Complement-mediated immune mechanisms in renal infection.
The belief that the inactivation of complement by renal ammonia enhances the susceptibility of renal tissue to infection has been held for some years. This thesis has been investigated in the present experiments using cultures of renal tissue maintained in vitro under physiological conditions. The experiments have confirmed that exposure of normal serum to renal issue in culture does result in the rapid loss of complement activity, but that the inactivation was not due to renal ammonia. Furthermore, in quantitative experiments, the liver was found to have even greater anti-complementary activity than renal tissue. In experiments where the biological significance of this phenomenon was examined, it was shown that the bactericidal capacity of serum was maintained even after exposure to renal tissue. The results of these investigations suggest that the biological significance of the inactivation of complement by renal tissue in vitro has been over-emphasized and requires further studies in vivo.
D000641:Ammonia / Q000378:metabolism; D000818:Animals; D001770:Blood Bactericidal Activity; D003167:Complement Activation; D003176:Complement C3 / Q000032:analysis; D003169:Complement Inactivator Proteins; D046508:Culture Techniques; D005260:Female; D005612:Freeze Drying; D007668:Kidney / Q000276:immunology* / Q000378:metabolism; D008099:Liver / Q000276:immunology / Q000378:metabolism; D011480:Protease Inhibitors / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D003176:Complement C3; D003169:Complement Inactivator Proteins; D011480:Protease Inhibitors; D000641:Ammonia