Activation of the alternative (properdin) pathway of complement by Candida albicans and related species.

Accumulations of neutrophilic granulocytes within the epidermis and beneath the stratum corneum of the skin are a prominent histologic feature of experimental and clinical candidiasis. The mechanism of cell accumulation was studied by standard chemotactic methods. Suspensions of viable or heat-killed Candida sp caused marked chemotaxis of human neutrophils in fresh serum. Culture supernatants of Candida sp were not chemotactic. Chemotaxis was dependent upon fresh serum, and could be abolished by heating the serum to 56 degress C for 30 min, suggesting that interaction of these organisms with a heat-labile serum factor generated a chemoattractant. Incubation of Candida sp with fresh human serum resulted in the conversion of the third component of complement and properdin factor B, as measured by immunoelectrophoresis. Conversion did not occur in serum chelated with EDTA, or heated to 50 degress C for 30 min (to destroy factor B). Conversion was present in serum chelated with EGTA (to deplete calcium), or genetically deficient in the fourth component of complement. By contrast, the three components of the kinin-forming system (Hageman factor, prekallikrein, high-molecular-weight kininogen) were not activated by Candida sp. We suggest that Candida sp do not release a chemotactic substance but, in the presence of serum, activate the alternative pathway of complement, generating chemotactic factors.