| The role and pathophysiological relevance of membrane transporter PepT1 in intestinal inflammation and inflammatory bowel disease. | |
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MedLine Citation:
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PMID: 22194420 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Intestinal inflammation is characterized by epithelial disruption, leading to loss of barrier function and the recruitment of immune cells, including neutrophils. Although the mechanisms are not yet completely understood, interactions between environmental and immunological factors are thought to be critical in the initiation and progression of intestinal inflammation. In recent years, it has become apparent that the di/tripeptide transporter PepT1 may play an important role in the pathogenesis of such inflammation. In healthy individuals, PepT1 is primarily expressed in the small intestine and transports di/tripeptides for metabolic purposes. However, during chronic inflammation such as that associated with inflammatory bowel disease, PepT1 expression is upregulated in the colon, wherein the protein is normally expressed either minimally or not at all. Several recent studies have shown that PepT1 binds to and transports various bacterial di/tripeptides into colon cells, leading to activation of downstream proinflammatory responses via peptide interactions with innate immune receptors. In the present review, we examine the relationship between colonic PepT1-mediated peptide transport in the colon and activation of innate immune responses during disease. It is important to understand the mechanisms of PepT1 action during chronic intestinal inflammation to develop future therapies addressing inappropriate immune activation in the colon. |
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Authors:
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Sarah A Ingersoll; Saravanan Ayyadurai; Moiz A Charania; Hamed Laroui; Yutao Yan; Didier Merlin |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review Date: 2011-12-22 |
Journal Detail:
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Title: American journal of physiology. Gastrointestinal and liver physiology Volume: 302 ISSN: 1522-1547 ISO Abbreviation: Am. J. Physiol. Gastrointest. Liver Physiol. Publication Date: 2012 Mar |
Date Detail:
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Created Date: 2012-02-22 Completed Date: 2012-04-16 Revised Date: 2012-05-23 |
Medline Journal Info:
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Nlm Unique ID: 100901227 Medline TA: Am J Physiol Gastrointest Liver Physiol Country: United States |
Other Details:
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Languages: eng Pagination: G484-92 Citation Subset: IM |
Affiliation:
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Center for Diagnostics & Therapeutics, Department of Biology, Georgia State University, Atlanta, 30302-5090, USA. singersoll@gsu.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Colorectal Neoplasms / physiopathology Gastroenteritis / drug therapy, etiology* Humans Inflammatory Bowel Diseases / etiology*, genetics, physiopathology Nod Signaling Adaptor Proteins / physiology Oligopeptides / metabolism Symporters / genetics, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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R56 DK084987/DK/NIDDK NIH HHS; R56-DK-061941/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Nod Signaling Adaptor Proteins; 0/Oligopeptides; 0/SLC15A1 protein, human; 0/Symporters |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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