Linked Life Data

17991290

Source:http://linkedlifedata.com/resource/pubmed/id/17991290

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-12-17
pubmed:abstractText
Environmental factors such as diet are known to play important roles in inflammatory bowel disease (IBD). Epidemiological studies have indicated that a high-fat diet is a risk factor for IBD. In addition, the balance between effector T cells (T(eff)) and regulatory T cells (T(reg)) contributes to the pathogenesis of mucosal inflammation. The aim of this study was to understand the mechanisms by which a high-fat diet can regulate susceptibility to intestinal inflammation. Wild-type C57BL/6 mice were fed either a commercial high-fat diet or a normal diet, then exposed to dextran sulphate sodium (DSS) to induce colonic inflammation. Intraepithelial lymphocytes (IEL) were isolated from the colon, and their phenotype and cytokine profile were analysed by flow cytometry. Mice receiving the high-fat diet were more susceptible to DSS-induced colitis. They had higher numbers of non-CD1d-restricted natural killer (NK) T cells in the colonic IEL, when compared to mice fed a normal diet. These cells expressed tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma, which are up-regulated by high-fat diets. Mice fed the high-fat diet also had decreased levels of colonic T(reg). Depletion of colonic NK T cells or adoptive transfer of T(reg) reduced the DSS colitis in these mice, and reduced the colonic expression of TNF-alpha and IFN-gamma. We conclude that a high-fat diet can increase non-CD1d-restricted NK T cells and decrease T(reg) in the colonic IEL population. This altered colonic IEL population leads to increased susceptibility to DSS-induced colitis. This effect may help to explain how environmental factors can increase the susceptibility to IBD.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-10096113, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-10352254, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-10499927, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-10596967, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-10657652, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-10694580, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-10763951, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-10889161, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-11034371, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-11046023, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-11681814, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-11745354, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-11861611, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-11968185, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-12483993, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-12682220, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-14557387, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-14607897, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-15039760, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-15146247, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-15153501, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-15168363, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-15188171, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-15489187, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-15677909, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-15893498, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-16175608, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-17404275, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-2783477, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-3044882, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-6973508, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-7520467, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-7866810, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-7903159, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-8345182, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-9245929, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-9585027, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-9585029, http://linkedlifedata.com/resource/pubmed/commentcorrection/17991290-9973454
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1365-2249
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
151
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
130-8
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
High-fat diet modulates non-CD1d-restricted natural killer T cells and regulatory T cells in mouse colon and exacerbates experimental colitis.
pubmed:affiliation
Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Institute of Digestive Disease, Shanghai, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't