| Role of innate immunity in Helicobacter pylori-induced gastric malignancy. | |
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MedLine Citation:
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PMID: 20664074 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Richard M Peek; Chris Fiske; Keith T Wilson |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review |
Journal Detail:
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Title: Physiological reviews Volume: 90 ISSN: 1522-1210 ISO Abbreviation: Physiol. Rev. Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-07-28 Completed Date: 2010-08-18 Revised Date: 2011-05-16 |
Medline Journal Info:
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Nlm Unique ID: 0231714 Medline TA: Physiol Rev Country: United States |
Other Details:
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Languages: eng Pagination: 831-58 Citation Subset: IM |
Affiliation:
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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 |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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:
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0/Toll-Like Receptors |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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