Role of innate immunity in Helicobacter pylori-induced gastric malignancy.
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.
Peek
Richard M
RM
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
Fiske
Chris
C
Wilson
Keith T
KT
D000818:Animals; D004847:Epithelial Cells / Q000382:microbiology; D005753:Gastric Mucosa / Q000382:microbiology; D005769:Gastrointestinal Motility; D041981:Gastrointestinal Tract / Q000276:immunology / Q000378:metabolism; D016481:Helicobacter Infections / Q000276:immunology* / Q000503:physiopathology; D016480:Helicobacter pylori / Q000472:pathogenicity; D006801:Humans; D007113:Immunity, Innate; D013274:Stomach Neoplasms / Q000276:immunology* / Q000382:microbiology*; D051193:Toll-Like Receptors / Q000378:metabolism
D051193:Toll-Like Receptors