Polymorphonuclear leucocyte locomotion and aggregation in patients with alcoholic liver disease.
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.
D000328:Adult; D000368:Aged; D002449:Cell Aggregation; D002465:Cell Movement; D002634:Chemotaxis, Leukocyte; D003182:Complement C5; D015936:Complement C5a; D005260:Female; D006801:Humans; D008108:Liver Diseases, Alcoholic / Q000097:blood* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009240:N-Formylmethionine Leucyl-Phenylalanine; D009504:Neutrophils / Q000502:physiology*
D003182:Complement C5; D009240:N-Formylmethionine Leucyl-Phenylalanine; D015936:Complement C5a