Rajkovic I A, Yousif-Kadaru A G, Wyke R J, Williams R
Clin Exp Immunol. 1984 Dec;58(3):654-62.
Defects in stimulated movement of polymorphonuclear (PMN) leucocytes was detected in 57% of patients with alcoholic liver disease. Serum from patients with the cellular defect had no effect on the function of normal PMN leucocytes. Aggregation responses of patients' PMN leucocytes suggest that the cellular defect may be related to specific abnormalities in the response to the C5a chemotactic factor. Defective serum attractant activity was found in 65% of the patients tested and the presence in the patients serum of humoral directed antagonists appeared to be responsible for the defect in majority of cases. Further analysis pointed to the presence of at least two distinct antagonists and the possible involvement of proteases in this serum abnormality. The activity of the serum antagonists or the severity of the cellular defect were unrelated to the presence of bacterial infection or elevations in serum IgA or IgG. The high frequency of cellular defects, possibly as a result of in vivo activation, in conjunction with serum abnormalities could account for the increased susceptibility of patients with alcoholic liver disease to bacterial infection.
在57%的酒精性肝病患者中检测到多形核（PMN）白细胞刺激运动缺陷。细胞缺陷患者的血清对正常PMN白细胞的功能没有影响。患者PMN白细胞的聚集反应表明，细胞缺陷可能与对C5a趋化因子反应的特定异常有关。在65%的检测患者中发现血清趋化活性缺陷，在大多数情况下，患者血清中存在体液定向拮抗剂似乎是导致该缺陷的原因。进一步分析表明至少存在两种不同的拮抗剂，并且蛋白酶可能参与了这种血清异常。血清拮抗剂的活性或细胞缺陷的严重程度与细菌感染的存在或血清IgA或IgG升高无关。细胞缺陷的高频率（可能是体内激活的结果）与血清异常相结合，可能解释了酒精性肝病患者对细菌感染易感性增加的原因。
