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Transcriptional profiling of C. albicans in the presence of mucin versus absence of mucin

ABSTRACT: Candida albicans is the most prevalent fungal pathogen of humans, causing a variety of diseases ranging from superficial mucosal infections to deep-seated systemic infections. Mucus, the gel that coats all wet epithelial surfaces, accommodates Candida albicans as part of the regular microbiome where C. albicans resides asymptomatically in healthy humans. Through a series of in vitro experiments combined with genome-wide transcriptional profiling, we show that mucin biopolymers, the main gel-forming constituents of mucus, induce a new oval-shaped morphology in C. albicans in which a range of genes related to adhesion, filamentation, and biofilm formation are down-regulated. We also show that corresponding phenotypes are suppressed, rendering Candida incapable of forming biofilms on a range of different synthetic surfaces and human epithelial cells. Our data suggests that mucins can manipulate Candida physiology and we hypothesize that they are key regulators for retaining Candida in the host-compatible, commensal state.

ORGANISM(S): Candida albicans

PROVIDER: GSE55766 | GEO | 2014/03/11

SECONDARY ACCESSION(S): PRJNA240961

REPOSITORIES: GEO

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Project description:Candida spp. are commensal opportunistic fungal pathogens that often colonize and infect mucosal surfaces of the human body. Candida, along with other microbes in the microbiota, generally grow as biofilms in a polymicrobial environment. Due to the nature of cellular growth in a biofilm (such as production of a protective extracellular matrix) and the recalcitrance of biofilms, infections involving biofilms are very difficult to treat with antibiotics and perpetuate the cycle of infection. The two most commonly isolated Candida spp. from Candida infections are Candida albicans and Candida glabrata, and the presence of both of these species results in increased patient inflammation and overall biofilm formation. This work aims to investigate the interspecies interactions between C. albicans (Ca) and C. glabrata (Cg) in co-culture through transcriptome analysis over the course of biofilm growth. We report that during co-culture, lipid biosynthesis and transporter genes were significantly modulated in both Ca and Cg. Differentially expressed genes in Ca during co-culture growth included putative transporter genes (C2_02180W_A and C1_09210C_B; up-regulated), amino acid biosynthesis (ARO7; up-regulated most in Ca:Cg 1:3), and lipid-related genes (LIP3 and IPT1; down-regulated). Differentially expressed genes in Cg in co-culture included putative transmembrane transporters (CAGL0H03399g and CAGL0K04609g; up-regulated), an oxidative stress response gene (CAGL0E04114g; down-regulated most in Ca:Cg 1:3), genes involved in the TCA cycle (LYS12 and CAGL0J06402g; down-regulated), and several genes involved in cell wall/membrane biosynthesis (SEC53, GAS2, VIG9; down-regulated). Additionally, confocal microscopy was utilized for membrane lipid analysis between monoculture and co-culture biofilms. Through filipin-stained lipid analysis, we found that there was a significant increase in cell membrane lipid content in Ca:Cg 1:3 biofilms compared to Ca and Ca:Cg 3:1 biofilms. These results suggest substantial modifications of both cell wall, cell membrane, and transporters in both Ca and Cg during the time course of co-culture growth, which allows for increased biofilm formation and virulence in Candida co-culture biofilms.

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Transcriptional profiling of C. albicans in the presence of mucin versus absence of mucin

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