期刊
EUKARYOTIC CELL
卷 5, 期 1, 页码 180-191出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/EC.5.1.180-191.2006
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资金
- NATIONAL CENTER FOR RESEARCH RESOURCES [C06RR016515] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [F31AI054328] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [R01DE014158] Funding Source: NIH RePORTER
- NCRR NIH HHS [C06 RR016515, C06 RR16515-01] Funding Source: Medline
- NIAID NIH HHS [F31 AI054328, F31 AI54328] Funding Source: Medline
- NIDCR NIH HHS [DE14158, R01 DE014158] Funding Source: Medline
Candida albicans is the most common etiological agent of vaginal candidiasis. Elevated host estrogen levels and the incidence of vaginal candidiasis are positively associated. Elevated estrogen levels may affect host and/or fungal cells. This study investigates the effect of 17-beta-estradiol, 17-alpha-estradiol, ethynyl estradiol, and estriol on several C albicans strains at concentrations ranging from 10(-5) to 10(-10) M. The addition of 17-beta-estradiol or ethynyl estradiol to C. albicans cells caused an increase in the number of cells forming germ tubes and an increase in germ tube length in a dose- and strain-dependent manner. The addition of 17-alpha-estradiol or estriol did not have a significant effect on germ tube formation by the cultured cells. Exposure to exogenous estrogens did not significantly change the biomass of any C albicans culture tested. The transcriptional profile of estrogen-treated C albicans cells showed increased expression of CDRI and CDR2 across several strain-estrogen concentration-time point combinations, suggesting that these genes are the most responsive to estrogen exposure. Analysis of strain DSY654, which lacks the CDR1 and CDR2 coding sequences, showed a significantly decreased number of germ tube-forming cells in the presence of 17-beta-estradiol. PDR16 was the most highly up-regulated gene in strain DSY654 under these growth conditions. The cell biology and gene expression data from this study led to a model that proposes how components of the phospholipid and sterol metabolic pathways may interact to affect C albicans germ tube formation and length.
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