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Updated: Aug 14, 2026
Viability Assay of Trichoderma stromaticum Conidia Inside Human Peripheral Blood Mononuclear-Derived Macrophages
Published on: October 20, 2023
Stimulation, inhibition and death of macrophages infected with Trichophyton rubrum
M R M Campos1, M Russo, E Gomes
1Departamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, Avenida Prof. Lineu Prestes, 580, Bloco 17, CEP 05508-900, São Paulo, Brazil.
Abstract:
Trichophyton rubrum is the most common pathogen causing dermatophytosis, accounting for approximately 80% of the reported cases of onychomycosis. Since 90% of the chronic dermatophyte infections are caused by T. rubrum, it is likely that this pathogen must have evolved mechanisms that evade or suppress cell-mediated immunity. Several reports have highlighted the participation of phagocytes in the immune defense against fungi; however, few studies have addressed the role of these cells in dermatophytosis. In this study, we investigated the interactions of resident and peritoneal macrophages with T. rubrum. We show here that the interaction of T. rubrum conidia with resident macrophages results in the production of TNF-alpha and IL-10 but not IL-12 and nitric oxide. Infected macrophages down-regulated the expression of co-stimulatory molecules (CD80 and CD54). We also show that phagocytosis of T. rubrum conidia is inhibited by the addition of fungal exoantigens or mannan. Cytotoxicity assays indicated that after 8 h of conidia ingestion macrophage viability decreased drastically. Electron microscopy revealed that the ingested conidia grow and differentiate into hyphae inside macrophages leading to rupture of the macrophage membrane.
Insights
Trichophyton rubrum evades immune responses by inhibiting macrophage functions. This common fungus suppresses key immune signals and grows inside macrophages, leading to cell death and chronic infections.
Area of Science:
- Immunology
- Mycology
- Dermatology
Background:
- Trichophyton rubrum is the primary cause of dermatophytosis and onychomycosis.
- Chronic infections suggest T. rubrum possesses immune evasion mechanisms.
- The role of phagocytes in dermatophytosis immunity is underexplored.
Purpose of the Study:
- To investigate the interaction between T. rubrum and macrophages.
- To understand how T. rubrum affects macrophage immune functions.
Main Methods:
- Co-culture of T. rubrum conidia with resident and peritoneal macrophages.
- Measurement of cytokine production (TNF-alpha, IL-10, IL-12) and nitric oxide.
- Analysis of co-stimulatory molecule expression (CD80, CD54).
- Inhibition assays using fungal exoantigens and mannan.
- Macrophage cytotoxicity assays and electron microscopy.
Main Results:
- T. rubrum conidia induced TNF-alpha and IL-10, but not IL-12 or nitric oxide, in macrophages.
- Macrophage expression of CD80 and CD54 was down-regulated.
- Phagocytosis was inhibited by fungal exoantigens and mannan.
- Macrophage viability decreased significantly after T. rubrum conidia ingestion.
- T. rubrum conidia grew into hyphae within macrophages, causing cell lysis.
Conclusions:
- T. rubrum actively suppresses macrophage-mediated immune responses.
- The fungus employs strategies to survive and proliferate intracellularly within macrophages.
- These mechanisms contribute to the chronicity and persistence of T. rubrum infections.
