Interaction between inflammatory mediators and miRNAs in Helicobacter pylori infection

Abstract

Summary Helicobacter pylori cause chronic inflammation favouring gastric carcinogenesis, and its eradication may prevent malignant transformation. We evaluated whether H. pylori infection and its eradication modify the expression of inflammatory mediators in patients with chronic gastritis. Furthermore, we assessed whether microRNAs modulate inflammatory pathways induced by H. pylori and identified miRNA–gene interaction networks. mRNA and protein expression of TNFA, IL6, IL1B, IL12A, IL2 and TGFBRII and miRNAs miR‐103a‐3p, miR‐181c‐5p, miR‐370‐3p, miR‐375 and miR‐223‐3p were evaluated in tissue samples from 20 patients with chronic gastritis H. pylori negative (Hp−) and 31 H. pylori positive (Hp+), before and three months after bacterium eradication therapy, in comparison with a pool of Hp− normal gastric mucosa. Our results showed that H. pylori infection leads to up‐regulation of TNFA, IL6, IL12A and IL2 and down‐regulation of miRNAs. Bacterium eradication reduces the expression of TNFA and IL6 and up‐regulates TGFBRII and all investigated miRNAs, except miR‐223‐3p. Moreover, transcriptional profiles of inflammatory mediators and miRNAs after eradication are different from the non‐infected group. Deregulated miRNA–mRNA interaction networks were observed in the Hp+ group before and after eradication. Therefore, miRNAs modulated cytokine expression in the presence of H. pylori and after its eradication, suggesting that miRNAs participate in the pathological process triggered by H. pylori in the gastric mucosa.

Involvement of Aryl Hydrocarbon Receptor and Aryl Hydrocarbon Receptor Repressor in Helicobacter Pylori-related Gastric Pathogenesis

“…Therefore, H. pylori infection may inhibit AHR and AHRR expression in the stomach, and the in vitro and in vivo results supported this speculation. H. pylori infection stimulated stomach cells to produce proinflammatory factors 32 , 33 , and these cytokines exerted provital roles in the pathogenesis of H. pylori infection-associated gastric diseases, including gastritis and gastric cancer 34 , 35 , 36 , 37 . The current study demonstrated that silencing of AHR or AHRR promoted TNF, IL-8 and IL-1β secretion in human stomach cells after coculture with H. pylori .…”

Helicobacter pylori Infection Is Associated with Decreased Expression of SLC5A8, a Cancer Suppressor Gene, in Young Children

“…At this point, it might be interesting to speculate on how reduced SLC5A8 expression in host cells may benefit H. pylori . Indeed, this pathogen has been shown to modulate host gene expression in ways that favor host infection (Matsushima et al, 2011 ; Kim et al, 2012 ; Hanada and Graham, 2014 ; O'Ryan et al, 2015 ; Rossi et al, 2016 ). As mentioned in this manuscript, SLC5A8 is implicated in the control of short-chain fatty acid uptake, which in turn modulates the expression of cell cycle control and pro-inflammatory genes.…”

<em>Helicobacter&nbsp;pylori</em> is associated with weakened pulmonary function and reduced incidence of allergic conditions in patients with chronic cough

“…While the pathogenetic mechanisms underlying the effects of a H. pylori on airway disorders remain to be determined, they may involve chronic inflammation promoted by persistent infection with a H. pylori (30,31). It is well-known that a H. pylori colonization of the gastric mucosa stimulates the release of various pro-inflammatory factors, including cytokines and eicosanoids.…”