Interactions between Candida albicans and host

Abstract

Candida albicans can cause grave infections in patients who are immunocompromised by disease, by surgery, or by immunesupressive therapy. The high levels of morbidity and mortality resulting from those infections in hospitalized patients show that C. albicans became a prominent human pathogen. Although the host immune system is the major factor balancing the transition from commensalism to pathogenicity, several virulence attributes expressed by C. albicans, such as adhesion factors, phenotypic switching, dimorphic behavior, and secretion of hydrolytic enzymes, might contribute to the persistence of colonization as well as the development of symptomatic episodes. Host defense against candidiasis relies mainly on the ingestion and elimination of C. albicans by phagocitic cells which present receptors Toll-like 4, dectin –1 associated to receptors Toll-like2 and mannose receptors. The cytokine IL-10 (IL-10) produced by phagocytes has a crucial role on susceptibility of host fungal infection, whereas IL-10 produced by regulatory T cells is mainly responsible by commensalism. In contrast, production of tumour necrosis factor - ? (TNF-?), interleukin –1 ? (lL-1 ?), (IL-6) and (Il-12) provided protetive cell–mediated immunity. The interferon-? produced by natural killer and TH1 cells estimulates migration of phagocytes and major efficacy on destruction of fungi.