Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-1-5
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.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1938-3673
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
87
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
51-8
pubmed:dateRevised
2010-3-11
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
pubmed:year
2010
pubmed:articleTitle
Enhanced production of IL-17A during zymosan-induced peritonitis in obese mice.
pubmed:affiliation
Department of Kinesiology, University of Illinois, Chicago, IL 60612, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, N.I.H., Extramural