Migration of the fungal pathogen Candida albicans across endothelial monolayers

Zink, Sigrid; Nass, T; Rösen, P.; Ernst, Joachim F.

doi:10.1128/iai.64.12.5085-5091.1996

Cited by 58 publications

(30 citation statements)

References 30 publications

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“…This phenomenon was not restricted to SIRC cells but was also seen in cell lines such as MDCK (canine kidney), HepG2 (human hepatocellular liver carcinoma), G-361 (human skin melanoma) and suspension cells SP2/OAg14 (mouse myeloma) (data not shown). The actin remodeling was very similar to remodeling reported previously during phagocytosis of C. albicans by macrophages, human umbilical vein endothelial cells and human oral epithelial lines during C. albicans infection (Zink et al, 1996;Káposzta et al, 1999;Tsarfaty et al, 2000).…”

Section: Actin Remodeling During C Albicans Invasionsupporting

confidence: 86%

Association of small Rho GTPases and actin ring formation in epithelial cells during the invasion byCandida albicans

Atre

Surve

Shouche

et al. 2009

FEMS Immunol Med Microbiol

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Invasion of epithelial cells is a major virulence determinant of Candida albicans; however, the molecular events that occur during invasion are not discerned. This study is aimed to elucidate the role of the host's actin remodeling and involvement of small GTPases during invasion. Actin filaments formed a rigid ring-like structure in the rabbit corneal epithelial cell line SIRC after C. albicans invasion. During invasion, an increase in the mRNA content of Cdc42, Rac1 and RhoA GTPase was observed in SIRC cells. Immunochemical staining and expression of chimeric green fluorescent protein (GFP)-GTPases showed that all three GTPases colocalize at invasion and actin polymerization sites. This colocalization was not seen in SIRC cells expressing a GFP-tagged dominant-negative mutant of GTPases. Inhibition of invasion was observed in SIRC cells expressing dominant-negative mutants of Rac1 and RhoA GTPases. Involvement of zonula occludens-1 (ZO-1) was observed in the process of actin-mediated endocytosis of C. albicans. Actin, GTPases and ZO-1 were colocalized in epithelial cells during uptake of polymethylmethacrylate beads coated with spent medium from a C. albicans culture. The results indicate that host actin remodeling and recruitment of small GTPases occur during invasion and molecules that are shed or secreted by C. albicans are probably responsible for cytoskeletal reorganization.

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Section: Actin Remodeling During C Albicans Invasionsupporting

confidence: 86%

Association of small Rho GTPases and actin ring formation in epithelial cells during the invasion byCandida albicans

Atre

Surve

Shouche

et al. 2009

FEMS Immunol Med Microbiol

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“…Although both, yeast and filamentous forms are found in infectious lesions caused by C. albicans, the morphological switch to filamentous forms, including germ-tubes, pseudohyphae and hyphae, has been associated with invasiveness (Kumamoto and Vinces, 2005). Several studies suggested that continuous elongation of filaments may contribute to host cell damage and lead to tissue destruction and invasion (Farrell et al, 1983;Zink et al, 1996;Hausauer et al, 2005;Kurzai et al, 2005). In addition, several proteins contributing to the pathogenesis of Candida infection have been shown to be predominantly expressed in filamentous forms.…”

Section: Discussionmentioning

confidence: 99%

Induction of ERK-kinase signalling triggers morphotype-specific killing of Candida albicans filaments by human neutrophils

Wozniok¹,

Hornbach²,

Schmitt³

et al. 2008

Cell Microbiol

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SummaryCandida 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.

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“…Several such in vitro assays to study C. albicans adhesion have already been described. In this regard, in vitro adhesion assays were established to analyse the mechanisms of adhesion to endothelia (Filler et al, 1995;Zink et al, 1996;Phan et al, 2000), leading among other results, to the detection of Ncadherin as a ligand for C. albicans in the extracellular matrix of endothelial cells (Phan et al, 2005). In addition, assays to study adhesion to the human epidermis (Korting et al, 1998;Schaller et al, 2000) as well as to intestinal epithelia (Dieterich et al, 2002;Wiesner et al, 2002) have been described recently.…”

Section: Discussionmentioning

confidence: 99%

Anin vitroassay to study the transcriptional response during adherence ofCandida albicansto different human epithelia

Sohn

Senyürek

Fertey

et al. 2006

FEMS Yeast Research

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Adhesion to mammalian epithelia is one of the prerequisites that are essential to accomplish pathogenesis of Candida albicans in the mammalian host. In this context C. albicans is able to adhere to a plethora of different cell types providing different microenvironments for colonization. To study the response of C. albicans adhering to different surfaces on the transcriptional level we have established an in vitro adhesion assay exploiting confluent monolayers of the human colorectal carcinoma cell line Caco-2 or epidermoid vulvo-vaginal A-431 cells. Candida albicans very efficiently adheres to these epithelia growing as hyphae. Using whole-genome DNA microarrays comprising probes for almost 7000 predicted ORFs we found that transcriptional profiles of C. albicans adhering to Caco-2 or to A-431 cells, although very similar, still significantly differ from those of Candida cells adhering to plastic surfaces. Differences became even more obvious when comparing C. albicans cells either growing in an adherent manner or in suspension culture. Correspondingly, we found for several cell surface genes, including PRA1, PGA23, PGA7 and HWP1, an adhesion-dependent induction of transcription. Obviously, C. albicans is able to respond specifically to very subtle differences in the environment during adhesion to various growth substrates.

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Migration of the fungal pathogen Candida albicans across endothelial monolayers

Cited by 58 publications

References 30 publications

Association of small Rho GTPases and actin ring formation in epithelial cells during the invasion byCandida albicans

Association of small Rho GTPases and actin ring formation in epithelial cells during the invasion byCandida albicans

Induction of ERK-kinase signalling triggers morphotype-specific killing of Candida albicans filaments by human neutrophils

Anin vitroassay to study the transcriptional response during adherence ofCandida albicansto different human epithelia

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