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INFLUENCE OF ENDOTOXIN AND COMPLEX BACTERIAL ANTIGENS IN THE PRESENCE OF SERUM FACTORS UPON THE FUNCTION OF HUMAN NEUTROPHILS IN VITRO
Author(s) -
Koch Christian
Publication year - 1975
Publication title -
acta pathologica microbiologica scandinavica section c immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0304-1328
DOI - 10.1111/j.1699-0463.1975.tb01626.x
Subject(s) - microbiology and biotechnology , antigen , in vivo , immune system , in vitro , ingestion , bacteria , intracellular , staphylococcus aureus , human serum albumin , biology , incubation , stimulation , bovine serum albumin , chemistry , immunology , biochemistry , genetics , neuroscience
Endotoxin, added to normal human neutrophils in the presence of serum, simultaneously with the addition of Staphylococcus aureus, caused stimulation of ingestion as well as intracellular killing of the bacteria in doses ranging from 0.1 to 1000 μg endotoxin per ml. Stimulation of ingestion was also induced by simultaneous addition of complex microbial antigens, heat‐killed bacteria, and precipitating as well as soluble human serum albumin (HSA)/anti‐HSA complexes. On the other hand, inhibition of intracellular killing could be induced when the leucocytes were pre‐incubated with endotoxin or precipitating HSA/anti‐HSA complexes. High doses of complex microbial antigens, particularly in the presence of immune serum containing multiple specific precipitating antibodies, resulted in inhibition of intracellular killing after pre‐incubation as well as by simultaneous addition to the neutrophils with the bacteria. It is suggested that the functional changes, induced by endotoxin and by microbial antigens, are secondary to ingestion of immune complexes. These changes are, however, not as pronounced as those previously demonstrated in circulating neutrophils from patients with severe bacterial infection. Direct interaction of endotoxin or microbial antigens with the neutrophils in vivo, is not solely responsible for the functional changes seen in patients with severe bacterial infection, but prolonged exposure of the neutrophils to such agents in vivo, may add to the killing defect observed in vitro.