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Staphylococcus aureus sigma B-dependent emergence of small-colony variants and biofilm production following exposure to Pseudomonas aeruginosa 4-hydroxy-2-heptylquinoline-N-oxide

Mitchell, Gabriel; Séguin, David Lalonde; Asselin, Ann-Elise; Déziel, Éric; Cantin, André M.; Frost, Éric; Michaud, Sophie; Malouin, François (2010). Staphylococcus aureus sigma B-dependent emergence of small-colony variants and biofilm production following exposure to Pseudomonas aeruginosa 4-hydroxy-2-heptylquinoline-N-oxide BMC Microbiology , vol. 10 . p. 1-15. DOI: 10.1186/1471-2180-10-33.

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Résumé

BACKGROUND: Staphylococcus aureus and Pseudomonas aeruginosa are often found together in the airways of cystic fibrosis (CF) patients. It was previously shown that the P. aeruginosa exoproduct 4-hydroxy-2-heptylquinoline-N-oxide (HQNO) suppresses the growth of S. aureus and provokes the emergence of small-colony variants (SCVs). The presence of S. aureus SCVs as well as biofilms have both been associated with chronic infections in CF. RESULTS: We demonstrated that HQNO stimulates S. aureus to form a biofilm in association with the formation of SCVs. The emergence of SCVs and biofilm production under HQNO exposure was shown to be dependent on the activity of the stress- and colonization-related alternative sigma factor B (SigB). Analysis of gene expression revealed that exposure of a prototypical S. aureus strain to HQNO activates SigB, which was leading to an increase in the expression of the fibronectin-binding protein A and the biofilm-associated sarA genes. Conversely, the quorum sensing accessory gene regulator (agr) system and the alpha-hemolysin gene were repressed by HQNO. Experiments using culture supernatants from P. aeruginosa PAO1 and a double chamber co-culture model confirmed that P. aeruginosa stimulates biofilm formation and activates SigB in a S. aureus strain isolated from a CF patient. Furthermore, the supernatant from P. aeruginosa mutants unable to produce HQNO induced the production of biofilms by S. aureus to a lesser extent than the wild-type strain only in a S. aureus SigB-functional background. CONCLUSIONS: These results suggest that S. aureus responds to HQNO from P. aeruginosa by forming SCVs and biofilms through SigB activation, a phenomenon that may contribute to the establishment of chronic infections in CF patient

Type de document:
Mots-clés libres: FIBRONECTIN-BINDING PROTEINS, VIRULENCE GENE-EXPRESSION, N-ACYLHOMOSERINE LACTONES, CYSTIC-FIBROSIS PATIENTS, ANTIBIOTIC-RESISTANCE, INTERSPECIES COMMUNICATION, BURKHOLDERIA-CEPACIA, BACTERIAL BIOFILMS, ALPHA-HEMOLYSIN, IN-VIVO
Centre: Centre INRS-Institut Armand Frappier
Date de dépôt: 30 avr. 2014 18:18
Dernière modification: 30 avr. 2014 18:18
URI: http://espace.inrs.ca/id/eprint/2209

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