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Review
, 114 (3), 491-7

Role of the Helicobacter Pylori-Induced Inflammatory Response in the Development of Gastric Cancer

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Review

Role of the Helicobacter Pylori-Induced Inflammatory Response in the Development of Gastric Cancer

Acacia Lamb et al. J Cell Biochem.

Abstract

Helicobacter pylori (H. pylori) infection causes chronic gastritis and peptic ulceration and is the strongest risk factor for the development of gastric cancer. The pathogenesis of H. pylori is believed to be associated with infection-initiated chronic gastritis, which is characterized by enhanced expression of many inflammatory genes. H. pylori utilizes various virulence factors, targeting different cellular proteins, to modulate the host inflammatory response. In this review, we explore the many different ways by which H. pylori initiates inflammation, leveling many "hits" on the gastric mucosa which can lead to the development of cancer. We also discuss some recent findings in understanding the pathogen-host interactions and the role of transcription factor NF-κB in H. pylori-induced inflammation.

Conflict of interest statement

Conflict of interest

The authors declare no conflict of interest

Figures

Figure 1
Figure 1
H. pylori induces gastric cancer-related inflammatory response. A) Schematic model for H. pylori-induced inflammation. H. pylori infection activates various transcription factors via its different virulence factors in gastric epithelial cells or inflammatory cells such as T cells and macrophages. Activated transcription factors then induce the expression of genes encoding pro-inflammatory cytokines, chemokines, inflammatory modulators and growth factors, creating an inflammatory microenvironment that facilitates the transformation of gastric epithelial cells. B) Modulation of TAK1 ubiquitination and activation by H. pylori CagA. After translocation into the epithelial cells, CagA enhances TRAF6- and Ubc13-mediated K63-linked polyubiquitination of TAK1 by directly associating with TRAF6 and TAK1. The enhanced ubiquitination of TAK1 might result from a stimulation of the activity of TRAF6 or Ubc13 or from an inhibition of an unidentified deubiquitinase (DUB) of TAK1. Polyubiquitinated TAK1 is then activated, leading to the activation of IKKs and NF-κB, and the subsequent inflammatory response.

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