ALCOHOL SUPPRESSES LIPOPOLYSACCHARIDE-INDUCED TUMOR NECROSIS FACTOR ACTIVITY IN SERUM AND LUNG
ALCOHOL SUPPRESSES LIPOPOLYSACCHARIDE-INDUCED TUMOR NECROSIS FACTOR ACTIVITY IN SERUM AND LUNG
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DOI：
10.1016/0024-3205(89)90472-4
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发表时间：
1989-01-01
期刊：
影响因子：
6.1
通讯作者：
SUMMER, WR
中科院分区：
文献类型：
--
作者：
NELSON, S;BAGBY, G;SUMMER, WR
乙醇中毒已被证明抑制免疫系统的选定功能，从而损害宿主对细菌感染的防御。肿瘤坏死因子是巨噬细胞对脂多糖产生的一种分泌性蛋白，介导炎症级联反应并刺激吞噬细胞功能。急性乙醇中毒明显抑制血清和肺肿瘤坏死因子引起的响应脂多糖。此外，乙醇可抑制内毒素诱导的中性粒细胞向肺泡的募集，并防止循环中性粒细胞对静脉内毒素的反应下降。因此，乙醇的抗炎作用可能是继发于抑制巨噬细胞源性肿瘤坏死因子。
Ethanol intoxication has been shown to suppress selected functions of the immune system thereby compromising host defense against bacterial infections. Tumor necrosis factor, a secretory protein produced by the macrophage in response to lipopolysaccharide, mediates the inflammatory cascade and stimulates phagocyte functions. Acute ethanol intoxication markedly suppressed both serum and lung tumor necrosis factor elicited in response to lipopolysaccharide. Furthermore, ethanol inhibited intratracheal lipopolysaccharide-induced neutrophil recruitment into the alveoli and prevented the fall in circulation neutrophils in response to intravenous lipopolysaccharide. Thus, the anti-inflammatory effects of ethanol may be secondary to suppression of macrophage-derived tumor necrosis factor.