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Regulation of Candida albicans Hyphal Morphogenesis by Endogenous Signals
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Candida albicans Morphology-Dependent Host FGF-2 Response as a Potential Therapeutic Target

South Texas Center for Emerging Infectious Diseases (STCEID), Department of Biology, The University of Texas at San Antonio, San Antonio, TX 78249, USA
Author to whom correspondence should be addressed.
J. Fungi 2019, 5(1), 22;
Received: 10 January 2019 / Revised: 20 February 2019 / Accepted: 1 March 2019 / Published: 5 March 2019
Angiogenesis mediated by proteins such as Fibroblast Growth Factor-2 (FGF-2) is a vital component of normal physiological processes and has also been implicated in contributing to the disease state associated with various microbial infections. Previous studies by our group and others have shown that Candida albicans, a common agent of candidiasis, induces FGF-2 secretion in vitro and angiogenesis in brains and kidneys during systemic infections. However, the underlying mechanism(s) via which the fungus increases FGF-2 production and the role(s) that FGF-2/angiogenesis plays in C. albicans disease remain unknown. Here we show, for the first time, that C. albicans hyphae (and not yeast cells) increase the FGF-2 response in human endothelial cells. Moreover, Candidalysin, a toxin secreted exclusively by C. albicans in the hyphal state, is required to induce this response. Our in vivo studies show that in the systemic C. albicans infection model, mice treated with FGF-2 exhibit significantly higher mortality rates when compared to untreated mice not given the angiogenic growth factor. Even treatment with fluconazole could not fully rescue infected animals that were administered FGF-2. Our data suggest that the increase of FGF-2 production/angiogenesis induced by Candidalysin contributes to the pathogenicity of C. albicans. View Full-Text
Keywords: angiogenesis; FGF-2; morphogenesis; Candidalysin angiogenesis; FGF-2; morphogenesis; Candidalysin
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Vellanki, S.; Huh, E.Y.; Saville, S.P.; Lee, S.C. Candida albicans Morphology-Dependent Host FGF-2 Response as a Potential Therapeutic Target. J. Fungi 2019, 5, 22.

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