Modulation of human monocyte functions during acute bacterial infection.
The in vitro functions of highly purified blood monocytes were studied in 11 patients suffering from acute bacterial infections (e.g. erysipelas, appendicitis, abscesses). Chemotaxis, superoxide-anion generation, and beta-glucuronidase release of the patients' monocytes in response to the receptor-dependent stimuli formyl-methionyl-leucyl-phenylalanine (FMLP), complement split product C5a, leukotriene B4 (LTB4), and opsonized zymosan particles were measured. All the patients were examined in a follow-up study during the course of illness. A group of 33 healthy volunteers served as control. The patients revealed a transient decrease in monocyte chemotactic migration in response to all stimuli between days 3 and 5 after onset of clinical symptoms. Superoxide-anion generation from patients' monocytes was found to be enhanced 3 days after impaired chemotaxis. Stimulated release of lysosomal beta-glucuronidase showed a decrease in the first days of the disease. However, spontaneous beta-glucuronidase release was enhanced between days 3 and 7 in the patients' monocytes. Serial measurements of monocyte responsiveness. These results indicate a distinct modulation of monocyte functions during the course of an acute bacterial infection. Changes in monocyte maturity and/or activation under inflammatory conditions may be responsible for these alterations in monocyte function.
Mrowietz
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Department of Dermatology, University of Kiel, FRG.
Christophers
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D000208:Acute Disease; D001424:Bacterial Infections / Q000097:blood*; D002465:Cell Movement; D002633:Chemotaxis; D005966:Glucuronidase / Q000378:metabolism; D006801:Humans; D009000:Monocytes / Q000166:cytology / Q000276:immunology / Q000502:physiology*; D013481:Superoxides / Q000378:metabolism
D013481:Superoxides; D005966:Glucuronidase