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Interactions of Candida albicans wit...

Frank, Charlotte Frances.

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Interactions of Candida albicans with intestinal epithelial cells.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Interactions of Candida albicans with intestinal epithelial cells./
作者:	Frank, Charlotte Frances.
面頁冊數:	205 p.
附註:	Source: Dissertation Abstracts International, Volume: 67-04, Section: B, page: 1810.
Contained By:	Dissertation Abstracts International67-04B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3214210
ISBN:	9780542651878

Interactions of Candida albicans with intestinal epithelial cells.
Frank, Charlotte Frances.

Interactions of Candida albicans with intestinal epithelial cells. - 205 p.

Source: Dissertation Abstracts International, Volume: 67-04, Section: B, page: 1810.

Thesis (Ph.D.)--Yale University, 2006.

Translocation of Candida albicans from the gastrointestinal tract to the bloodstream is a key step in the pathogenesis of invasive candidal disease, and the interaction of C. albicans with human intestinal epithelium plays a central role in this process. Experiments were designed to determine whether physiologic alterations of cultured human epithelial cells were specific to C. albicans and to identify the relevant proteins in C. albicans and human epithelial cells. After incubations of 7.5 to 24 hours, C. albicans, but not Saccharomyces cerevisiae decreased transepithelial electrical resistance (TER) of Caco-2 monolayers. TER decrease required live, replicating C. albicans cells and the expression of transcriptional regulators of filamentation particularly Efg1p. This model enabled us to evaluate the roles of inoculum, duration of infection, viability, filamentation, and virulence genes in the ability of C. albicans to alter the integrity of a monolayer of epithelial cells.

ISBN: 9780542651878Subjects--Topical Terms:

1017734
Biology, Microbiology.

Interactions of Candida albicans with intestinal epithelial cells.
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520 $a Translocation of Candida albicans from the gastrointestinal tract to the bloodstream is a key step in the pathogenesis of invasive candidal disease, and the interaction of C. albicans with human intestinal epithelium plays a central role in this process. Experiments were designed to determine whether physiologic alterations of cultured human epithelial cells were specific to C. albicans and to identify the relevant proteins in C. albicans and human epithelial cells. After incubations of 7.5 to 24 hours, C. albicans, but not Saccharomyces cerevisiae decreased transepithelial electrical resistance (TER) of Caco-2 monolayers. TER decrease required live, replicating C. albicans cells and the expression of transcriptional regulators of filamentation particularly Efg1p. This model enabled us to evaluate the roles of inoculum, duration of infection, viability, filamentation, and virulence genes in the ability of C. albicans to alter the integrity of a monolayer of epithelial cells.
520 $a Statistical analysis of a C. albicans microarray identified five MRNAs upregulated specific for epithelial cell contact. For these five, C. albicans homozygous mutants were constructed and tested in the TER assay. Only one of the mutants was impaired in its ability to decrease TER. However, the mutant's prolonged doubling time may contribute to this phenotype.
520 $a By densitometry, immunoblots from lysates of Caco-2 monolayers inoculated with C. albicans exhibited significantly decreased intensity of bands corresponding to the epithelial junction proteins occludin, E-cadherin, and desmoglein-2 compared to lysates of uninoculated monolayers and monolayers inoculated with S. cerevisiae. C. albicans enhanced the release of an 89 kDa extracellular E-cadherin fragment into the supernatant; simultaneously the accumulation of a 35 kDa intracellular E-cadherin fragment was specifically enhanced by C. albicans in the presence of gamma-secretase inhibitors. Correlation of the formation of the 35 kDa fragment with a decrease in the TER of a C. albicans-inoculated monolayer confirmed that changes in host cell proteins are temporally linked to TER decrease.
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