Abstract
Candida albicans is an opportunistic pathogenic fungus considered to be a common member of the human microflora. Similar to some other opportunistic microbes, C. albicans can invade and benefit from its host when the immune status of that host is weakened. Most often this happens to immunocompromised individuals, leading to the infection of oral and vaginal mucosae or the systemic spread of the pathogen throughout the entire body. Oropharyngeal candidiasis (OPC) occurs in up to 90 percent of patients with acquired immunodeficiency syndrome (AIDS), making it the most frequent opportunistic infection for this group. Upon first signs of fungal invasion, a range of host signaling activates in order to eliminate the threat. Epithelial and myeloid type cells detect C. albicans mainly through receptor tyrosine kinases and pattern-recognition receptors. This review provides an overview of downstream signaling resulting in an adequate immune response through the activation of various transcription factors. The study discusses recent advances in research of the interleukin-17 (IL-17) producing innate cells, including natural T helper 17 (nTh17) cells, γδ T cells, invariant natural killer T (iNKT) cells and type 3 innate lymphoid cells (ILC3) that are involved in response to oral C. albicans infections.
Highlights
The oral environment is characterized by a complex microflora consisting of fungal and bacterial species tightly coexisting with each other [1]
The signaling cascade starts from the host–pathogen contact in epithelial cells, following with the interleukin-17 (IL-17)-dependent recruitment of phagocytic cells, such as neutrophils, macrophages, and dendritic cells (DCs) to the site of infection [23,24]
The main source of IL-17 in humans are T helper 17 (Th17) cells, whereas in mice it is mainly produced by γδT cells and natural Th17 cells [28]
Summary
The oral environment is characterized by a complex microflora consisting of fungal and bacterial species tightly coexisting with each other [1]. Major fungal invasins Als and Ssa can interact with host RTKs, resulting in epithelial cell endocytosis of C. albicans [86] In this process, the toxin called candidalysin plays a major role in the activation of immune response through EGFR tyrosine phosphorylation at Y-845 and Y-1068, [84,87]. C-Fos appears to be a major regulator of inflammatory response in oral epithelial cells, in particular upon C. albicans invasion and candidalysin release Another RTK ephrin type-A receptor 2 (EphA2) has been recently shown to interact with β-glucans of yeast-phase C. albicans, which results in downstream phosphorylation of MAPK/ERK kinase 1/2 (MEK1/2), p38-mediated activation of c-Fos and signal transducer and activator of transcription 3 (STAT3) [91]. Both TLR4 and dectin-1 were shown to play a modest role in IL-8 signaling, known to be important in the recruitment of PMLs such as macrophages and neutrophils
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