Related Experiment Videos
Polymorphonuclear leukocytes, complement, and Trichophyton rubrum
Abstract:
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.
Insights
Complement activation by Trichophyton rubrum generates chemotactic factors and enhances polymorphonuclear leukocyte (PMNL) interaction with fungi. Complement opsonization significantly boosts PMNL
Area of Science:
- Immunology
- Mycology
- Dermatophytosis
Background:
- Trichophyton rubrum is a common dermatophyte causing superficial fungal infections.
- The role of the complement system and polymorphonuclear leukocytes (PMNL) in host defense against T. rubrum is not fully elucidated.
- Understanding these interactions is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To investigate the role of complement activation in the host immune response to Trichophyton rubrum.
- To assess the synergistic effects of complement and PMNL in controlling fungal growth and viability.
Main Methods:
- Incubation of T. rubrum with fresh human serum to activate complement.
- Assessing chemotaxis of PMNL towards fungal components.
- Measuring fungal growth and metabolic activity (radiolabeled N-acetylglucosamine incorporation) after incubation with serum and PMNL.
- Evaluating PMNL adherence and respiratory burst activity (chemiluminescence) in response to opsonized and unopsonized fungi.
Main Results:
- Complement activation produced factors chemotactic for PMNL.
- Complement opsonization significantly enhanced PMNL adherence to fungal hyphae and stimulated a faster respiratory burst.
- Opsonized T. rubrum hyphae showed significantly inhibited metabolic activity when incubated with PMNL.
- Opsonized fungal spores were killed by PMNL, preventing subsequent growth, unlike unopsonized spores or spores incubated with heat-inactivated serum.
Conclusions:
- Complement activation is essential for generating PMNL-attracting factors and facilitating PMNL-fungal interactions.
- Complement-mediated opsonization significantly enhances the fungistatic and fungicidal capabilities of PMNL against T. rubrum.
- The combined action of complement and PMNL represents a key host defense mechanism against dermatophyte infections.