Bautista A P, D'Souza N B, Lang C H, Spitzer J J
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.
Alcohol Clin Exp Res. 1992 Aug;16(4):788-94. doi: 10.1111/j.1530-0277.1992.tb00680.x.
Chronic alcohol consumption has been associated with increased migration of neutrophils into liver that could contribute to the development of alcoholic liver disease. Mild endotoxemia may be at least partially responsible for this condition since endotoxemia was shown to be present in virtually all chronic alcoholics. This study examines the release of superoxide anion and chemotactic activity by Kupffer cells and sequestered hepatic as well as blood neutrophils during chronic alcohol intoxication (16 weeks) alone, and following an intravenous injection of Escherichia coli lipopolysaccharide (LPS) (1 mg/kg) 3 hr before cell isolation. Chronic ethanol consumption increased the total neutrophil yield per liver, but did not change the f-met-leu-phe induced chemotactic activity by both hepatic and blood neutrophils. However, the combined insults of ethanol and LPS increased the chemotactic activity and superoxide anion generation by these cells. Plasma from ethanol-fed rats was highly chemotactic to syngeneic normal rat neutrophils. This activity was increased 1.75-fold in the plasma obtained from chronic ethanol plus endotoxin-injected rats. The chemotactic activity of Kupffer cells was not significantly modulated during ethanol intoxication plus endotoxin treatment. The f-met-leu-phe-induced superoxide anion release by Kupffer cells was enhanced after LPS treatment. Chronic ethanol consumption did not induce any effect on this parameter. These observations suggest that functional alterations in neutrophils during chronic ethanol intoxication may contribute to hepatic injury.
长期饮酒与中性粒细胞向肝脏的迁移增加有关，这可能促进酒精性肝病的发展。轻度内毒素血症可能至少部分导致了这种情况，因为几乎所有慢性酗酒者都存在内毒素血症。本研究考察了单独慢性酒精中毒（16周）期间，以及在细胞分离前3小时静脉注射大肠杆菌脂多糖（LPS）（1mg/kg）后，库普弗细胞、肝内及血液中隔离的中性粒细胞释放超氧阴离子和趋化活性的情况。长期摄入乙醇增加了每只肝脏中性粒细胞的总产量，但并未改变肝内和血液中性粒细胞对f-甲硫-亮-苯丙氨酸诱导的趋化活性。然而，乙醇和LPS的联合损伤增加了这些细胞的趋化活性和超氧阴离子生成。乙醇喂养大鼠的血浆对同基因正常大鼠中性粒细胞具有高度趋化性。在慢性乙醇加内毒素注射大鼠的血浆中，这种活性增加了1.75倍。在乙醇中毒加内毒素治疗期间，库普弗细胞的趋化活性没有受到显著调节。LPS处理后，库普弗细胞对f-甲硫-亮-苯丙氨酸诱导的超氧阴离子释放增强。长期摄入乙醇对该参数没有诱导任何影响。这些观察结果表明，慢性乙醇中毒期间中性粒细胞的功能改变可能导致肝损伤。
