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J Biol Chem ; 288(4): 2882-92, 2013 Jan 25.
Article in English | MEDLINE | ID: mdl-23235150

ABSTRACT

Inflammation induced by wound healing or infection activates local vascular endothelial cells to mediate leukocyte rolling, adhesion, and extravasation by up-regulation of leukocyte adhesion molecules such as E-selectin and P-selectin. Obesity-associated adipose tissue inflammation has been suggested to cause insulin resistance, but weight loss and lipolysis also promote adipose tissue immune responses. While leukocyte-endothelial interactions are required for obesity-induced inflammation of adipose tissue, it is not known whether lipolysis-induced inflammation requires activation of endothelial cells. Here, we show that ß(3)-adrenergic receptor stimulation by CL 316,243 promotes adipose tissue neutrophil infiltration in wild type and P-selectin-null mice but not in E-selectin-null mice. Increased expression of adipose tissue cytokines IL-1ß, CCL2, and TNF-α in response to CL 316,243 administration is also dependent upon E-selectin but not P-selectin. In contrast, fasting increases adipose-resident macrophages but not neutrophils, and does not activate adipose-resident endothelium. Thus, two models of lipolysis-induced inflammation induce distinct immune cell populations within adipose tissue and exhibit distinct dependences on endothelial activation. Importantly, our results indicate that ß(3)-adrenergic stimulation acts through up-regulation of E-selectin in adipose tissue endothelial cells to induce neutrophil infiltration.


Subject(s)
Adipose Tissue/pathology , E-Selectin/metabolism , Receptors, Adrenergic, beta-3/metabolism , Adipose Tissue/metabolism , Animals , Chemokine CCL2/metabolism , Diabetes Mellitus, Type 2/metabolism , Human Umbilical Vein Endothelial Cells , Humans , Immune System , Inflammation , Interleukin-1beta/metabolism , Lipolysis , Mice , Mice, Inbred C57BL , Mice, Knockout , Neutrophils/metabolism , Tumor Necrosis Factor-alpha/metabolism
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