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首页> 外文期刊>Infection and immunity >Stimulation of the ceramide pathway partially mimics lipopolysaccharide-induced responses in murine peritoneal macrophages.
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Stimulation of the ceramide pathway partially mimics lipopolysaccharide-induced responses in murine peritoneal macrophages.

机译：刺激神经酰胺途径部分模拟血红素血糖诱导的鼠腹膜巨噬细胞的反应。

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Recent studies have suggested that lipolysaccharide (LPS) stimulates cells by mimicking the second-messenger function of ceramide, a lipid generated in the cell by the action of sphingomyelinase (SMase). To examine this possibility further, we compared the abilities of LPS, SMase, and/or ceramide analogs to induce cytokine secretion, modulate gene expression, and induce endotoxin tolerance in macrophages. SMase and LPS induced secretion of tumor necrosis factor alpha (TNF-alpha) to comparable degrees; however, unlike LPS, SMase failed to stimulate detectable interferon activity. Cell-permeable analogs of ceramide induced the expression of many LPS-inducible genes; however, the expression of interferon-inducible protein 10 (IP-10) and interferon consensus sequence-binding protein (ICSBP) mRNAs was significantly lower than that induced by LPS. Both SMase-induced TNF-alpha secretion and LPS-induced TNF-alpha secretion were inhibited by pretreatment with a serine/threonine phosphatase inhibitor, calyculin A. Macrophages preexposed in vitro to LPS to induce a well-characterized state of endotoxin tolerance secreted little or no TNF-alpha upon secondary challenge with either LPS or SMase, whereas macrophages preexposed to SMase secreted high levels of TNF-alpha upon secondary stimulation with LPS or SMase. Collectively, these results suggest that ceramide activates a subset of LPS-induced signaling pathways in murine peritoneal exudate macrophages.
机译：最近的研究表明，通过模仿神经酰胺的第二信使函数，通过鞘氨基氨基酶（SMASE）的作用，通过模拟透明酰胺的第二信使函数来刺激细胞的脂肪组糖（LPS）。为了进一步检查这种可能性，我们比较了LPS，Smase和/或神经酰胺类似物的能力，以诱导细胞因子分泌，调节基因表达，并诱导巨噬细胞内毒素耐受性。 SMASE和LPS诱导肿瘤坏死因子α（TNF-alpha）分泌到可比程度;但是，与LPS不同，SMASE未能刺激可检测的干扰素活动。神经酰胺的细胞渗透性类似物诱导许多LPS诱导基因的表达;然而，干扰素可诱导蛋白10（IP-10）和干扰素共有序列结合蛋白（ICSBP）MRNA的表达明显低于LPS诱导的。通过用丝氨酸/苏氨酸磷酸酶抑制剂预处理抑制SMASE诱导的TNF-α分泌和LPS诱导的TNF-α分泌物，抑制剂，巨噬细胞在体外预测到LPS，以诱导细分内毒素耐受性的良好表征状态没有LPS或Smase对次级攻击产生TNF-α，而预先筛选的巨噬细胞在用LPS或SMASE时在二次刺激时分泌高水平的TNF-α。总的来说，这些结果表明神经酰胺激活鼠腹膜渗出物巨噬细胞中的LPS诱导的信号通路的子集。

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