HS and AFM performed the NMR studies and assisted in data analysis. MAA assisted in the conception of the study and contributed to data analysis and manuscript editing. All authors

read and approved the final manuscript.”
“Background Candida albicans is a commensal of human microflora, residing at the oral cavity, https://www.selleckchem.com/products/empagliflozin-bi10773.html the gastrointestinal tract, the vaginal and the urinary environments, that acts as an opportunistic pathogen [Necrostatin-1 manufacturer reviewed by 1]. C. albicans commonly causes infections such as denture stomatitis, thrush, and urinary tract-infections, but can also provoke more severe systemic infections. These are frequently life-threatening, in particular in immuno-compromised individuals, whose numbers are constantly increasing due to organ transplant, chemotherapy, or, more importantly, to the prevalence of AIDS and Hepatitis C [reviewed by [1]]. Given the limited number of suitable and effective antifungal drugs, together with increasing drug resistance of the pathogens, it is important that research community addresses, and ultimately discloses, the

following yet unsolved questions: a) how the transformation from commensal to pathogen takes place, b) how it can be prevented, c) which are the mechanisms underlying antifungal drugs resistance. All of these culminate in the need to search for new and better agents that target fundamental biological processes and/or GSK872 molecular weight pathogenic determinants. C. albicans, as most pathogens, has developed P-type ATPase an effective

battery of virulence factors and specific strategies to assist the ability to colonize host tissues, cause disease, and overcome host defences [reviewed by [2]]. An outstanding attribute of C. albicans biology is its capacity to grow in a diversity of morphological forms, ranging from unicellular budding yeast (blastospores), pseudohyphae, to true hyphae with parallel-sided walls [3–5]. The yeast-hyphae transition contributes to tissue invasion and to the escape from phagocyte cells after host internalization [6], and is therefore considered an important virulence factor [4, 5, 8–11]. Additionally, several other factors have been described in association with virulence, including the production of proteins that mediate adherence, the colonization and invasion of host tissues, the maintenance of cell wall integrity, phenotypic switching, and the avoidance of the host immune response [12–18]. Many of these virulence factors are glycosylphosphatidylinositol (GPI) – anchored proteins, which comprise 88% of all covalently linked cell wall proteins in C. albicans [14], many of which associated with the lipid-ordered domains. In spite of all these knowledge, we are still far from fully understanding the precise mechanism(s) driven by Candida switch from commensal to pathogen status.