Affordable Access

deepdyve-link deepdyve-link
Publisher Website

Staphylococcus aureus hemolysin A disrupts cell-matrix adhesions in human airway epithelial cells.

Authors
  • Hermann, Ina
  • Räth, Susann
  • Ziesemer, Sabine
  • Volksdorf, Thomas
  • Dress, Regine J
  • Gutjahr, Melanie
  • Müller, Christian
  • Beule, Achim G
  • Hildebrandt, Jan-Peter
Type
Published Article
Journal
American Journal of Respiratory Cell and Molecular Biology
Publisher
American Thoracic Society
Publication Date
Jan 01, 2015
Volume
52
Issue
1
Pages
14–24
Identifiers
DOI: 10.1165/rcmb.2014-0082OC
PMID: 24918472
Source
Medline
Keywords
License
Unknown

Abstract

Treatment of primary or immortalized human airway epithelial cells (16HBE14o-, S9) or alveolar cancer cells (A549) with recombinant hemolysin A (rHla), a major virulence-associated factor of Staphylococcus aureus, induces alterations in cell shape and formation of paracellular gaps in the cell layer. Semiquantitative Western blotting using extracts of freshly isolated airway tissue (nasal epithelium) or 16HBE14o- model cells revealed that phosphorylation levels of focal adhesion kinase (Fak) and paxillin were altered upon treatment of tissue or cells with rHla. Immune fluorescence analyses showed that rHla treatment of 16HBE14o- cells results in losses of vinculin and paxillin from focal contacts and a net reduction in the number of focal contacts. The actin cytoskeleton was strongly remodeled. We concluded that treatment of cells with rHla activates Fak signaling, which accelerates focal contact turnover and prevents newly formed focal contacts (focal complexes) from maturation to focal adhesions. The inability of rHla-treated cells to form stable focal adhesions may be one factor that contributes to gap formation in the cell layer. In vivo, such changes may disturb the defensive barrier function of the airway epithelium and may facilitate lung infections by S. aureus.

Report this publication

Statistics

Seen <100 times