Macrophage secretion and the complement cleavage product C3a in the pathogenesis of infections by mycoplasmas and L-forms of bacteria and in immunity to these organisms.
Mouse peritoneal macrophages in culture exposed to Mycoplasma pulmonis show marked biochemical changes. This micro-organism induces the release of hydrolytic enzymes from macrophages. The release is time- and dose-dependent and is not associated with loss of the cytoplasmic enzyme lactate dehydrogenase or any other sign of cell death. Secretory products of macrophages may play a role in the pathogenesis of chronic inflammatory responses elicited by mycoplasma infections. One of the products of activated macrophages is the complement cleavage product C3a. Purified C3a was incubated with M. hominis, M. pulmonis, Proteus mirabilis and an L-phase variant of this organism. All mycoplasmas and the L-phase variant were lysed by low concentrations of C3a, whereas the bacterial form of Pr. mirabilis was resistant.
D000818:Animals; D002478:Cells, Cultured; D003176:Complement C3 / Q000276:immunology*; D004306:Dose-Response Relationship, Immunologic; D006867:Hydrolases / Q000378:metabolism; D007740:L Forms; D008264:Macrophages / Q000201:enzymology / Q000276:immunology*; D051379:Mice; D008854:Microscopy, Electron; D009174:Mycoplasma / Q000648:ultrastructure; D009175:Mycoplasma Infections / Q000276:immunology*; D011512:Proteus Infections / Q000276:immunology; D011513:Proteus mirabilis; D013997:Time Factors
D003176:Complement C3; D006867:Hydrolases