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Maria Labandeira-Rey,1Florence Couzon,2,3,4,5Sandrine Boisset,2,3,4,5Eric L. Brown,1*Michele Bes,2,3,4,5Yvonne Benito,2,3,4,5Elena M. Barbu,1Vanessa Vazquez,1Magnus Höök,1Jerome Etienne,2,3,4,5François Vandenesch,2,3,4,5M. Gabriela Bowden1
The Staphylococcus aureus Panton-Valentine leukocidin (PVL)is a pore-forming toxin secreted by strains epidemiologicallyassociated with the current outbreak of community-associatedmethicillin-resistant Staphylococcus aureus (CA-MRSA) and withthe often-lethal necrotizing pneumonia. To investigate the roleof PVL in pulmonary disease, we tested the pathogenicity ofclinical isolates, isogenic PVL-negative and PVL-positive S.aureus strains, as well as purified PVL, in a mouse acute pneumoniamodel. Here we show that PVL is sufficient to cause pneumoniaand that the expression of this leukotoxin induces global changesin transcriptional levels of genes encoding secreted and cellwallanchored staphylococcal proteins, including the lunginflammatory factor staphylococcal protein A (Spa).
1 Center for Extracellular Matrix Biology, Institute of Biosciences and Technology, The Texas A&M University System Health Science Center, Houston, TX 77030, USA. 2 Université de Lyon, Lyon, F-69008, France. 3 Université de Lyon 1, Faculté Laennec, Lyon, F-69008, France. 4 INSERM E0230, Centre National de référence des staphylocoques, Lyon, F-69008, France. 5 Hospices Civils de Lyon, Hôpital Edouard Herriot, Lyon, F-69003, France.
* Present address: University of Texas School of Public Health,Houston, TX 77030, USA.
These authors contributed equally to this work.
To whom correspondence should be addressed. E-mail: gbowden{at}ibt.tamhsc.edu and denesch{at}univ-lyon1.fr
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Barbara C. Kahl and Georg Peters (23 February 2007) Science315 (5815), 1082.
[DOI: 10.1126/science.1139628] |Summary »|Full Text »|PDF »
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