intestinal ischemia.The incidence of NEC in neonates with critical CHD is 6.8%-13%.However,the role of the intestinal microbiome in NEC pathogenesis in infants with ductal-dependent CHD remains unclear.CASE SUMMARY A male term neonate with right atrial isomerism underwent modified Blalock-Taussig shunt placement on the 14^(th)day of life and had persistent mesenteric hypoperfusion after surgery.The patient had episodes of NEC stageⅡA on the 1^(st)and 28^(th)days after cardiac surgery.Fecal microbial composition was analyzed before and after cardiac surgery by sequencing region V4 of the 16S rRNA gene.Before surgery,species belonging to genera Veillonella and Clostridia and class Gammaproteobacteria were detected,Bifidobacteriaceae showed a low abundance.The first NEC episode was associated with postoperative hemodynamic instability,intestinal ischemiareperfusion injury during cardiopulmonary bypass,and a high abundance of Clostridium paraputrificum(Clostridium sensu stricto I)(56.1%).Antibacterial therapy after the first NEC episode resulted in increased abundance of Gammaproteobacteria,decreased abundance of Firmicutes,and low alpha diversity.These changes in the microbial composition promoted the growth of Clostridium sensu strictoⅠ(72.0%)before the second NEC episode.CONCLUSION A high abundance of Clostridium sensu strictoⅠand mesenteric hypoperfusion may have contributed to NEC in the present case.
