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幽门螺杆菌感染中固有免疫应答的诱导和调节。

Induction and Regulation of the Innate Immune Response in Helicobacter pylori Infection.

机构信息

Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Nashville, Tennessee; Center for Mucosal Inflammation and Cancer, Nashville, Tennessee; Program in Cancer Biology, Nashville, Tennessee.

Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Nashville, Tennessee; Center for Mucosal Inflammation and Cancer, Nashville, Tennessee; Program in Cancer Biology, Nashville, Tennessee; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee.

出版信息

Cell Mol Gastroenterol Hepatol. 2022;13(5):1347-1363. doi: 10.1016/j.jcmgh.2022.01.022. Epub 2022 Feb 3.

DOI:10.1016/j.jcmgh.2022.01.022
PMID:35124288
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8933844/
Abstract

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.

摘要

胃癌(GC)是全球第五大常见癌症和第四大癌症相关死亡原因。肠型 GC 由急性胃炎、多灶性萎缩性胃炎、肠上皮化生、异型增生和癌演变而来。全球约有 50%的人口感染革兰氏阴性细菌幽门螺杆菌(H. pylori),它感染胃部,引发胃部炎症,继而导致疾病进展。在这种情况下,H. pylori 效应物诱导胃上皮细胞和髓样细胞固有免疫反应在感染结局中发挥关键作用。然而,只有 1%至 3%的感染患者会发展为胃腺癌,这强调了其他机制调节局部非特异性反应,包括胃微生物组和遗传因素。本文综述了描述在 H. pylori 感染过程中诱导和调节黏膜固有免疫反应的因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/778f/8933844/d26b01c64a19/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/778f/8933844/3259020f9520/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/778f/8933844/d26b01c64a19/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/778f/8933844/3259020f9520/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/778f/8933844/d26b01c64a19/gr2.jpg

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