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Physiol Rev. 2010 Jul;90(3):831-58. doi: 10.1152/physrev.00039.2009.

Role of innate immunity in Helicobacter pylori-induced gastric malignancy.

Author information

1
Division of Gastroenterology, Department of Medicine, Vanderbilt University School of Medicine, and Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee 37232-2279, USA. richard.peek@vanderbilt.edu

Abstract

Helicobacter pylori colonizes the majority of persons worldwide, and the ensuing gastric inflammatory response is the strongest singular risk factor for peptic ulceration and gastric cancer. However, only a fraction of colonized individuals ever develop clinically significant outcomes. Disease risk is combinatorial and can be modified by bacterial factors, host responses, and/or specific interactions between host and microbe. Several H. pylori constituents that are required for colonization or virulence have been identified, and their ability to manipulate the host innate immune response will be the focus of this review. Identification of bacterial and host mediators that augment disease risk has profound ramifications for both biomedical researchers and clinicians as such findings will not only provide mechanistic insights into inflammatory carcinogenesis but may also serve to identify high-risk populations of H. pylori-infected individuals who can then be targeted for therapeutic intervention.

PMID:
20664074
PMCID:
PMC2990353
DOI:
10.1152/physrev.00039.2009
[Indexed for MEDLINE]
Free PMC Article

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