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Oropharyngeal candidiasis (OPC) occurs in a diverse group of patients. Risk factors for OPC include the use of dentures, corticosteroid inhalers, cigarettes, broad-spectrum antibiotics, and immunosuppressive and chemotherapeutic agents. Patients with HIV, diabetes, and iatrogenic or autoimmune-induced dry mouth are also at substantial risk for OPC. This infection is caused primarily by Candida albicans, a ubiquitous polymorphic fungus that is part of the normal microbiota of the gastrointestinal and reproductive tracts of healthy individuals. In order to persistently colonize the oropharynx, C. albicans must adhere to the epithelial cell lining of the oral mucosa while avoiding being killed by host antimicrobial factors. OPC develops when local host defenses are weakened, permitting the fungus to invade and damage oral epithelial cells. The epithelial cells respond to fungal infection by secreting antimicrobial peptides that directly kill the fungus and by releasing pro-inflammatory cytokines that recruit neutrophils to the focus of infection, where they can kill C. albicans and limit the extent of epithelial cell damage [1,2]. In this Pearl, we summarize recent advances in our knowledge of the pathogenesis of OPC, focusing on fungal-epithelial interactions.

Oropharyngeal Candidiasis: Fungal Invasion and Epithelial Cell Responses