Antibody-independent complement consumption by Micropolyspora faeni.
Micropolyspora faeni is an etiologic agent of hypersensitivity pneumonitis, a disease with an ill-defined mechanism of pathogenesis. Many reports have suggested an immunologic mechanism. A number of laboratories have demonstrated a nonantibody-mediated activation of the complement cascade. This study was undertaken to define the pathway of the complement consumption induced by M. faeni. We utilized an extract of M. faeni grown on synthetic media rather than the more common double dialysis extracts. Complement consumption by this extract was easily demonstrable in the absence of detectable antibody, but was inhibited by EDTA and MgEGTA. With the exception f C1, all of the early components of the classical pathway were markedly reduced following incubation of normal human serum with this extract. C1 was poorly consumed. In addition, factor B conversion to B was not inhibited by 10 mM MgEGTA suggests that the alternative pathway may also be affected. The generation of M. faeni-dependent chemotactic factor(s) from serum demonstrates that the complement cascade is being activated rather than inhibited.
D000906:Antibodies; D003172:Complement C1; D003176:Complement C3; D003181:Complement C4; D003165:Complement System Proteins; D004492:Edetic Acid / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D004591:Electrophoresis, Polyacrylamide Gel; D005203:Farmer's Lung / Q000276:immunology; D005455:Fluorescent Antibody Technique; D008848:Micromonosporaceae / Q000276:immunology*; D011951:Receptors, Complement
D000906:Antibodies; D003172:Complement C1; D003176:Complement C3; D003181:Complement C4; D011951:Receptors, Complement; D004533:Egtazic Acid; D003165:Complement System Proteins; D004492:Edetic Acid