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(searched for: doi:10.1126/scitranslmed.aay5691)
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Published: 6 February 2021
Journal of Fungi, Volume 7; doi:10.3390/jof7020119

Abstract:
Candida albicans infections range from superficial to systemic and are one of the leading causes of fungus-associated nosocomial infections. The innate immune responses during these various infection types differ, suggesting that the host environment plays a key role in modulating the host–pathogen interaction. In addition, C. albicans is able to remodel its cell wall in response to environmental conditions to evade host clearance mechanisms and establish infection in niches, such as the oral and vaginal mucosa. Phagocytes play a key role in clearing C. albicans, which is primarily mediated by Pathogen Associated Molecular Pattern (PAMP)–Pattern Recognition Receptor (PRR) interactions. PRRs such as Dectin-1, DC-SIGN, and TLR2 and TLR4 interact with PAMPs such as β-glucans, N-mannan and O-mannan, respectively, to trigger the activation of innate immune cells. Innate immune cells exhibit distinct yet overlapping repertoires of PAMPs, resulting in the preferential recognition of particular Candida morphotypes by them. The role of phagocytes in the context of individual infection types also differs, with neutrophils playing a prominent role in kidney infections, and dendritic cells playing a prominent role in skin infections. In this review, we provide an overview of the key receptors involved in the detection of C. albicans and discuss the differential innate immune responses to C. albicans seen in different infection types such as vulvovaginal candidiasis (VVC) and oral candidiasis.
Harshini Weerasinghe,
Published: 1 December 2020
Current Opinion in Microbiology, Volume 58, pp 32-40; doi:10.1016/j.mib.2020.07.001

Abstract:
Immune cells, including macrophages and monocytes, remodel their metabolism and have specific nutritional needs when dealing with microbial pathogens. While we are just beginning to understand immunometabolism in fungal infections, emerging themes include recognition of fungal cell surface molecule driving metabolic remodelling to increase glycolysis, the critical role of glycolysis in the production of antifungal cytokines and fungicidal effector molecules, and the need for maintaining host glucose homeostasis to defeat fungal infections. A crosstalk between host and pathogen metabolic pathways determines the fate of immune cells and fungi when they interact. Thus, immunometabolic interactions offer potential for innovation in antifungal treatments in the future. For this to become a reality, we must decipher the mechanisms by which diverse fungal pathogens activate and manipulate immunometabolism.
Comment
Nature Reviews Nephrology, Volume 16, pp 484-484; doi:10.1038/s41581-020-0322-5

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