Publication: Micafungin enhances the human macrophage response to Candida albicans through β-glucan exposure
Authors
Guirao-Abad, José Pedro ; Sánchez-Fresneda, Ruth ; Machado, Francisco ; Argüelles, Juan Carlos ; Martínez-Esparza Alvargonzález, María Concepción
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Publisher
American Society for Microbiology
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DOI
https://doi.org/10.1128/AAC.02161-17
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info:eu-repo/semantics/article
Description
© 2018 American Society for Microbiology. This document is the Published version of a Published Work that appeared in final form in Antimicrobial Agents and Chemotherapy. To access the final edited and published work see https://doi.org/10.1128/aac.02161-17
Abstract
Micafungin belongs to the antifungal family of echinocandins, which act as noncompetitive inhibitors of the fungal cell wall β-1,3-d-glucan synthase. Since Candida albicans is the most prevalent pathogenic fungus in humans, we study the involvement of micafungin in the modulation of the inflammatory response developed by human tissue macrophages against C. albicans The MIC for micafungin was 0.016 μg/ml on the C. albicans SC5314 standard strain. Micafungin induced a drastic reduction in the number of exponential SC5314 viable cells, with the fungicidal effect being dependent on the cellular metabolic activity. Notably, micafungin also caused a structural remodelling of the cell wall, leading to exposure of the β-glucan and chitin content on the external surface. At the higher doses used (0.05 μg/ml), the antifungal also induced the blowing up of budding yeasts. In addition, preincubation with micafungin before exposure to human tissue macrophages enhanced the secretion of tumor necrosis factor alpha (TNF-α), interleukin-17A (IL-17A), and IL-10 cytokines. Our results strongly suggest that in C. albicans treatment with micafungin, in addition to having the expected toxic antifungal effect, it potentiates the immune response, improving the interaction and activation of human macrophages, probably through the unmasking of β-glucans on the cell wall surface.
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Citation
Antimicrobial Agents and Chemotherapy 2018 May 62(5): e02161-17
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