C5a-specific modulation of phagocyte functions in patients with localized bacterial infections.
Chemotaxis, enzyme release and superoxide-anion (O2-) generation of purified peripheral blood neutrophils (PMN) and monocytes were studied in a total of 87 patients suffering from localized bacterial infections. Shortly after disease onset, single or several PMN functions became non-responsive to the complement split product C5a. Functional activities elicited by the synthetic peptide f-met-leu-phe or leukotriene B4 remained unaltered. C5a-specific impairment lasted one to several days and returned to normal with the subsidence of the disease. C5a elicited release of beta-glucuronidase as well as generation of superoxide-anions was seen more often to be impaired as compared to chemotactic migration. In contrast to PMN, monocytes from the same patients failed to show paralleling C5a-specific functional alterations. There was no correlation between impairment of PMN functions and plasma levels of the complement split-products C3a and C4a as determined by RIA. It is concluded that in acute infectious disease a graded C5a-specific modulation of PMN functions may be present. This phenomenon is transient and not paralleled by functional alterations of monocytes or changes in plasma complement levels.
Mrowietz
U
U
Department of Dermatology, University of Kiel, Federal Republic of Germany.
Christophers
E
E
Schröder
J M
JM
D001424:Bacterial Infections / Q000276:immunology*; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D003182:Complement C5 / Q000276:immunology*; D005966:Glucuronidase / Q000096:biosynthesis; D006801:Humans; D009000:Monocytes / Q000201:enzymology / Q000276:immunology / Q000378:metabolism; D009504:Neutrophils / Q000201:enzymology / Q000276:immunology* / Q000378:metabolism; D013481:Superoxides / Q000096:biosynthesis
D003182:Complement C5; D013481:Superoxides; D005966:Glucuronidase