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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.
Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.
Acknowledgments
We thank Maira Cristina Nakamura and Dario Simões Zamboni from School of Medicine of Ribeirão Preto (University of São Paulo) for providing knockout animals.
Funding
This work was supported by São Paulo Research Foundation (FAPESP): Grant FAPESP 2012/14684-6.
Supplemental Material
Supplemental data for this article can be accessed on the publisher's website.
Author Contributions
FSYY and LGF performed the experiments; FSYY and SRA designed the study; FSYY wrote and SRA edited the manuscript.