Enterohepatic Helicobacter Species as a Potential Causative Factor in Inflammatory Bowel Disease

Yu, Qiao; Zhang, Shenghong; Li, Li; Xiong, Liang; Chao, Kang; Zhong, Bihui; Li, Yuwen; Wang, Huiling; Chen, Minhu

doi:10.1097/md.0000000000001773

Cited by 27 publications

(20 citation statements)

References 48 publications

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“…Notably, inflammationpromoting OTUs related to Helicobacter, Peptostreptococcaceae, Streptococcus, and E. faecalis were increased in the stress-treated group. These findings fit well with evidence that Helicobacter is linked to IBD (42), as are Peptostreptococcaceae (43), Streptococcus (44), and E. faecalis (45). Lachnospiraceae, which has shown protection against colitis (46), were significantly decreased after stress.…”

Section: Discussionsupporting

confidence: 87%

Chronic stress promotes colitis by disturbing the gut microbiota and triggering immune system response

Gao

Cao

Cheng

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

307

218

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Chronic stress is known to promote inflammatory bowel disease (IBD), but the underlying mechanism remains largely unresolved. Here, we found chronic stress to sensitize mice to dextran sulfate sodium (DSS)-induced colitis; to increase the infiltration of B cells, neutrophils, and proinflammatory ly6C macrophages in colonic lamina propria; and to present with decreased thymus and mesenteric lymph node (MLN) coefficients. Circulating total white blood cells were significantly increased after stress, and the proportion of MLN-associated immune cells were largely changed. Results showed a marked activation of IL-6/STAT3 signaling by stress. The detrimental action of stress was not terminated in IL-6 mice. Interestingly, the composition of gut microbiota was dramatically changed after stress, with expansion of inflammation-promoting bacteria. Furthermore, results showed stress-induced deficient expression of mucin-2 and lysozyme, which may contribute to the disorder of gut microbiota. Of note is that, in the case of cohousing, the stress-induced immune reaction and decreased body weight were abrogated, and transferred gut microbiota from stressed mice to control mice was sufficient to facilitate DSS-induced colitis. The important role of gut microbiota was further reinforced by broad-spectrum antibiotic treatment. Taken together, our results reveal that chronic stress disturbs gut microbiota, triggering immune system response and facilitating DSS-induced colitis.

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Section: Discussionsupporting

confidence: 87%

Chronic stress promotes colitis by disturbing the gut microbiota and triggering immune system response

Gao

Cao

Cheng

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

307

218

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“…The Helicobacter species in the gastrointestinal microbiota comprise Helicobacter pylori and enterohepatic Helicobacter species, which can colonize the intestinal mucosa. A recent meta‐analysis study indicated that the prevalence of Helicobacter species was higher among the patients with IBD, compared to controls . It appears that enterohepatic Helicobacter species was associated with IBD, while intestinal H. pylori infection was not significantly associated with IBD.…”

Section: Inflammatory Bowel Disease and The Gastrointestinal Tract MImentioning

confidence: 99%

The human gastrointestinal tract and oral microbiota in inflammatory bowel disease: a state of the science review

López

Grande

Galvez

et al. 2016

APMIS

102

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Inflammatory bowel disease (IBD) includes a spectrum of diseases from ulcerative colitis (UC) to Crohn's disease (CD). Many studies have addressed the changes in the microbiota of individuals affected by UC and CD. A decrease in biodiversity and depletion of the phyla Bacteroidetes and Firmicutes has been reported, among others. Changes in microbial composition also result in changes in the metabolites generated in the gut from microbial activity that may involve the amount of butyrate and other metabolites such as H S being produced. Other factors such as diet, age, or medication need to be taken into consideration when studying dysbiosis associated with IBD. Diverse bacterial species have been associated specifically or non-specifically to IBD, but none of them have been demonstrated to be its ethiological agent. Recent studies also suggest that micro-eukaryotic populations may also be altered in IBD patients. Last, but not least, viruses, and specially bacteriophages, can play a role in controlling microbial populations in the gastrointestinal tract. This may affect both bacterial diversity and metabolism, but possible implications for IBD still remain to be solved. Dysbiosis in the oral microbiome associated with IBD remains an emerging field for future research.

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“…were over-represented in colitis-induced Villin-Cre;Gankyrin f/f mice. Enterohepatic Helicobacter species (EHS) are known to colonize the intestine and are also associated with IBD [41]. In fact, the elevated abundance of EHS in IBD patients in comparison to healthy subjects was revealed by a meta-analysis based on 14 clinical studies [41].…”

Section: Discussionmentioning

confidence: 99%

Deficiency of Gankyrin in the small intestine is associated with augmented colitis accompanied by altered bacterial composition of intestinal microbiota

et al. 2020

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Background: Gankyrin (GK) is an oncoprotein which regulates inflammatory responses and its inhibition is considered as a possible anti-inflammatory therapy for inflammatory bowel disease (IBD). Methods: In this study, we investigated the role of GK in epithelial cells using mice with intestinal epithelial cellspecific GK deletion in (i) the entire small intestine and colon (Villin-Cre;Gankyrin f/f) and (ii) the distal intestine and colon (Cdx2-Cre;Gankyrin f/f). Result: Unexpectedly, GK-deficiency in the upper small bowel augmented inflammatory activity compared with control mice when colitis was induced with dextran sodium sulfate. Biochemical analyses have revealed GKdeficiency to have caused reduction in the expression of antimicrobial peptides, α-Defensin-5 and-6, in the upper small bowel. Examination of human samples have further confirmed that the reduction of GK expression in the small bowel is associated with colonic involvement in human Crohn's disease. Through the sequencing of bacterial 16S rRNA gene amplicons, bacteria potentially deleterious to intestinal homeostasis such as Helicobacter japonicum and Bilophila were found to be over-represented in colitis induced Villin-Cre;Gankyrin f/f mice when compared to Gankyrin f/f control mice under the same condition. Conclusion: These results highlight the distinct site dependence of the pro-and anti-inflammatory functions of GK and provide important insights into the pathogenesis of IBD.

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Enterohepatic Helicobacter Species as a Potential Causative Factor in Inflammatory Bowel Disease

Cited by 27 publications

References 48 publications

Chronic stress promotes colitis by disturbing the gut microbiota and triggering immune system response

Chronic stress promotes colitis by disturbing the gut microbiota and triggering immune system response

The human gastrointestinal tract and oral microbiota in inflammatory bowel disease: a state of the science review

Deficiency of Gankyrin in the small intestine is associated with augmented colitis accompanied by altered bacterial composition of intestinal microbiota

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