Abstract
Candida albicans is a commensal fungus that asymptomatically colonizes the skin and mucosa of 60% of healthy individuals. Breaches in the cutaneous and mucosal barriers trigger candidiasis that ranges from asymptomatic candidemia and mucosal infections to fulminant sepsis with 70% mortality rates. Fungi influence at least several diseases, in part by mechanisms such as the production of pro-carcinogenic agents, molecular mimicking, and triggering of the inflammation cascade. These processes impact the interactions among human pathogenic and resident fungi, the bacteriome in various organs/tissues, and the host immune system, dictating the outcomes of invasive infections, metabolic diseases, and cancer. Although mechanistic investigations are at stages of infancy, recent studies have advanced our understanding of host–fungal interactions, their role in immune homeostasis, and their associated pathologies. This review summarizes the role of C. albicans and other opportunistic fungi, specifically their association with various diseases, providing a glimpse at the recent developments and our current knowledge in the context of inflammatory-bowel disease (IBD), cancers, and COVID-19. Two of the most common human diseases where fungal interactions have been previously well-studied are cancer and IBD. Here we also discuss the emerging role of fungi in the ongoing and evolving pandemic of COVID-19, as it is relevant to current health affairs.
Highlights
The past century has witnessed a significant increase in the wealth of knowledge on infectious diseases caused by viruses, bacteria, fungi, protozoa, and prions
These findings are in line with the initial studies establishing that C. albicans can act as a promoter of carcinogenesis in the rat/mouse tongue following recurrent applications of nitroquinoline (4-nitroquinoline 1-oxide; 4-NQO), thereby mimicking the human neck and head cancer [65,66]
This is in agreement with in vitro studies that showed intestinally conditioned Clec7a -/- dendritic cells (DCs) were less effective in clearing C. tropicalis
Summary
The past century has witnessed a significant increase in the wealth of knowledge on infectious diseases caused by viruses, bacteria, fungi, protozoa, and prions. Upon the binding of Dectin-1, fungal β-glucans lead to the phosphorylation of the cytoplasmic domain of Dectin-1 by Src kinase and the docking and activation of spleen tyrosine kinase (Syk) These events induce the assembly of a scaffold comprising of caspase-recruitment domain 9 (CARD9), adaptor-protein B-cell lymophoma-10 (Bcl-10) and mucosa-associated lymphoid-tissue-lymphoma-translocation protein 1 (MALT1) [27,28,29]. Candida, being the highly represented genera in the mycobiome, is best-studied for its relationship with the host as an opportunistic pathogen as well as its non-pathogenic interactions and contributions to the host’s immune development [37] The invasion by this yeast occurs through its morphological transition to the hyphal form thereby breaching mucosal barriers and gaining access to underlying host tissues. Fungal dysbiosis modulates local immune milieu and alters Th functions, which significantly switches the balance between health and disease states
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