Abstract

One of the ubiquitous hospital-acquired infections is associated with Candida albicans fungus. Usually, this commensal fungus causes no harm to its human host, as it lives mutually with mucosal/epithelial tissue surface cells. Nevertheless, due to the activity of various immune weakening factors, this commensal starts reinforcing its virulence attributes with filamentation/hyphal growth and building an absolute microcolony composed of yeast, hyphal, and pseudohyphal cells, which is suspended in an extracellular gel-like polymeric substance (EPS) called biofilms. This polymeric substance is the mixture of the secreted compounds from C. albicans as well as several host cell proteins. Indeed, the presence of these host factors makes their identification and differentiation process difficult by host immune components. The gel-like texture of the EPS makes it sticky, which adsorbs most of the extracolonial compounds traversing through it that aid in penetration hindrance. All these factors further contribute to the multidrug resistance phenotype of C. albicans biofilm that is spotlighted in this article. The mechanisms it employs to escape the host immune system are also addressed effectively. The article focuses on cellular and molecular determinants involved in the resistance of C. albicans biofilm against multidrug and the host immune system.

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