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首页> 外文期刊>American Journal of Physiology >Interleukin-6 and interleukin-15 are selectively regulated by lipopolysaccharide and interferon-gamma in primary pig adipocytes.
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Interleukin-6 and interleukin-15 are selectively regulated by lipopolysaccharide and interferon-gamma in primary pig adipocytes.

机译：白细胞介素6和白细胞介素15由脂多糖和干扰素-γ在猪原代脂肪细胞中选择性调节。

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3T3-L1 adipocytes express the lipopolysaccharide (LPS) receptor and respond to direct stimulation with the antigen by increasing the expression of inflammatory mediators. Activation of this receptor by its ligand in the macrophage causes the activation and translocation of nuclear factor-kappaB (NF-kappaB) to the nucleus where it regulates the expression of proinflammatory cytokines and other target genes. We investigated whether LPS could stimulate NF-kappaB translocation in primary pig adipocytes and regulate the expression and secretion of TNF-alpha and IL-6. LPS clearly induced the nuclear translocation of NF-kappaB and also upregulated (P < 0.05) the mRNA expression and secretion of IL-6 into the culture medium. An induction of TNF-alpha expression by LPS was not detected, but with extended incubation (8 h), there was a modest increase (P < 0.09) in the media concentration of this cytokine. Inhibition of either ERK1/2, PKC, or the inhibitory G protein (Gi) with U-0126, bisindolylmaleimide HCl, andpertussis toxin, respectively, blocked (P < 0.05) the increase in IL-6 expression caused by LPS. Because LPS administration in vivo increases circulating concentrations of IFN-gamma, and because this cytokine also regulates multiple immune modulators in the adipocyte, we also determined whether IFN-gamma regulates cytokine expression in primary adipocytes. Although the expression of IL-6 and TNF-alpha was unresponsive to IFN-gamma, the expression of IL-15 was markedly upregulated (P < 0.01). Furthermore, the induction of IL-15 expression by IFN-gamma was blocked by inhibition of PKC. These data indicate that NF-kappaB is responsive to LPS in the adipocyte and also identify key mediators of LPS-induced IL-6 expression. In addition, we provide novel evidence that IFN-gamma targets the adipocyte to induce IL-15 expression, thus indicating a possible role for the adipocyte in the regulation of T-cell function and muscle metabolism during the innate immune response.
机译：3T3-L1脂肪细胞表达脂多糖（LPS）受体，并通过增加炎症介质的表达来响应抗原的直接刺激。该受体通过其配体在巨噬细胞中的活化引起核因子-κB（NF-κB）的活化和易位至细胞核，在核中调节促炎细胞因子和其他靶基因的表达。我们调查了LPS是否可以刺激原代猪脂肪细胞中的NF-κB易位并调节TNF-α和IL-6的表达和分泌。 LPS明显诱导NF-κB的核易位，并且还上调（P <0.05）IL-6的mRNA表达和分泌到培养基中。没有检测到LPS诱导TNF-α表达，但是随着孵育时间的延长（8小时），该细胞因子的培养基浓度略有增加（P <0.09）。用U-0126，双吲哚基马来酰亚胺HCl和百日咳毒素分别抑制ERK1 / 2，PKC或抑制性G蛋白（Gi），可以阻止（P <0.05）LPS引起的IL-6表达增加。由于在体内进行LPS给药会增加IFN-γ的循环浓度，并且由于该细胞因子还调节脂肪细胞中的多种免疫调节剂，因此我们还确定了IFN-γ是否调节原代脂肪细胞中的细胞因子表达。尽管IL-6和TNF-α的表达对IFN-γ无反应，但IL-15的表达却显着上调（P <0.01）。此外，通过抑制PKC来阻断IFN-γ对IL-15表达的诱导。这些数据表明NF-κB对脂肪细胞中的LPS有反应，并且还确定了LPS诱导的IL-6表达的关键介体。此外，我们提供了新的证据，证明IFN-γ靶向脂肪细胞以诱导IL-15表达，从而表明脂肪细胞在先天性免疫应答过程中调节T细胞功能和肌肉代谢的可能作用。

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