Source:http://linkedlifedata.com/resource/pubmed/id/19745158
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2010-1-5
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pubmed:abstractText |
IL-17A is a proinflammatory cytokine critical for host defense and involved in the pathogenesis of autoimmune disorders. Obesity is associated with chronic low-grade inflammation but also with a heightened acute inflammatory response. We investigated the effect of obesity on IL-17A production using the model of ZY-induced peritonitis. Compared with lean controls, administration of ZY induced a significantly exacerbated inflammatory response in obese leptin-deficient ob/ob mice and in mice with diet-induced obesity (DIO). Levels of IL-17A in the peritoneal fluid in response to ZY were elevated significantly in ob/ob and DIO mice compared with lean animals. Reconstitution of ob/ob mice with exogenous leptin did not alter production of IL-17A significantly in response to ZY. Peritoneal cells and adipose tissue obtained from ZY-injected obese mice expressed significantly higher levels of IL-17A mRNA compared with lean mice. Approximately 2% of peritoneal Ly6G(+) neutrophils from ZY-injected obese mice expressed IL-17A protein, compared with 0.2% of cells obtained from lean mice. Neutralization of IL-17 in ob/ob mice inhibited neutrophil recruitment and production of neutrophil-attracting CXC chemokines and IL-6, without affecting macrophage infiltration or levels of IL-10 and the chemokine CCL2. In contrast, neutralization of IL-6 did not affect production of IL-17A or chemokines while reducing production of the acute-phase protein serum amyloid A significantly. These data demonstrate that neutrophil-derived IL-17A is increased in obese mice during acute inflammation and contributes to exacerbation of inflammatory responses.
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pubmed:grant | |
pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC,
http://linkedlifedata.com/resource/pubmed/chemical/Dietary Fats,
http://linkedlifedata.com/resource/pubmed/chemical/Il17a protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/Zymosan
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1938-3673
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
87
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
51-8
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pubmed:dateRevised |
2010-3-11
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pubmed:meshHeading |
pubmed-meshheading:19745158-Acute Disease,
pubmed-meshheading:19745158-Animals,
pubmed-meshheading:19745158-Ascitic Fluid,
pubmed-meshheading:19745158-Chemokines, CXC,
pubmed-meshheading:19745158-Dietary Fats,
pubmed-meshheading:19745158-Female,
pubmed-meshheading:19745158-Gene Expression Regulation,
pubmed-meshheading:19745158-Inflammation,
pubmed-meshheading:19745158-Interleukin-17,
pubmed-meshheading:19745158-Interleukin-6,
pubmed-meshheading:19745158-Intra-Abdominal Fat,
pubmed-meshheading:19745158-Leptin,
pubmed-meshheading:19745158-Male,
pubmed-meshheading:19745158-Mice,
pubmed-meshheading:19745158-Mice, Inbred C57BL,
pubmed-meshheading:19745158-Mice, Obese,
pubmed-meshheading:19745158-Neutrophils,
pubmed-meshheading:19745158-Obesity,
pubmed-meshheading:19745158-Peritonitis,
pubmed-meshheading:19745158-T-Lymphocyte Subsets,
pubmed-meshheading:19745158-Thinness,
pubmed-meshheading:19745158-Zymosan
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pubmed:year |
2010
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pubmed:articleTitle |
Enhanced production of IL-17A during zymosan-induced peritonitis in obese mice.
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pubmed:affiliation |
Department of Kinesiology, University of Illinois, Chicago, IL 60612, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, N.I.H., Extramural
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