Nilsson E, Lindström P, Patarroyo M, Ringertz B, Lerner R, Rincon J, Palmblad J
Department of Medicine III, Karolinska Institute, Södersjukhuset, Stockholm, Sweden.
J Infect Dis. 1991 Mar;163(3):591-7. doi: 10.1093/infdis/163.3.591.
Since ethanol impairs polymorphonuclear leukocyte (PMNL) delivery to inflammatory sites, the effect of ethanol on PMNL adhesiveness was studied in vitro. Ethanol inhibited PMNL aggregation induced by formylmethionylleucylphenylalanine (FMLP) but not by phorbol myristate acetate (PMA), whereas responses to both stimuli were abolished by treating PMNL with monoclonal antibody 60.3 (against the adhesion protein CD18). This antibody also abrogated spontaneous and FMLP-stimulated PMNL adhesion to plastic, whereas ethanol reduced spontaneous but not FMLP-induced adherence. Chemotaxis in Boyden or agarose systems was not diminished by ethanol, but high concentrations of MAb 60.3 inhibited migration under agarose. Nonetheless, upregulation of cell surface expression of CD18 (assessed by immunofluorescence flow cytometry) induced by FMLP or PMA was similarly reduced by ethanol. Thus, ethanol inhibited only certain of PMNL adhesion, and although the stimulated up-regulation of CD18 expression was reduced it is unlikely that ethanol effects were mediated only by this inhibition.
由于乙醇会损害多形核白细胞（PMNL）向炎症部位的输送，因此在体外研究了乙醇对PMNL黏附性的影响。乙醇抑制甲酰甲硫氨酰亮氨酰苯丙氨酸（FMLP）诱导的PMNL聚集，但不抑制佛波酯肉豆蔻酸酯乙酸酯（PMA）诱导的聚集，而用单克隆抗体60.3（针对黏附蛋白CD18）处理PMNL后，对这两种刺激的反应均被消除。该抗体还消除了自发的和FMLP刺激的PMNL与塑料的黏附，而乙醇降低了自发黏附，但没有降低FMLP诱导的黏附。乙醇不会降低Boyden或琼脂糖系统中的趋化作用，但高浓度的单克隆抗体60.3会抑制琼脂糖下的迁移。尽管如此，乙醇同样降低了由FMLP或PMA诱导的CD18细胞表面表达上调（通过免疫荧光流式细胞术评估）。因此，乙醇仅抑制PMNL的某些黏附，并且尽管CD18表达的刺激上调有所降低，但乙醇的作用不太可能仅通过这种抑制介导。
