Abstract
Candida spp. are colonizing fungi of human skin and mucosae of the gastrointestinal and genitourinary tract, present in 30–50% of healthy individuals in a population at any given moment. The host defense mechanisms prevent this commensal fungus from invading and causing disease. Loss of skin or mucosal barrier function, microbiome imbalances, or defects of immune defense mechanisms can lead to an increased susceptibility to severe mucocutaneous or invasive candidiasis. A comprehensive understanding of the immune defense against Candida is essential for developing adjunctive immunotherapy. The important role of underlying genetic susceptibility to Candida infections has become apparent over the years. In most patients, the cause of increased susceptibility to fungal infections is complex, based on a combination of immune regulation gene polymorphisms together with other non-genetic predisposing factors. Identification of patients with an underlying genetic predisposition could help determine which patients could benefit from prophylactic antifungal treatment or adjunctive immunotherapy. This review will provide an overview of patient susceptibility to mucocutaneous and invasive candidiasis and the potential for adjunctive immunotherapy.
Highlights
Candida spp., especially Candida albicans, are colonizing fungi of human skin and mucosae of the gastrointestinal and genitourinary tract of 30–50% of healthy individuals in any given human population at a certain moment, with the majority of the individuals being colonized during certain periods of their lives
The cell populations of the innate immune system involved in recognition of C. albicans are monocytes, macrophages, dendritic cells and neutrophils
The neutrophil response was normal, Candida colonization was persistent due to absent induction of epithelial antimicrobial peptides. These findings suggest that the main role of IL-17 in mucosal host defense against Candida is the stimulation of epithelial cells to release antimicrobial peptides, and to a lesser extent neutrophil recruitment [84]
Summary
Candida spp., especially Candida albicans, are colonizing fungi of human skin and mucosae of the gastrointestinal and genitourinary tract of 30–50% of healthy individuals in any given human population at a certain moment, with the majority of the individuals being colonized during certain periods of their lives. Loss of skin or mucosal barrier function, microbiome imbalances, or defects of immune defense mechanisms can all lead to an increased susceptibility to severe mucocutaneous or invasive candidiasis [1]. Nails, oropharyngeal mucosa, esophagus, and genital tract are occasional and not severe. Candida infections in the absence of commonly predisposing factors such as diabetes, and this condition has been termed chronic mucocutaneous candidiasis (CMC) [2]. Most patients admitted to the intensive care unit (ICU) have several of these risk factors but only a few develop invasive candidiasis [3]. This review will provide an overview of the mechanisms that increase patient susceptibility to mucocutaneous and invasive candidiasis and will provide a rationale of the potential for adjunctive immunotherapy
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