Combined B- and T-cell deficiency does not protect against obesity-induced glucose intolerance and inflammation

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• 作者：Dov B. Ballak^a ; ^b ; ^{d.ballak@aig.umcn.nl} ; Rinke Stienstra^a ; ^b ; Anneke Hijmans^b ; Leo A.B. Joosten^a ; Mihai G. Netea^a ; Cees J. Tack^b
• 关键词：Obesity-induced inflammation ; Adaptive immune system ; Adipose tissue ; Glucose intolerance ; Macrophages
• 刊名：Cytokine
• 出版年：2013
• 出版时间：April, 2013
• 年：2013
• 卷：62
• 期：1
• 页码：96-103
• 全文大小：944 K

文摘

Obesity-induced inflammation is associated with insulin resistance and morphologically characterized by macrophage influx into the adipose tissue. Recently, various other immune cells, including B- and T-cells, have been shown to participate in modulating adipose tissue inflammation during the development of obesity. We show that HFD-feeding modulates the influx of B and T-cells into adipose tissue of obese animals, suggestive of a role of the adaptive immune system in the development of adipose tissue inflammation. Despite a lower bodyweight after HFD-feeding, gene expression levels of CD68, F4/80 and MCP-1 in white adipose tissue were enhanced in SCID animals that lack B- and T-cells. Moreover, conditioned medium from adipose tissue explants of HFD-fed SCID mice revealed increased release of IL-6 and CXCL1 compared to WT animals. Compared to WT mice, glucose tolerance was impaired in B- and T-cell deficient mice after HFD-feeding. Thus, complete B- and T-cell deficiency does not protect against HFD-induced adipose tissue inflammation and glucose intolerance. In contrast, SCID mice showed an increased pro-inflammatory status at the level of the adipose tissue in some cytokines. Our findings suggest that a delicate balance between various B- and T-cell populations controls adipose tissue inflammation.