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.
Highlights
Candida albicans is both a commensal and opportunistic fungal pathogen of humans, the delicate balance of which is maintained by the actions of the innate immune system and resident microbiota
We provide an overview of the key receptors involved in the detection of C. albicans, summarise the immune sensing of C. albicans occurring in different infection types, and discuss the potential role the host environment plays in modulating these responses
These innate immune cells recognise C. albicans by its cell wall Pathogen Associated Molecular Pattern (PAMP); β-1,3-glucan is recognised by the C-type lectin receptor Dectin-1 and complement receptor 3 (CR3); N-mannan, by Dectin-2, Dendritic cells (DCs)-SIGN and MINCLE; and O-mannan, by TLR4 (Table 1 and Figure 1) [14,36,37,38,39]
Summary
Candida albicans is both a commensal and opportunistic fungal pathogen of humans, the delicate balance of which is maintained by the actions of the innate immune system and resident microbiota. C. albicans can form biofilms in nail infections; on teeth exacerbating, tooth decay; on mucosal surfaces; and on the surfaces of medical devices, including catheters, long lines and voice prostheses [5,6]. This capacity to form biofilms has made C. albicans one of. The Candida cell wall consists of an inner skeletal layer of β-glucan and chitin, and an outer layer of glycosylated proteins [7,8] These proteins play essential roles in adhesion to host cells, while carbohydrate PAMPs are recognised by PRRs on the surface of innate immune cells. We provide an overview of the key receptors involved in the detection of C. albicans, summarise the immune sensing of C. albicans occurring in different infection types, and discuss the potential role the host environment plays in modulating these responses
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