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The Host Cytokine Responses and Protective Immunity in Oropharyngeal Candidiasis

¹ University of Connecticut, School of Dental Medicine, Department of Oral Health and Diagnostic Sciences, 263 Farmington Ave., Farmington, CT 06030-1710, USA; and
² Center for Excellence in Oral and Craniofacial Biology, School of Dentistry, Louisiana State University Health Science Center, New Orleans, LA 70119, USA;

^* corresponding author, adongari{at}uchc.edu

Over the last three decades, the prevalence of oropharyngeal fungal infections has increased enormously, mainly due to an increasing population of immunocompromised patients, including individuals with HIV infection, transplant recipients, and patients receiving cancer therapy. The vast majority of these infections are caused by Candida species. The presence of cytokines in infected tissues ultimately dictates the host defense processes that are specific to each pathogenic organism. During oral infection with Candida, a large number of pro-inflammatory and immunoregulatory cytokines are generated in the oral mucosa. The main sources of these cytokines are oral epithelial cells, which maintain a central role in the protection against fungal organisms. These cytokines may drive the chemotaxis and effector functions of innate and/or adaptive effector cells, such as infiltrating neutrophils and T-cells in immunocompetent hosts, and CD8⁺ T-cells in HIV⁺ hosts. Epithelial cells also have direct anti-Candida activity. Several studies have provided a potential link between lower levels of certain pro-inflammatory cytokines and susceptibility to oral C. albicans infection, suggesting that such cytokines may be involved in immune protection. The exact role of these cytokines in immune protection against oropharyngeal candidiasis is still incompletely understood and requires further investigation. Identification of such cytokines with the ability to enhance anti-fungal activities of immune effector cells may have therapeutic implications in the treatment of this oral infection in the severely immunocompromised host.

KEY WORDS: oral candidiasis • cytokines • immune response.

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