共查询到20条相似文献,搜索用时 31 毫秒
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Duncan Wilson Sascha Thewes Katherina Zakikhany Chantal Fradin Antje Albrecht Ricardo Almeida Sascha Brunke Katharina Grosse Ronny Martin Francois Mayer Ines Leonhardt Lydia Schild Katja Seider Melanie Skibbe Silvia Slesiona Betty Waechtler Ilse Jacobsen & Bernhard Hube 《FEMS yeast research》2009,9(5):688-700
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Li F Svarovsky MJ Karlsson AJ Wagner JP Marchillo K Oshel P Andes D Palecek SP 《Eukaryotic cell》2007,6(6):931-939
Candida albicans is the leading cause of systemic fungal infections in immunocompromised humans. The ability to form biofilms on surfaces in the host or on implanted medical devices enhances C. albicans virulence, leading to antimicrobial resistance and providing a reservoir for infection. Biofilm formation is a complex multicellular process consisting of cell adhesion, cell growth, morphogenic switching between yeast form and filamentous states, and quorum sensing. Here we describe the role of the C. albicans EAP1 gene, which encodes a glycosylphosphatidylinositol-anchored, glucan-cross-linked cell wall protein, in adhesion and biofilm formation in vitro and in vivo. Deleting EAP1 reduced cell adhesion to polystyrene and epithelial cells in a gene dosage-dependent manner. Furthermore, EAP1 expression was required for C. albicans biofilm formation in an in vitro parallel plate flow chamber model and in an in vivo rat central venous catheter model. EAP1 expression was upregulated in biofilm-associated cells in vitro and in vivo. Our results illustrate an association between Eap1p-mediated adhesion and biofilm formation in vitro and in vivo. 相似文献
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Global analysis of in vivo Foxa2-binding sites in mouse adult liver using massively parallel sequencing 总被引:1,自引:0,他引:1
Wederell ED Bilenky M Cullum R Thiessen N Dagpinar M Delaney A Varhol R Zhao Y Zeng T Bernier B Ingham M Hirst M Robertson G Marra MA Jones S Hoodless PA 《Nucleic acids research》2008,36(14):4549-4564
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Wozniok I Hornbach A Schmitt C Frosch M Einsele H Hube B Löffler J Kurzai O 《Cellular microbiology》2008,10(3):807-820
Candida albicans is among the most important fungal pathogens in humans. Morphological plasticity has been linked to its pathogenic potential as filamentous forms are associated with tissue invasion and infection. Here we show that human neutrophils discriminate between yeasts and filaments of C. albicans . Whereas filaments induced targeted motility, resulting in the establishment of close contact between neutrophils and fungal cells, yeast forms were largely ignored during coincubation. In transwell assays, C. albicans filaments induced significantly higher migratory activity in neutrophils than yeasts. Neutrophil motility based on actin rearrangement was essential for killing of C. albicans filaments but not involved in killing of yeast forms. Using inhibitors for MAP-kinase cascades, it was shown that recognition of C. albicans filaments by neutrophils is mediated via the MEK/ERK cascade and independent of JNK or p38 activation. Inhibition of the ERK signalling pathway abolished neutrophil migration induced by C. albicans filaments and selectively impaired the ability to kill this morphotype. These data show that invasive filamentous forms of C. albicans trigger a morphotype-specific activation of neutrophils, which is strongly dependent on neutrophil motility. Therefore, human neutrophils are capable of sensing C. albicans invasion and initiating an appropriate early immune response. 相似文献
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