Abstract
Mucosal epithelial tissues are exposed to high numbers of microbes, including commensal fungi, and are able to distinguish between those that are avirulent and those that cause disease. Epithelial cells have evolved multiple mechanisms to defend against colonization and invasion by Candida species. The interplay between mucosal epithelial tissues and immune cells is key for control and clearance of fungal infections. Our understanding of the mucosal innate host defense system has expanded recently with new studies bringing to light the importance of epithelial cell responses, innate T cells, neutrophils, and other phagocytes during Candida infections. Epithelial tissues release cytokines, host defense peptides, and alarmins during Candida invasion that act in concert to limit fungal proliferation and recruit immune effector cells. The innate T cell/IL-17 axis and recruitment of neutrophils are of central importance in controlling mucosal fungal infections. Here, we review current knowledge of the innate immunity at sites of mucosal Candida infection, with a focus on infections caused by C. albicans.
Highlights
Mucosal candidiasis is a significant problem in both immunocompetent and immunocompromised individuals [1]
The release of inflammatory mediators from epithelial cells is a critical step for the generation of protective host responses, including recruitment of inflammatory leukocytes and the generation of host defense peptides (HDPs) [7]
Oral epithelial cells respond to damage induced by C. albicans by releasing IL-1α, which stimulates the production of granulocyte-colony stimulating factor (G-CSF) on endothelial cells, a key trigger of emergency granulopoiesis [40]
Summary
Mucosal candidiasis is a significant problem in both immunocompetent and immunocompromised individuals [1]. Vulvovaginal candidiasis (VVC) is common in women who are immunocompetent and immunocompromised, while oropharyngeal candidiasis (OPC) causes significant morbidity in patients who are immunocompromised due to AIDS, neutropenia, diabetes mellitus, or the use of immunosuppressive drugs [2,3]. The development of a mucosal Candida infection is usually attributed to the disturbance of the balance between fungal colonization and changes in the host environment. Healthy individuals have a protective Candida-specific mucosal immunity. These antifungal mechanisms are comprised of numerous components that act in concert to limit fungal invasion, proliferation, and prevent disease. This review will provide an overview of various host cell types that contribute to the innate mucosal immune response
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