Summary and Future Directions

Oral candidiasis is characterized by a recurrent, persistent, acute inflammatory reaction to Candida infection, which is limited to the uppermost epithelial layers of the oral mucosa. The inflammatory response to this pathogen elicits chronic pain and discomfort upon mastication, but it may also be responsible for activation of immunoef-

fector cells and the prevention of invasive infection. Although this chapter has concentrated on the innate immune and nonimmune mechanisms of the oral mucosal defense against Candida, it is well recognized that an intact arm of the adaptive immunity, represented mainly by Th1 cells, plays an instrumental role in regulating the clearance of this infection by innate immu-noeffectors. The mechanisms that trigger the acute inflammatory response in the oral mucosa are currently unknown. However, dissection of this process is critical to the understanding of the pathogenesis of this fungal infection and may be important for the development of strategies to prevent invasive infection in immunocompromised hosts. Evidence is accumulating that demonstrates that the acute host response to oral infection with Candida is initiated and perpetuated by oral epithelial cells, the first and principal targets of infection. A number of studies support the hypothesis that oral epithelial cells, just like epithelial cells from other mucosal sites that normally harbor a great number of commensal organisms (e.g., colon, vagina), require contact with the microorganism and active invasion of the host cell cytoplasm, possibly via destruction of the plasma membrane, for a proinflam-matory response. Further studies are needed to demonstrate that induction of specific cytokines in oral epithelial cells in vivo may promote the ability of PMN, monocyte, and/or keratinocyte antifungal activities. Increased production of proinflammatory cytokines by oral epithelial cells combined with the cytolytic activity of the inflammation-inducing hyphal forms of C. albicans, are also likely responsible for the clinical findings of redness and surface ulceration of the oral mucosa during this superficial oral infection. Further studies are also necessary to explore the contribution of other Candida species such as C. glabrata or C. krusei to the oral mucosal inflammatory response and epithelial cell damage in a monoinfection as well coinfection model system with C. albi-

cans. Future animal studies are also needed to determine whether mitigation of these proinflammatory cytokine responses and the ensuing acute inflammation would ameliorate the clinical symptoms of oral candidiasis, and/or promote invasion into the submucosal tissues. Limited knowledge is available about the contribution of salivary and oral epithelial cell antifungal peptides in the innate defense mechanisms in oral can-didiasis in vivo. Knockout animal model systems will be instrumental in fully elucidating the role of such antifungal peptides (histatins, defensins, calprotectin) in the innate immune protection of the oral mucosa from this microorganism in vivo.

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