|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 UMRS 514, Institut National de la Sante et de la Recherche Medicale (INSERM), Reims, France; Institute of Microbiology "Prof. Paulo de Goes", Rio de Janeiro, Brazil
2 UMRS 514, Institut National de la Sante et de la Recherche Medicale (INSERM), Reims, France
3 Department of Microbiology and Immunology, State University of Rio de Janeiro (UERJ), Rio de Janeiro, Brazil
4 EPI 0014, INSERM, Vandoeuvre les Nancy, France
* To whom correspondence should be addressed. E-mail: edith.puchelle{at}univ-reims.fr.
Staphylococcus aureus (S. aureus) is a major cause of pulmonary infection, particularly in cystic fibrosis (CF) patients. However, only a few aspects of the interplay between S. aureus and host airway epithelial cells have been investigated thus far. We investigated by videomicroscopy the time and bacterial concentration-dependent (104, 106 and 108 CFU/mL) effect of S. aureus on adherence, internalization, the associated damage of the airway epithelial cells and the balance between the secretion of the S. aureus virulence factor (
-toxin) and the airway cell antibacterial secretory leukocyte proteinase inhibitor (SLPI). After 1h of interaction, whatever the initial bacterial concentration, a low percentage of S. aureus (less than 8%) adhered to airway cells and no airway epithelial cell damage was observed. In contrast, after 24h of incubation, more bacteria adhered to airway epithelial cells, internalized bacteria were observed and a bacterial concentration-dependent effect on airway cell damage was observed. At 24h, most airway cells incubated with bacteria at 108 CFU/mL exhibited a necrotic phenotype. The necrosis was preceded by a transient apoptotic process. In parallel, we observed a time and bacterial concentration-dependent decrease in SLPI and increase in
-toxin expression. These results suggest that airway cells are able to defend against S. aureus in early stages of infection. However, in later phases, there is a marked imbalance between the bactericidal capacity of host cells and bacterial virulence. These findings reinforce the potential importance of S. aureus in the pathogenicity of airway infections, including those observed early in CF patients.
This article has been cited by other articles:
![]() |
M. J. J. B. Sibbald, A. K. Ziebandt, S. Engelmann, M. Hecker, A. de Jong, H. J. M. Harmsen, G. C. Raangs, I. Stokroos, J. P. Arends, J. Y. F. Dubois, et al. Mapping the Pathways to Staphylococcal Pathogenesis by Comparative Secretomics Microbiol. Mol. Biol. Rev., September 1, 2006; 70(3): 755 - 788. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Fragaki, C. Kileztky, C. Trentesaux, J.-M. Zahm, O. Bajolet, M. Johnson, and E. Puchelle Downregulation by a long-acting beta2-adrenergic receptor agonist and corticosteroid of Staphylococcus aureus-induced airway epithelial inflammatory mediator production Am J Physiol Lung Cell Mol Physiol, July 1, 2006; 291(1): L11 - L18. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Escotte, D. Al Alam, R. Le Naour, E. Puchelle, M. Guenounou, and S. C. Gangloff T Cell Chemotaxis and Chemokine Release after Staphylococcus aureus Interaction with Polarized Airway Epithelium Am. J. Respir. Cell Mol. Biol., March 1, 2006; 34(3): 348 - 354. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Moreilhon, D. Gras, C. Hologne, O. Bajolet, F. Cottrez, V. Magnone, M. Merten, H. Groux, E. Puchelle, and P. Barbry Live Staphylococcus aureus and bacterial soluble factors induce different transcriptional responses in human airway cells Physiol Genomics, February 10, 2005; 20(3): 244 - 255. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |