Journal
CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
Volume 13, Issue 5, Pages 1347-1363Publisher
ELSEVIER INC
DOI: 10.1016/j.jcmgh.2022.01.022
Keywords
Gastric Cancer; Gastritis; Microbiota; Polymorphism; Virulence Factors
Categories
Funding
- National Institutes of Health [R01DK128200, R01CA190612, P01CA116087, P01CA028842, R41CA257262]
- Veterans Affairs Merit Review [I01BX001453, I01CX002171]
- Crohn's & Colitis Foundation [703003]
- Department of Defense [W81XWH-21-1-0617]
- Thomas F. Frist Sr. Endowment (KTW)
- Vanderbilt Center for Mucosal Inflammation and Cancer (KTW)
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Gastric cancer is the fifth most common cancer and the fourth most common cause of cancer-related death worldwide. The key factor in the development of gastric inflammation and disease progression is Helicobacter pylori infection, although only a small percentage of infected individuals develop gastric adenocarcinoma.
Gastric cancer (GC) is the fifth most common cancer and the fourth most common cause of cancer-related death worldwide. The intestinal type of GC progresses from acute to chronic gastritis, multifocal atrophic gastritis, intestinal metaplasia, dysplasia, and carcinoma. Infection of the stomach by Helicobacter pylori, a Gram-negative bacterium that infects approximately 50% of the world's population, is the causal determinant that initiates the gastric inflammation and then disease progression. In this context, the induction of the innate immune response of gastric epithelial cells and myeloid cells by H. pylori effectors plays a critical role in the outcome of the infection. However, only 1% to 3% of infected patients develop gastric adenocarcinoma, emphasizing that other mechanisms regulate the localized non-specific response, including the gastric microbiota and genetic factors. This review summarizes studies describing the factors that induce and regulate the mucosal innate immune response during H. pylori infection.
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