Please use this identifier to cite or link to this item: doi:10.22028/D291-28895
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Title: The extracellular adherence protein (Eap) of Staphylococcus aureus acts as a proliferation and migration repressing factor that alters the cell morphology of keratinocytes
Author(s): Eisenbeis, Janina
Peisker, Henrik
Backes, Christian S
Bur, Stephanie
Hölters, Sebastian
Thewes, Nicolas
Greiner, Markus
Junker, Christian
Schwarz, Eva C
Hoth, Markus
Junker, Kerstin
Preissner, Klaus T
Jacobs, Karin
Herrmann, Mathias
Bischoff, Markus
Language: English
Title: International journal of medical microbiology
Volume: 307
Issue: 2
Startpage: 116
Endpage: 125
Publisher/Platform: Elsevier
Year of Publication: 2017
Publikation type: Journal Article
Abstract: Staphyloccocus aureus is a major human pathogen and a common cause for superficial and deep seated wound infections. The pathogen is equipped with a large arsenal of virulence factors, which facilitate attachment to various eukaryotic cell structures and modulate the host immune response. One of these factors is the extracellular adherence protein Eap, a member of the "secretable expanded repertoire adhesive molecules" (SERAM) protein family that possesses adhesive and immune modulatory properties. The secreted protein was previously shown to impair wound healing by interfering with host defense and neovascularization. However, its impact on keratinocyte proliferation and migration, two major steps in the re-epithelialization process of wounds, is not known. Here, we report that Eap affects the proliferation and migration capacities of keratinocytes by altering their morphology and adhesive properties. In particular, treatment of non-confluent HaCaT cell cultures with Eap resulted in cell morphology changes as well as a significant reduction in cell proliferation and migration. Eap-treated HaCaT cells changed their appearance from an oblong via a trapezoid to an astral-like shape, accompanied by decreases in cell volume and cell stiffness, and exhibited significantly increased cell adhesion. Eap had a similar influence on endothelial and cancer cells, indicative for a general effect of Eap on eukaryotic cell morphology and functions. Specifically, Eap was found to interfere with growth factor-stimulated activation of the mitogen-activated protein kinase (MAPK) pathway that is known to be responsible for cell shape modulation, induction of proliferation and migration of epithelial cells. Western blot analyses revealed that Eap blocked the phosphorylation of extracellular signal-regulated kinase 1 and 2 (Erk1/2) in keratinocyte growth factor (KGF)-stimulated HaCaT cells. Together, these data add another antagonistic mechanism of Eap in wound healing, whereby the bacterial protein interferes with keratinocyte migration and proliferation.
DOI of the first publication: 10.1016/j.ijmm.2017.01.002
Link to this record: hdl:20.500.11880/27774
http://dx.doi.org/10.22028/D291-28895
ISSN: 14384221
Date of registration: 13-Sep-2019
Faculty: NT - Naturwissenschaftlich- Technische Fakultät
Department: NT - Physik
Collections:UniBib – Die Universitätsbibliographie

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