<b><i>Helicobacter pylori</i></b>: Does Gastritis Prevent Colitis?

Abstract

Background: Since its discovery in the early 1980s, Helicobacter pylori has been linked to a variety of gastric and extragastric diseases. Chronic infection with H. pylori causes histologically evident gastritis in all colonized individuals and is the predominant risk factor for gastric and duodenal ulcers as well as gastric adenocarcinoma. However, increasingly robust experimental and epidemiological evidence suggests that H. pylori may at the same time be beneficial to its carriers, as it efficiently prevents allergic disorders and chronic inflammatory conditions. The purpose of this review is to summarize and document the latest evidence for a possible inverse association of H. pylori infection status and the risk of inflammatory bowel disease (IBD), as provided in both experimental and human observational studies. The pathogenesis of IBDs, the available mouse models for these diseases and the dual role of H. pylori in health and disease are presented in dedicated chapters. Summary and Key Messages: Almost all available epidemiological data suggest that H. pylori infection is inversely associated with both Crohn's disease (CD) and ulcerative colitis in European, Asian as well as American populations; large meta-analyses reviewing 30 original articles or more document that this inverse association is especially strong in CD patients and in children and young adults. Experimental data available from various mouse models of IBD confirm that live H. pylori infection as well as treatment with immunomodulatory molecules of H. pylori reduce clinical and histopathological IBD symptoms. Various proposed mechanisms involving the tolerization of dendritic cells, the production of protective cytokines and the preferential induction and differentiation of regulatory T-cells are presented. The implications of the beneficial aspects of the Helicobacter-host interaction for H. pylori eradication decisions, as well as potential new therapeutic options in the treatment of IBD are discussed in this review.

Short‐term and long‐term impacts of Helicobacter pylori eradication with reverse hybrid therapy on the gut microbiota

“…Additionally, several studies revealed that probiotic supplementation could reduce the antibiotic‐induced dysbiosis and decrease the frequency of adverse effects of H. pylori eradication therapy . In addition, there is emerging experimental and epidemiological evidence suggesting that H. pylori may be beneficial to its carriers by preventing the development of inflammatory bowel disease . Future research is warranted to clarify the benefits and risk of eradication therapy in the development of intestinal disorders and the relationships between alterations of the gut microbiota following eradication therapy and the risk of developing intestinal diseases.…”

Is the Presence of Helicobacter Pylori in the Colonic Mucosa, Provocative of Activity in Ulcerative Colitis?

“…This possibility has been previously reported that the initiation of the human IBD can be triggered by other types of Helicobacter organisms from colon such as Helicobacter bilis, Helicobacter fennelliae, Helicobacter hepaticus, and Helicobacter trogontum. 7 Also, CagA positivity was higher in the patients with more active IBDs.…”

“…5,6 In recent years diagnosis of IBD cases are being increased. 7 At the same time with improved hygiene especially in developing countries, H.P infection in gastrointestinal tract is being decreased. 8 So, there are reports about protective effects of H.P infection and gastritis against IBD development.…”

Gab2 and Gab3 Redundantly Suppress Colitis by Modulating Macrophage and CD8+ T-Cell Activation

“…Human CD8 + T-cells are emerging as major mediators of human IBD and the identification of a key role for Gab2/3 in suppression of T-cell and macrophage function, fills in major gaps in our understanding of how CD8 + T-cells drive IBD. Furthermore, the H. pylori virulence factor CagA has been shown to protect against DSS-induced experimental colitis ( 79 ) and is inversely associated with human IBD ( 40 ) but no functional roles have been previously attributed to Gab adaptor proteins in promoting a healthy colon under normal physiological conditions. The findings of this study thus provide a deeper understanding of how Gab2 and Gab3 redundantly function to ultimately control CD8 + T-cell and this finding could lead to new therapeutic avenues.…”