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Updated: Apr 12, 2026
Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
Published on: February 18, 2015
IL-1 signaling inhibits Trichophyton rubrum conidia development and modulates the IL-17 response in vivo
Fábio Seiti Yamada Yoshikawa1, Lucas Gonçalves Ferreira, Sandro Rogério de Almeida
1a Faculty of Pharmaceutical Sciences; Department of Clinical e Toxicological Analysis; University of São Paulo ; São Paulo , Brazil.
Abstract:
Dermatophytosis are one of the most common fungal infections in the world. They compromise keratinized tissues and the main etiological agent is Trichophyton rubrum. Macrophages are key cells in innate immunity and prominent sources of IL-1β, a potent inflammatory cytokine whose main production pathway is by the activation of inflammasomes and caspase-1. However, the role of inflammasomes and IL-1 signaling against T.rubrum has not been reported. In this work, we observed that bone marrow-derived macrophages produce IL-1β in response to T.rubrum conidia in a NLRP3-, ASC- and caspase-1-dependent fashion. Curiously, lack of IL-1 signaling promoted hyphae development, uncovering a protective role for IL-1β in macrophages. In addition, mice lacking IL-1R showed reduced IL-17 production, a key cytokine in the antifungal defense, in response to T.rubrum. Our findings point to a prominent role of IL-1 signaling in the immune response to T.rubrum, opening the venue for the study of this pathway in other fungal infections.
Insights
Interleukin-1 beta (IL-1β) signaling is crucial for controlling the fungal pathogen Trichophyton rubrum. This pathway limits fungal growth and enhances antifungal defenses, highlighting its importance in dermatophytosis immunity.
Area of Science:
- Immunology
- Mycology
- Infectious Diseases
Background:
- Dermatophytosis, a common fungal infection, is primarily caused by Trichophyton rubrum.
- Macrophages are vital for innate immunity and produce IL-1β via inflammasome activation.
- The role of IL-1 signaling in T. rubrum infections was previously unknown.
Purpose of the Study:
- To investigate the role of inflammasomes and IL-1 signaling in the host response to T. rubrum.
- To determine if macrophages utilize IL-1β production against T. rubrum.
- To elucidate the function of IL-1 signaling in T. rubrum infection and associated immune responses.
Main Methods:
- Bone marrow-derived macrophages were stimulated with T. rubrum conidia.
- Experiments involved wild-type and knockout mice lacking key inflammasome components (NLRP3, ASC, caspase-1) and IL-1 receptor (IL-1R).
- IL-1β, IL-17, and fungal hyphae development were assessed.
Main Results:
- Macrophages produced IL-1β in a NLRP3-, ASC-, and caspase-1-dependent manner upon T. rubrum exposure.
- Absence of IL-1 signaling led to increased T. rubrum hyphae development, indicating a protective role for IL-1β.
- Mice lacking IL-1R exhibited diminished IL-17 production in response to T. rubrum.
Conclusions:
- IL-1 signaling plays a significant protective role against T. rubrum infection by macrophages.
- IL-1β limits fungal hyphae development and influences IL-17 production, crucial for antifungal defense.
- These findings suggest IL-1 signaling as a potential therapeutic target for dermatophytosis and other fungal infections.
