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reagents/materials/analysis tools: AMT MW RL. Wrote the paper: AEZ OB WOM UG. All authors read and approved the final manuscript.”
“Background The innate defense system plays a key role in protecting the host against microorganism-fueled infections such as candidiasis caused by Candida albicans. C. albicans colonizes several body sites, including the oral cavity; however, as a commensal organism, it causes no apparent damage or inflammation in the surrounding tissue [1, 2]. C. albicans is a polymorphic organism that adheres to different surfaces in the body and can grow as yeast, pseudohyphae, and hyphae [3], usually in the form of biofilm. C. albicans transition, biofilm formation, and pathogenesis are under the control of various genes. The HWP1 gene encodes the hyphal cell wall protein, which is a hyphal-specific adhesin that is essential to biofilm formation [4]. The involvement of HWP1 in C. albicans adhesion is supported by the EAP1 gene which encodes a glucan-crosslinked cell wall protein (adhesin Eap1p). Together, these components mediate C. albicans adhesion to various surfaces, such as epithelial cells and polystyrene [5].