Interplay between Candida albicans and the mammalian innate host defense

Abstract

Candida albicans is both the most common fungal commensal microorganism in healthy individuals and the major fungal pathogen causing high mortality in at-risk populations, especially immunocompromised patients. In this review, we summarize the interplay between the host innate system and C. albicans, ranging from how the host recognizes, responds, and clears C. albicans infection to how C. albicans evades, dampens, and escapes from host innate immunity.

Fig 1

Major pattern recognition receptors (PRRs) and their corresponding Candida PAMPs. Candida cell wall components are mainly recognized extracellularly by Toll-like receptors and C-type lectin receptors on the host cell surface and lead to different downstream signaling, such as chemokine/cytokine production and phagocytosis. Once Candida is internalized/phagocytosed, the fungal PAMPs can further activate TLR9 or NLRP3 inflammasome activation.

Fig 2

Candida albicans host innate system evasion strategies. (A) Yeast- to hyphal-phase transition. (B) Downregulation of epithelial TLR4 expression. (C) Shielding of PAMP from PRR recognition. (D) Inhibition or degradation of complement system. (E) Inhibition of phagolysosome formation. (F) Modulation of T cell function.

Fig 3

Schematic diagram of the interplay between Candida albicans and host innate immune systems at the mucosal surface. Black lines denote host defense mechanisms. Red lines denote Candida invasion/escape mechanisms.