Deletion of the Candida albicans PIR32 Results in Increased Virulence, Stress Response, and Upregulation of Cell Wall Chitin Deposition

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dc.contributor.author Bahnan, Wael
dc.contributor.author Koussa, Joseph
dc.contributor.author Younes, Samer
dc.contributor.author Abi Rizk, Marybel
dc.contributor.author Khalil, Bassem
dc.contributor.author El Sitt, Sally
dc.contributor.author Hanna, Samer
dc.contributor.author El-Sibai, Mirvat
dc.contributor.author Khalaf, Roy A.
dc.date.accessioned 2016-03-18T08:14:00Z
dc.date.available 2016-03-18T08:14:00Z
dc.date.copyright 2012
dc.date.issued 2016-03-18
dc.identifier.issn 0301-486X en_US
dc.identifier.uri http://hdl.handle.net/10725/3360
dc.description.abstract Candida albicans is a common opportunistic pathogen that causes a wide variety of diseases in a human immunocompromised host leading to death. In a pathogen, cell wall proteins are important for stability as well as for acting as antigenic determinants and virulence factors. Pir32 is a cell wall protein and member of the Pir protein family previously shown to be upregulated in response to macrophage contact and whose other member, Pir1, was found to be necessary for cell wall rigidity. The purpose of this study is to characterize Pir32 by generating a homozygous null strain and comparing the phenotype of the null with that of the wild-type parental strain as far as filamentation, virulence in a mouse model of disseminated candidiasis, resistance to oxidative stress and cell wall disrupting agents, in addition to adhesion, biofilm capacities, and cell wall chitin content. Our mutant was shown to be hyperfilamentous, resistant to sodium dodecyl sulfate, hydrogen peroxide, sodium chloride, and more virulent in a mouse model when compared to the wild type. These results were unexpected, considering that most cell wall mutations weaken the wall and render it more susceptible to external stress factors and suggests the possibility of a cell surface compensatory mechanism. As such, we measured cell wall chitin deposition and found a twofold increase in the mutant, possibly explaining the above-observed phenotypes. en_US
dc.language.iso en en_US
dc.title Deletion of the Candida albicans PIR32 Results in Increased Virulence, Stress Response, and Upregulation of Cell Wall Chitin Deposition en_US
dc.type Article en_US
dc.description.version Published en_US
dc.author.school SAS en_US
dc.author.idnumber 200703859 en_US
dc.author.idnumber 200300427
dc.author.woa N/A en_US
dc.author.department Natural Sciences en_US
dc.description.embargo N/A en_US
dc.relation.journal Mycopathologia en_US
dc.journal.volume 174 en_US
dc.journal.issue 2 en_US
dc.article.pages 107-119 en_US
dc.keywords Candida albicans en_US
dc.keywords Virulence en_US
dc.keywords Adhesion en_US
dc.keywords Cell wall en_US
dc.identifier.doi http://dx.doi.org/10.1007/s11046-012-9533-z en_US
dc.identifier.ctation Bahnan, W., Koussa, J., Younes, S., Rizk, M. A., Khalil, B., El Sitt, S., ... & Khalaf, R. A. (2012). Deletion of the Candida albicans PIR32 results in increased virulence, stress response, and upregulation of cell wall chitin deposition. Mycopathologia, 174(2), 107-119. en_US
dc.author.email mirvat.elsibai@lau.edu.lb
dc.author.email roy.khalaf@lau.edu.lb
dc.identifier.url http://link.springer.com/article/10.1007/s11046-012-9533-z
dc.orcid.id https://orcid.org/0000-0003-4084-6759 en_US

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