Low prevalence of <i>Helicobacter pylori</i> infection among patients with inflammatory bowel disease

Sonnenberg, Amnon; Genta, Robert M.

doi:10.1111/j.1365-2036.2011.04969.x

Cited by 94 publications

(78 citation statements)

References 23 publications

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“…Our data are consistent with a strong inverse correlation of H. pylori seropositivity with the risk of developing both CD and UC, 13,15 as well as with experimental data documenting a protective effect of live H. pylori infection on acute Salmonella typhimurium-induced typhlocolitis. 34 The enteroprotective effects of H. pylori in the latter model have been attributed to immunoregulatory sequences in the genomic DNA of H. pylori, which downregulate proinflammatory cytokine production and induce tolerogenic properties in dendritic cells.…”

Section: Discussionsupporting

confidence: 90%

“…From the *Institutes of Molecular Cancer Research, University of Zürich, Zürich, Switzerland; ‡ Experimental Immunology, University of Zürich, Zürich, Switzerland; and meta-analyses. [13][14][15] We have shown in various models that experimental H. pylori infection prevents allergen-induced asthma by inducing tolerogenic DCs, which acquire the ability to direct the differentiation of protective FoxP3 + regulatory T cells. [16][17][18][19] We report here that experimental H. pylori infection and regular administration of H. pylori extract protect against chronic colitis in the dextran sodium sulfate (DSS) and T-cell transfer models of the disease.…”

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confidence: 99%

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Helicobacter pylori–specific Protection Against Inflammatory Bowel Disease Requires the NLRP3 Inflammasome and IL-18

Engler

Leonardi

Hartung

et al. 2015

Inflammatory Bowel Diseases

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BACKGROUND The Gram-negative bacterium Helicobacter pylori is a constituent of the human gastric microbiota. Chronic infection with H. pylori causes gastritis and predisposes to gastric carcinoma but has also been inversely linked to various allergic and chronic inflammatory conditions. In particular, large meta-analyses have documented an inverse association between H. pylori infection and the risk of developing ulcerative colitis and Crohn's disease. METHODS We investigated possible protective effects of experimental H. pylori infection and of regular treatment with H. pylori extract in 2 mouse models of colitis and in mouse models of type I diabetes and multiple sclerosis. The mechanism of protection was examined in mouse strains lacking specific innate immune recognition pathways and cytokines. RESULTS We show here that experimental infection with H. pylori and administration of regular doses of H. pylori extract both alleviate the clinical and histopathological features of dextran sodium sulfateinduced chronic colitis and of T-cell transfer-induced colitis. High resolution endoscopy of the protected animals revealed the accumulation of large amounts of colonic mucus upon H. pylori exposure, which could be attributed to transcriptional activation of the mucin 2 gene. The protection against dextran sodium sulfate-induced colitis was dependent on the NLRP3 inflammasome and interleukin-18 signaling. Other autoimmune diseases, i.e., experimental autoimmune encephalomyelitis and type I diabetes, were not controlled by H. pylori. CONCLUSIONS In summary, we propose here that the immunomodulatory activity of an ancient constituent of the gut microbiota, H. pylori, may be exploited for the prevention and/or treatment of inflammatory bowel diseases.

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Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 99%

Helicobacter pylori–specific Protection Against Inflammatory Bowel Disease Requires the NLRP3 Inflammasome and IL-18

Engler

Leonardi

Hartung

et al. 2015

Inflammatory Bowel Diseases

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“…The analysis showed an inverse relationship between HP and IBD, both for UC and CD. On the other hand, a positive relationship was found between HP-negative chronic gastritis and IBD [63,64] . Data obtained in the different types of studies performed to date (epidemiological, clinical and experimental) suggest that HP infection reduces the risk of developing IBD, by producing a protective effect that hinders the appearance of IBD.…”

Section: Helicobacter Pylorimentioning

confidence: 92%

“…The authors concluded that the inverse correlation between IBD and HP, observed in epidemiological studies, could be partially explained by HP DNA's capacity to reduce typeⅠIFN [61] . More recently, in 2012 Sonnenberg et al [63,64] , carried out a study in which they performed upper and lower endoscopy (on the same day) to a large sample of patients. Biopsies obtained in the upper endoscopy were examined for esophagitis, gastritis and HP infection.…”

Section: Helicobacter Pylorimentioning

confidence: 99%

Pathogenesis of Crohn’s disease: Bug or no bug

Bosca-Watts

Tosca

Antón

et al. 2015

WJGP

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“…The HP infection rate in CD patients was reported to be low [17,[37][38][39][40][41][42][43][44][45][46], Halme et al reported that the incidence of HP infection in CD patients was 9.7% and concluded that CD-associated HP-negative gastritis was relatively common [46]. The low HP infection rate in CD patients might be due to the long-term administration of medicines, such as antibiotics and SASP [17,40,41,45].…”

Section: Gastric Lesionsmentioning

confidence: 99%

The endoscopic findings of the upper gastrointestinal tract in patients with Crohn’s disease

Nomura

Moriichi

Fujiya

et al. 2017

Clin J Gastroenterol

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Crohn's disease (CD) is a type of chronic inflammatory bowel disease (IBD) associated with ulceration, and the main foci of the inflammation in CD patients are typically the terminal ileum and colon. However, in the upper gastrointestinal tract (GIT), including the esophagus, stomach and duodenum, inflammatory lesions are also detected as well, with a relatively high frequency (30-75%). Recent advances in imaging modalities, including endoscopy, have aided in the diagnosis of CD. Various lesions, including aphtha, erosion, ulcers, bamboojoint-like appearance and notch-like appearance, are detected in the upper GI of CD patients. Of these lesions, the bamboo-joint-like appearance in the gastric cardiac region and notch-like appearance in the second portion of the duodenum are highly specific for CD, regardless of the disease activity at other sites. These two findings, particularly a bamboo-joint-like appearance, have therefore been considered as potential biomarkers for CD. Although proton pump inhibitors (PPIs) are administered as an initial treatment for upper GIT lesions of CD, the efficacy of this treatment remains controversial. The administration of mesalazine, steroids, immunosuppressant and biologic agents is expected to be effective for treating such lesions.

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Low prevalence of Helicobacter pylori infection among patients with inflammatory bowel disease

Abstract: SUMMARY BackgroundThere is some preliminary evidence to suggest that patients with inflammatory bowel disease (IBD) are less frequently infected with Helicobacter pylori than the general population.

Cited by 94 publications

References 23 publications

Helicobacter pylori–specific Protection Against Inflammatory Bowel Disease Requires the NLRP3 Inflammasome and IL-18

Helicobacter pylori–specific Protection Against Inflammatory Bowel Disease Requires the NLRP3 Inflammasome and IL-18

Pathogenesis of Crohn’s disease: Bug or no bug

The endoscopic findings of the upper gastrointestinal tract in patients with Crohn’s disease

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