Document Detail


Role of innate immunity in Helicobacter pylori-induced gastric malignancy.
MedLine Citation:
PMID:  20664074     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Richard M Peek; Chris Fiske; Keith T Wilson
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review    
Journal Detail:
Title:  Physiological reviews     Volume:  90     ISSN:  1522-1210     ISO Abbreviation:  Physiol. Rev.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-28     Completed Date:  2010-08-18     Revised Date:  2011-05-16    
Medline Journal Info:
Nlm Unique ID:  0231714     Medline TA:  Physiol Rev     Country:  United States    
Other Details:
Languages:  eng     Pagination:  831-58     Citation Subset:  IM    
Affiliation:
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
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MeSH Terms
Descriptor/Qualifier:
Animals
Epithelial Cells / microbiology
Gastric Mucosa / microbiology
Gastrointestinal Motility
Gastrointestinal Tract / immunology,  metabolism
Helicobacter Infections / immunology*,  physiopathology
Helicobacter pylori* / pathogenicity
Humans
Immunity, Innate*
Stomach Neoplasms / immunology*,  microbiology*
Toll-Like Receptors / metabolism
Grant Support
ID/Acronym/Agency:
CA-116087/CA/NCI NIH HHS; DK-53620/DK/NIDDK NIH HHS; DK-58587/DK/NIDDK NIH HHS; DK-77955/DK/NIDDK NIH HHS; P01 CA116087-01A2/CA/NCI NIH HHS; P30 DK058404-09/DK/NIDDK NIH HHS; R01 AT004821-04/AT/NCCAM NIH HHS; R01 CA077955-06/CA/NCI NIH HHS; R01 DK053620-06A2/DK/NIDDK NIH HHS; R01 DK058587-01A1/DK/NIDDK NIH HHS; R01 DK073902-01/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Toll-Like Receptors

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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