{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,8,25]],"date-time":"2024-08-25T19:06:42Z","timestamp":1724612802284},"reference-count":43,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2010,10,1]],"date-time":"2010-10-01T00:00:00Z","timestamp":1285891200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Eukaryot Cell"],"published-print":{"date-parts":[[2010,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The transcription factors that regulate\n            <jats:named-content content-type=\"genus-species\">Aspergillus fumigatus<\/jats:named-content>\n            interactions with host cells and virulence are incompletely defined. We investigated the role of the putative C2H2 transcription factor DvrA in governing these processes. Although DvrA was identified by its limited homology to\n            <jats:named-content content-type=\"genus-species\">Candida albicans<\/jats:named-content>\n            Bcr1, a \u0394\n            <jats:italic>dvrA<\/jats:italic>\n            mutant strain of\n            <jats:named-content content-type=\"genus-species\">A. fumigatus<\/jats:named-content>\n            had wild-type adherence to host constituents\n            <jats:italic>in vitro<\/jats:italic>\n            . However, it had increased capacity to damage both endothelial cells and a pulmonary epithelial cell line compared to the ability of the wild-type strain and a \u0394\n            <jats:italic>dvrA<\/jats:italic>\n            ::\n            <jats:italic>dvrA<\/jats:italic>\n            -complemented strain. This increase in damage required direct contact between the mutant and host cells. The \u0394\n            <jats:italic>dvrA<\/jats:italic>\n            mutant also stimulated greater CCL20, interleukin-8, and tumor necrosis factor mRNA expression in a pulmonary epithelial cell line compared to levels induced by the control strains. Also, it was resistant to nikkomycin Z, suggesting an altered cell wall composition. As predicted by these\n            <jats:italic>in vitro<\/jats:italic>\n            results, the \u0394\n            <jats:italic>dvrA<\/jats:italic>\n            mutant had increased virulence and stimulated a greater pulmonary inflammatory response than the wild-type strain and \u0394\n            <jats:italic>dvrA<\/jats:italic>\n            ::\n            <jats:italic>dvrA<\/jats:italic>\n            -complemented strains in the nonneutropenic mouse model of invasive pulmonary aspergillosis. These results indicate that DvrA influences\n            <jats:named-content content-type=\"genus-species\">A. fumigatus<\/jats:named-content>\n            virulence as well as its capacity to damage host cells and stimulate a proinflammatory response.\n          <\/jats:p>","DOI":"10.1128\/ec.00055-10","type":"journal-article","created":{"date-parts":[[2010,7,31]],"date-time":"2010-07-31T02:12:23Z","timestamp":1280542343000},"page":"1432-1440","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":28,"title":["Role of Aspergillus fumigatus DvrA in Host Cell Interactions and Virulence"],"prefix":"10.1128","volume":"9","author":[{"given":"Daniele E.","family":"Ejzykowicz","sequence":"first","affiliation":[{"name":"Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Norma V.","family":"Solis","sequence":"additional","affiliation":[{"name":"Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fabrice N.","family":"Gravelat","sequence":"additional","affiliation":[{"name":"McGill University, Montreal, Quebec, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Josee","family":"Chabot","sequence":"additional","affiliation":[{"name":"McGill University, Montreal, Quebec, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xuexian","family":"Li","sequence":"additional","affiliation":[{"name":"Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Donald C.","family":"Sheppard","sequence":"additional","affiliation":[{"name":"McGill University, Montreal, Quebec, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Scott G.","family":"Filler","sequence":"additional","affiliation":[{"name":"Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California"},{"name":"David Geffen School of Medicine at UCLA, Los Angeles, California"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00813-09"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.63.9.3266-3271.1995"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.73.1.494-503.2005"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.72.8.4731-4740.2004"},{"key":"e_1_3_3_6_2","first-page":"9","article-title":"Split-marker recombination for efficient targeted deletion of fungal genes","volume":"50","author":"Catlett N. 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