title: Dynamic interaction between airway epithelial cells and Staphylococcus aureus.
abstract: Staphylococcus aureus is a major cause of pulmonary infection, particularly in cystic fibrosis (CF) patients. However, 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 (10(4), 10(6), and 10(8) CFU/ml) effect of S. aureus on adherence, internalization, and the associated damage of the airway epithelial cells. The balance between the secretion by S. aureus of the alpha-toxin virulence factor and by the airway cells of the antibacterial secretory leukoproteinase inhibitor (SLPI) was also analyzed. After 1 h of interaction, whatever the initial bacterial concentration, a low percentage of S. aureus (<8%) adhered to airway cells, and no airway epithelial cell damage was observed. In contrast, after 24 h 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 24 h, most airway cells incubated with bacteria at 10(8) 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 alpha-toxin expression. These results suggest that airway cells can defend against S. aureus in the 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.
authors.affiliation: INSERM UMRS 514, 45 rue Cognacq-Jay, 51092 Reims Cedex, France.
authors.forename: Mauricio C A
authors.initials: MC
authors.lastname: da Silva
authors.forename: Jean-Marie
authors.initials: JM
authors.lastname: Zahm
authors.forename: Delphine
authors.initials: D
authors.lastname: Gras
authors.forename: Odile
authors.initials: O
authors.lastname: Bajolet
authors.forename: Michel
authors.initials: M
authors.lastname: Abely
authors.forename: Jocelyne
authors.initials: J
authors.lastname: Hinnrasky
authors.forename: Magali
authors.initials: M
authors.lastname: Milliot
authors.forename: Maria Cristina
authors.initials: MC
authors.lastname: de Assis
authors.forename: Coralie
authors.initials: C
authors.lastname: Hologne
authors.forename: Noël
authors.initials: N
authors.lastname: Bonnet
authors.forename: Marc
authors.initials: M
authors.lastname: Merten
authors.forename: Maria Cristina
authors.initials: MC
authors.lastname: Plotkowski
authors.forename: Edith
authors.initials: E
authors.lastname: Puchelle
mesh_terms: D017209:Apoptosis; D001422:Bacterial Adhesion; D001427:Bacterial Toxins / Q000378:metabolism; D002461:Cell Line, Transformed; D003470:Culture Media; D006460:Hemolysin Proteins / Q000378:metabolism; D006801:Humans; D009336:Necrosis; D011023:Pneumonia, Staphylococcal / Q000382:microbiology / Q000503:physiopathology*; D053491:Proteinase Inhibitory Proteins, Secretory; D011506:Proteins / Q000378:metabolism; D020545:Respiratory Mucosa / Q000166:cytology / Q000378:metabolism / Q000382:microbiology*; D053481:Secretory Leukocyte Peptidase Inhibitor; D013211:Staphylococcus aureus / Q000472:pathogenicity*; D014132:Trachea / Q000166:cytology; D014774:Virulence
chemical_list: D001427:Bacterial Toxins; D003470:Culture Media; D006460:Hemolysin Proteins; D053491:Proteinase Inhibitory Proteins, Secretory; D011506:Proteins; C506814:SLPI protein, human; D053481:Secretory Leukocyte Peptidase Inhibitor; C021091:staphylococcal alpha-toxin