@article{mbs:/content/journal/jmm/10.1099/jmm.0.049650-0, author = "Ridley, Robert A. and Douglas, Ian and Whawell, Simon A.", title = "Differential adhesion and invasion by Staphylococcus aureus of epithelial cells derived from different anatomical sites", journal= "Journal of Medical Microbiology", year = "2012", volume = "61", number = "12", pages = "1654-1661", doi = "https://doi.org/10.1099/jmm.0.049650-0", url = "https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.049650-0", publisher = "Microbiology Society", issn = "1473-5644", type = "Journal Article", abstract = " Staphylococcus aureus can invade epithelial cells, and the host-cell receptor α5β1 integrin is thought to mediate this process. The aim of this study was to investigate S. aureus invasion of epithelial cell lines derived from oral (H357), skin (UP) and nasopharyngeal (Detroit 562) sites and to determine whether any differences were due to the levels of α5β1 integrin expressed. While the adhesion and invasion of two S. aureus strains were similar in both oral and skin-derived keratinocytes, this was markedly reduced in the nasopharyngeal cell line, despite it expressing similar levels of α5β1. While this might be explainable on the basis of availability of cell receptor, adhesion to and invasion of H357 and UP cells by S. aureus were enhanced when the epithelial cells were in suspension rather than on a surface, and levels of α5 integrin subunit mRNA were also increased. Detroit 562 cells exhibited a similar α5 gene upregulation, but this did not result in enhanced adhesion and invasion of S. aureus. The Detroit 562 cells also showed reduced adhesion to fibronectin compared with the other cell types. This, and the low S. aureus invasion, may result from reduced α5β1 integrin activity or from variation in an as-yet-unidentified additional receptor or accessory molecule. These studies shed further light on the mechanisms of S. aureus invasion of human cells.", }