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首页> 外文期刊>Alcohol >Acute alcohol intoxication suppresses the pulmonary ELR-negative CXC chemokine response to lipopolysaccharide.
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Acute alcohol intoxication suppresses the pulmonary ELR-negative CXC chemokine response to lipopolysaccharide.

机译：急性酒精中毒可抑制肺ELR阴性CXC趋化因子对脂多糖的反应。

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Alcohol abuse impairs the pulmonary immune response to infection and increases the morbidity and mortality of bacterial pneumonia. Acute alcohol intoxication suppresses lung expression of CXC chemokines bearing the Glu-Leu-Arg motif (ELR+) following lipopolysaccharide (LPS) challenge, but its effect on the structurally related ELR- CXC chemokines, which attract T cells, is unknown. We therefore investigated the effect of acute alcohol intoxication on the pulmonary response to intratracheal (i.t.) LPS challenge for the ELR- CXC chemokines monokine induced by gamma (MIG or CXCL9), interferon-inducible protein 10 (IP-10 or CXCL10), and interferon-inducible T cell alpha chemoattractant (I-TAC or CXCL11). Male C57BL/6 or C3H/HeN mice were given an intraperitoneal injection of ethanol (3.0 g/kg) or phosphate buffered saline 30 min before i.t. LPS challenge. Chemokine mRNA transcripts were measured at 0, 2, 6, and 16 h. Acute alcohol intoxication inhibited the lung's expression of all three chemokine genes inresponse to LPS. Lung IFN-gamma mRNA was also inhibited by acute intoxication over the same time course. The in vitro effect of ethanol on chemokine secretion was further studied in the MH-S alveolar macrophage cell line. IP-10, MIG, and I-TAC in response to LPS were enhanced by exogenous interferon (IFN)-gamma, and these responses were blunted by exposure to ethanol. Alcohol exposure did not affect MH-S cell nuclear factor kappa beta p65 nuclear localization during challenge, despite dose-dependent inhibition of Erk 1/2 phosphorylation. In addition, phospho-signal transduction and activator of transcription 1 was not decreased in the presence of acute ethanol, thereby indicating that acute intoxication does not affect IFN-gamma signaling in MH-S cells. Recruitment of CD3+ T cells into the alveolar space 4 days after LPS challenge was moderately impaired by acute ethanol intoxication. These results implicate acute ethanol intoxication as a significant inhibitor of lymphocyte chemoattractant expression during pulmonary inflammation.
机译：滥用酒精会损害肺部对感染的免疫反应，并增加细菌性肺炎的发病率和死亡率。急性酒精中毒会抑制脂多糖（LPS）攻击后带有Glu-Leu-Arg基序（ELR +）的CXC趋化因子的肺表达，但其对结构相关的吸引T细胞的ELR-CXC趋化因子的作用尚不清楚。因此，我们研究了急性酒精中毒对由伽玛（MIG或CXCL9），干扰素诱导型蛋白10（IP-10或CXCL10）诱导的ELR-CXC趋化因子单因子对气管内LPS激发的肺部反应的影响。干扰素诱导性T细胞α化学引诱剂（I-TAC或CXCL11）。雄性C57BL / 6或C3H / HeN小鼠在腹膜内注射前30分钟进行腹膜内注射乙醇（3.0 g / kg）或磷酸盐缓冲液。 LPS挑战。在0、2、6和16小时测量趋化因子mRNA转录物。急性酒精中毒抑制了LPS响应的所有三个趋化因子基因的肺表达。在同一时间段，急性中毒也抑制了肺IFN-γmRNA。在MH-S肺泡巨噬细胞系中进一步研究了乙醇对趋化因子分泌的体外作用。外源干扰素（IFN）-γ可增强IP-10，MIG和I-TAC对LPS的反应，而暴露于乙醇会使这些反应变得迟钝。尽管剂量依赖性抑制Erk 1/2磷酸化，但在暴露过程中，酒精暴露不会影响MH-S细胞核因子kappa beta p65的核定位。另外，在急性乙醇的存在下磷酸信号转导和转录激活因子1没有降低，因此表明急性中毒并不影响MH-S细胞中的IFN-γ信号传导。 LPS攻击后第4天，急性乙醇中毒会损害CD3 + T细胞向肺泡腔的募集。这些结果暗示急性乙醇中毒是肺炎症期间淋巴细胞趋化因子表达的重要抑制剂。

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