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首页> 外文期刊>American Journal of Physiology >Lipopolysaccharide regulates proinflammatory cytokine expression in mouse myoblasts and skeletal muscle.
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Lipopolysaccharide regulates proinflammatory cytokine expression in mouse myoblasts and skeletal muscle.

机译：脂多糖调节小鼠成肌细胞和骨骼肌中促炎细胞因子的表达。

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摘要

The purpose of the present study was to examine the regulation of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 by lipopolysaccharide (LPS) in C2C12 myoblasts and mouse skeletal muscle. LPS produced dose- and time-dependent increases in TNF-alpha and IL-6 mRNA content in C2C12 myoblasts. The LPS-induced cytokine response could be mimicked by peptidoglycan from the cell wall of Staphylococcus aureus but not by zymosan A, a cell wall component from Saccharomyces cerevisiae. Ongoing protein synthesis was not necessary for the increase in the two cytokine mRNAs. The transcriptional inhibitor 5,6-dichloro-beta-D-ribofuranosyl-benzimidazole blocked LPS-stimulated IL-6 mRNA expression without changing its mRNA half-life. The anti-inflammatory glucocorticoid dexamethasone selectively blocked LPS-stimulated IL-6 mRNA accumulation but not TNF-alpha. In contrast, the proteasomal inhibitor MG-132 blocked TNF-alpha mRNA expression but not IL-6. Exposure of myoblasts to LPS was associated with a rapid decrease in the inhibitor of nuclear factor-kappaB (I kappaB, alpha, and epsilon), and this response was also blocked by MG-132. Treatment of myocytes with IL-1 or TNF-alpha also increased IL-6 mRNA content, but the increase in IL-6 mRNA due to LPS could not be prevented by pretreatment with antagonists to either IL-1 or TNF. Under in vivo conditions, LPS increased the plasma concentration of TNF-alpha and IL-6 and stimulated the accumulation of their mRNAs in multiple tissues including skeletal muscle from wild-type mice. In contrast, the ability of LPS to stimulate the same cytokines was markedly decreased in mice that harbor a mutation in the Toll-like receptor 4. Our data suggest that LPS stimulates cytokine expression not only in classical immune tissues but also in skeletal muscle.
机译：本研究的目的是研究脂多糖（LPS）对C2C12成肌细胞和小鼠骨骼肌中肿瘤坏死因子（TNF）-α和白介素（IL）-6的调节。 LPS导致C2C12成肌细胞中TNF-alpha和IL-6 mRNA含量呈剂量和时间依赖性增加。 LPS诱导的细胞因子反应可以通过金黄色葡萄球菌细胞壁上的肽聚糖来模拟，而不能通过酵母菌（酵母菌的细胞壁成分）zymosan A来模拟。正在进行的蛋白质合成对于两个细胞因子mRNA的增加不是必需的。转录抑制剂5，6-二氯-β-D-呋喃核糖基-苯并咪唑可阻断LPS刺激的IL-6 mRNA表达，而不会改变其mRNA半衰期。抗炎糖皮质激素地塞米松选择性阻断LPS刺激的IL-6 mRNA积累，但不能阻断TNF-α。相反，蛋白酶体抑制剂MG-132阻断TNF-αmRNA表达，但不阻断IL-6。成肌细胞暴露于LPS与核因子-kappaB（I kappaB，α和ε）抑制剂的快速减少有关，并且该反应也被MG-132阻断。用IL-1或TNF-α处理心肌细胞也会增加IL-6 mRNA的含量，但是通过用IL-1或TNF拮抗剂进行预处理无法防止由于LPS引起的IL-6 mRNA的增加。在体内条件下，LPS可增加TNF-α和IL-6的血浆浓度，并刺激其mRNA在野生型小鼠骨骼肌等多种组织中的积累。相反，在具有Toll样受体4突变的小鼠中，LPS刺激相同细胞因子的能力明显降低。我们的数据表明，LPS不仅刺激经典免疫组织而且还刺激骨骼肌的细胞因子表达。

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