4.4 Article

Comparison between Candida albicans agglutinin-like sequence gene expression patterns in human clinical specimens and models of vaginal candidiasis

Journal

INFECTION AND IMMUNITY
Volume 73, Issue 3, Pages 1656-1663

Publisher

AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.73.3.1656-1663.2005

Keywords

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Funding

  1. NIAID NIH HHS [R01 AI032556, AI32556, R29 AI032556] Funding Source: Medline
  2. NIDCR NIH HHS [R01 DE014158, DE14158] Funding Source: Medline

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Expression of the eight genes in the Candida albicans agglutinin-like sequence (ALS) family was studied by reverse transcription-PCR of RNA isolated from clinical vaginal fluid specimens and vaginal candidiasis model systems. Although expression of all ALS genes was detected across the set or clinical specimens, ALS1, ALS2, ALS3, and ALS9 transcripts were detected most frequently, and expression of ALS4 and ALS5 was detected least frequently. Laboratory strain 3153A and two C. albicans strains isolated from the clinical specimens were studied using two models of vaginal candidiasis to determine how closely these models mimicked the clinical specimens at the level of gene expression. ALS gene expression patterns in a murine vaginitis model were identical to those from the clinical specimens. Expression of more ALS genes was detected in specimens collected 7 days after infection compared to those collected at 4 days. Similar patterns of ALS gene expression were observed when the three C. albicans strains were tested in the reconstituted human vaginal epithelium model. In this model, expression of ALS4, ALS5, ALS6, and ALS7 was least frequently detected. Negative or weakened signals for ALS4 expression were observed at early time points, suggesting that ALS4 expression, which was strong in the inoculum cells, was down-regulated upon contact of C. albicans with vaginal epithelial cells in this model. The data presented here support the conclusion of host-site-specific influences on AILS gene expression and validate the use of the experimental models for evaluating the phenotype of als/als mutant strains.

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