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

被引:64
作者
Cheng, G
Wozniak, K
Wallig, MA
Fidel, PL
Trupin, SR
Hoyer, LL
机构
[1] Univ Illinois, Dept Vet Pathobiol, Urbana, IL 61802 USA
[2] Univ Illinois, Dept Obstet & Gynecol, Urbana, IL 61802 USA
[3] Louisiana State Univ, Hlth Sci Ctr, Dept Microbiol Immunol & Parasitol, New Orleans, LA USA
关键词
D O I
10.1128/IAI.73.3.1656-1663.2005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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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页码:1656 / 1663
页数:8
相关论文
共 42 条
[21]  
2-9
[22]   Secreted lipases of Candida albicans:: cloning, characterisation and expression analysis of a new gene family with at least ten members [J].
Hube, B ;
Stehr, F ;
Bossenz, M ;
Mazur, A ;
Kretschmar, M ;
Schäfer, W .
ARCHIVES OF MICROBIOLOGY, 2000, 174 (05) :362-374
[23]   Dimorphism and virulence in Candida albicans [J].
Mitchell, AP .
CURRENT OPINION IN MICROBIOLOGY, 1998, 1 (06) :687-692
[24]   Secreted aspartic proteases as virulence factors of Candida species [J].
Monod, M ;
Borg-von Zepelin, M .
BIOLOGICAL CHEMISTRY, 2002, 383 (7-8) :1087-1093
[25]   Antifungal drug susceptibilities of oral Candida dubliniensis isolates from human immunodeficiency virus (HIV)-infected and non-HIV-infected subjects and generation of stable fluconazole-resistant derivatives in vitro [J].
Moran, GP ;
Sullivan, DJ ;
Henman, MC ;
McCreary, CE ;
Harrington, BJ ;
Shanley, DB ;
Coleman, DC .
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 1997, 41 (03) :617-623
[26]   Candida albicans secreted aspartyl proteinases in virulence and pathogenesis [J].
Naglik, JR ;
Challacombe, SJ ;
Hube, B .
MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS, 2003, 67 (03) :400-+
[27]   In vivo analysis of secreted aspartyl proteinase expression in human oral candidiasis [J].
Naglik, JR ;
Newport, G ;
White, TC ;
Fernandes-Naglik, LL ;
Greenspan, JS ;
Greenspan, D ;
Sweet, SP ;
Challacombe, SJ ;
Agabian, N .
INFECTION AND IMMUNITY, 1999, 67 (05) :2482-2490
[28]   Differential expression of Candida albicans secreted aspartyl proteinase and phospholipase B genes in humans correlates with active oral and vaginal infections [J].
Naglik, JR ;
Rodgers, CA ;
Shirlaw, PJ ;
Dobbie, JL ;
Fernandes-Naglik, LL ;
Greenspan, D ;
Agabian, N ;
Challacombe, SJ .
JOURNAL OF INFECTIOUS DISEASES, 2003, 188 (03) :469-479
[29]   Evidence for differential expression of Candida albicans virulence genes during oral infection in intact and human immunodeficiency virus type 1-transgenic mice [J].
Ripeau, JS ;
Fiorillo, M ;
Aumont, F ;
Belhumeur, P ;
de Repentigny, L .
JOURNAL OF INFECTIOUS DISEASES, 2002, 185 (08) :1094-1102
[30]  
*SAS I INC, 2000, SAS STAT SOFTW VERS