The Library
Staphylococcal Esx proteins modulate apoptosis and release of intracellular staphylococcus aureus during infection in epithelial cells
Tools
Korea, C. G., Balsamo, G., Pezzicoli, A., Merakou, C., Tavarini, S., Bagnoli, F., Serruto, D. and Unnikrishnan, Meera (2014) Staphylococcal Esx proteins modulate apoptosis and release of intracellular staphylococcus aureus during infection in epithelial cells. Infection and Immunity, Volume 82 (Number 10). pp. 4144-4153. doi:10.1128/IAI.01576-14 ISSN 0019-9567.
Research output not available from this repository.
Request-a-Copy directly from author or use local Library Get it For Me service.
Official URL: http://dx.doi.org/10.1128/IAI.01576-14
Abstract
The opportunistic pathogen Staphylococcus aureus is one of the major causes of healthcare-associated infections. S. aureus is primarily an extracellular pathogen, but recently it has been reported to invade and replicate in several host cell types. The ability of S. aureus to persist within cells has been implicated in resistance to antimicrobials and recurrent infections. However, few staphylococcal proteins that mediate intracellular survival have been identified. Here, we examine if EsxA and EsxB, substrates of the ESAT 6-like secretion system (Ess), are important during intracellular S. aureus infection. The Esx proteins are required for staphylococcal virulence but their functions during infection are unclear. While isogenic S. aureus esxA or esxB mutants are not defective for epithelial cell invasion in vitro, a significant increase in early/late apoptosis was observed in esxA mutant-infected cells as compared to wildtype. Impeding secretion of EsxA, by deleting C-terminal residues of the protein, also resulted in a significant increase of epithelial cell apoptosis. Furthermore, cells transfected with esxA showed an increased protection from apoptotic cell death. A double mutant lacking both EsxA and EsxB also induced increased apoptosis, but remarkably was unable to escape from cells as efficiently as the single mutants or wildtype. Thus, using in vitro models of intracellular staphylococcal infection, we demonstrate that EsxA interferes with host cell apoptotic pathways and, together with EsxB, mediates the release of S. aureus from the host cell.
Item Type: | Journal Article | ||||
---|---|---|---|---|---|
Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School | ||||
Journal or Publication Title: | Infection and Immunity | ||||
Publisher: | American Society for Microbiology | ||||
ISSN: | 0019-9567 | ||||
Official Date: | 21 July 2014 | ||||
Dates: |
|
||||
Volume: | Volume 82 | ||||
Number: | Number 10 | ||||
Page Range: | pp. 4144-4153 | ||||
DOI: | 10.1128/IAI.01576-14 | ||||
Status: | Peer Reviewed | ||||
Publication Status: | Published | ||||
Access rights to Published version: | Restricted or Subscription Access |
Request changes or add full text files to a record
Repository staff actions (login required)
View Item |