Sopasakis V R, Nagaev I, Smith U
The Lundberg Laboratory for Diabetes Research, Department of Internal Medicine, The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden.
Int J Obes (Lond). 2005 Sep;29(9):1144-7. doi: 10.1038/sj.ijo.0803002.
Explants of human adipose tissue from nonobese subjects were cultured for 24 h with or without the presence of 20 ng/ml TNFalpha. Gene expression and/or medium concentrations of interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1 RA), TNFalpha, IL-6, IL-8, resistin, PAI-1 and leptin were analysed. TNFalpha increased the mRNA levels of TNFalpha itself as well as IL-6, IL-8, IL-1beta and PAI-1, but not leptin. The medium concentrations of IL-1 RA, IL-6 and IL-8 were markedly increased by TNFalpha while no measurable release of TNFalpha, resistin or IL-1beta to the medium was found. Thus, human adipose tissue from nonobese individuals releases substantial amounts of IL-6, IL-8 and IL-1 RA and the gene expression of these cytokines, like that of IL-1beta and PAI-1, is regulated by TNFalpha. However, since neither TNFalpha, resistin or IL-1beta was found in the culture medium, such a regulatory effect by TNFalpha on adipose tissue in vivo is likely to be mediated through a paracrine mechanism where invaded inflammatory cells may play a critical role.
将来自非肥胖受试者的人脂肪组织外植体在有或无20 ng/ml肿瘤坏死因子α（TNFα）存在的情况下培养24小时。分析白细胞介素（IL）-1β、IL-1受体拮抗剂（IL-1 RA）、TNFα、IL-6、IL-8、抵抗素、纤溶酶原激活物抑制剂-1（PAI-1）和瘦素的基因表达及/或培养基浓度。TNFα增加了其自身以及IL-6、IL-8、IL-1β和PAI-1的mRNA水平，但未增加瘦素的mRNA水平。TNFα显著增加了IL-1 RA、IL-6和IL-8的培养基浓度，而未发现TNFα、抵抗素或IL-1β向培养基中的可测量释放。因此，来自非肥胖个体的人脂肪组织释放大量的IL-6、IL-8和IL-1 RA，并且这些细胞因子的基因表达，如IL-1β和PAI-1的基因表达，受TNFα调节。然而，由于在培养基中未发现TNFα、抵抗素或IL-1β，TNFα对体内脂肪组织的这种调节作用可能通过旁分泌机制介导，其中侵入的炎症细胞可能起关键作用。
