Contribution of complement component C5 to the pathogenesis of experimental murine cryptococcosis

Abstract

C5-deficient (C5⁻) mice succumb much sooner after intravenous inoculation with Cryptococcus neoformans than do C5-sufficient (C5⁺) mice. The C5⁻ mice developed acute, fatal cryptococcal pneumonia, whereas the C5⁺ mice did not. The pneumonia was characterized by lung viable counts in C5⁻ mice up to 1000-fold higher than in C5⁺, initial sequestration of twice as much ⁵⁹Fe-labeled C. neoformans, and subsequent development of pulmonary edema. Chemotaxis of heterophils (PMNs) and mononuclear cells in response to C. neoformans was markedly greater in C5⁺ mice than in C5⁻ animals. The effect of C5 on localization and growth of C. neoformans in the lung appeared to account for the disparate survival times of C5⁺ and C5⁺ mice after intravenous inoculation with C. neoformans.