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Review
. 2014 Feb 14;20(6):1424-37.
doi: 10.3748/wjg.v20.i6.1424.

Helicobacter pylori infection: host immune response, implications on gene expression and microRNAs

Aline Cristina Targa Cadamuro  1 , Ana Flávia Teixeira Rossi  1 , Nathália Maciel Maniezzo  1 , Ana Elizabete Silva  1
Affiliations
Review

Helicobacter pylori infection: host immune response, implications on gene expression and microRNAs

Aline Cristina Targa Cadamuro et al. World J Gastroenterol. .

Abstract

Helicobacter pylori (H. pylori) infection is the most common bacterial infection worldwide. Persistent infection of the gastric mucosa leads to inflammatory processes and may remain silent for decades or progress causing more severe diseases, such as gastric adenocarcinoma. The clinical consequences of H. pylori infection are determined by multiple factors, including host genetic predisposition, gene regulation, environmental factors and heterogeneity of H. pylori virulence factors. After decades of studies of this successful relationship between pathogen and human host, various mechanisms have been elucidated. In this review, we have made an introduction on H. pylori infection and its virulence factors, and focused mainly on modulation of host immune response triggered by bacteria, changes in the pattern of gene expression in H. pylori-infected gastric mucosa, with activation of gene transcription involved in defense mechanisms, inflammatory and immunological response, cell proliferation and apoptosis. We also highlighted the role of bacteria eradication on gene expression levels. In addition, we addressed the recent involvement of different microRNAs in precancerous lesions, gastric cancer, and inflammatory processes induced by bacteria. New discoveries in this field may allow a better understanding of the role of major factors involved in the pathogenic mechanisms of H. pylori.

Keywords: Gastric cancer; Gastric lesions; Gene expression; Helicobacter pylori; Immune response; Inflammation; MicroRNAs; Virulence factors.

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Figures

Figure 1
Figure 1
Pathogenesis of Helicobacter pylori infection and host immune response. A: Bacterial urease neutralizes the gastric pH, enabling the colonization of gastric epithelial cells by the bacteria and their motility in the mucus layer. Adhesion of the bacteria to the gastric epithelium is mediated by BabA and SabA adhesins, allowing the release of factors CagA and VacA into the host cells, which causes a strong systemic immune response and inflammation of the gastric mucosa. Helicobacter pylori LPS is recognized by toll-like receptors, mainly TLR4 and TLR2, in cooperation with the adapter molecule MyD88 associated with IRAK1 and IRAK4 that leads to activation of transcription factor NF-κB, activating inflammatory signaling pathways; B: The immune response is also activated, with the recruitment of inflammatory cells at the infection site, inducing the production of various pro- and anti-inflammatory mediators; C: After NF-κB activation, rapid expression of multiple pro-inflammatory cytokines, chemokines such as the tumor necrosis factor alpha (TNF-α) and interleukins, and consequently activation of oncogenic pathways may culminate in cancer; D: The expression of some miRNAs is changed by H. pylori infection and the host immune response is regulated accordingly. LPS: Lipopolysaccharides; IL: Interleukin; COX-2: Cyclooxygenase; RNS: Reactive nitrogen species; ROS: Reactive oxygen species; IFN: Interferon.
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