Trichophyton rubrum can activate complement. In order to assess the role of complement in host defense, fresh human serum was incubated with fungus. Factors were produced which were chemotactic for polymorphonuclear leukocytes (PMNL), but only if complement activation was allowed. This suggests that the chemotactic factor or factors were derived from complement. Incubation of T. rubrum with fresh serum did not prevent fungal growth on subsequent culture, but did inhibit incorporation of radiolabeled N-acetylglucosoamine. The interaction of PMNL and fungi was studied, and the role of complement as a mediator was assessed. PMNL adhered well to fungi provided that the fungal hyphae had been preincubated with fresh human serum to provide complement opsonins. Opsonized and unopsonized fungi both stimulated a respiratory burst in normal PMNL as measured by chemiluminescence, but the burst was generated much faster with opsonized hyphae. Although hyphae with adherent PMNL subsequently proliferated in culture, the incorporation of N-acetylglucosoamine was inhibited 96% when the hyphae were opsonized with fresh serum and then incubated with PMNL. Inhibition was also observed with unopsonized fungi, but to a lesser degree. Varying the ratio of PMNL to hyphae showed that inhibition by PMNL was far more efficient if hyphae were opsonized. In contrast to hyphae, opsonized fungal spores were killed by PMNL so that no growth was observed in subsequent cultures. This killing was not observed if PMNL were omitted or if spores were preincubated with heat-inactivated serum rather than fresh serum. Activation of complement apparently opsonizes the spores so that they can be ingested and killed by viable PMNL. Contents of disrupted PMNL failed to inhibit fungal growth. Complement and PMNL may aid the host in defending itself against infection by dermatophytes.
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