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Title: | Attachment and entry of Candida famata in monocytes and epithelial cells |
Authors: | Pacheco, María CSIC; Pisa, Diana CSIC; García-Gómez, Patricia; Carrasco Llamas, Luis CSIC ORCID; Juarranz, Ángeles | Keywords: | Candida famata Yeast attachment Cellular infection Actin alteration |
Issue Date: | 27-Jul-2007 | Publisher: | John Wiley & Sons | Citation: | Microscopy Research & Technique Vol. 70 Issue 11, Pages 975 - 986 | Abstract: | Candida albicans is considered the main pathogenic yeast responsible for a multitude of infective disorders. However, other yeasts, such as Candida famata, are being recognized as potential emerging pathogens that cause several types of infections in humans and animals. Consequently, we have investigated the adhesion and internalization of Candida famata into monocytes and epithelial cells. The interaction of the yeast with the cells is very rapid and takes place during the first 15 min of injection. However, the affinity of the yeast for the cells varies, THP-1 (human monocytes) being the highest and followed in decreasing order by HeLa (human carcinoma), HaCaT, and Pam-212 (human and mouse keratinocytes, respectively). Heat inactivation or treatment with nystatin, significantly decreases yeast adhesion to cells. Immunofluorescence, as well as scanning and transmission electron microscopy, reveals that cell lines are able to internalize C. famata. At 48 h after infection, most of the yeasts located inside cells appear degraded, but some yeasts recovered from lysed cells, were still viable. Adhesion and internalization of C. famata into HeLa cells were found to be lower than those of C. albicans and C. glabrata, but higher than those of S. cerevisiae. In addition, infection with C. famata results in actin microfilaments rearrangement. This article presents novel data in the interaction of this pathogenic yeast with mammalian cells | Description: | Attachment and entry of Candida famata in monocytes and epithelial cells, Pacheco M., Microsc. Res. Tech., vol. 70, issue 11 © [2007] John Wiley & Sons | URI: | http://hdl.handle.net/10261/5047 | ISSN: | 1059-910X (Print) |
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