Abstract
Staphylococcus aureus is a predominant cause of fatal pneumonia following influenza A virus (IAV) infection. Herein we investigate the influence of antecedent IAV infection on S. aureus virulence gene expression. Using a murine model, comparing the USA300 and USA300ΔsaeR/S strains, we demonstrate that S. aureus pathogenesis following IAV infection is SaeR/S dependent. Furthermore, we show that IAV modulates the lung environment to rapidly up-regulate S. aureus virulence factors containing the SaeR-binding domain. Data demonstrate that the pathogen response to IAV infection impacts host outcome and provides evidence that the ability of S. aureus to sense and respond to the lung environment determines severity of pneumonia.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Bacterial Proteins / genetics
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Bacterial Proteins / metabolism*
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Disease Models, Animal
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Female
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Gene Deletion
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Male
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Mice, Inbred BALB C
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Orthomyxoviridae Infections / complications*
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Orthomyxoviridae Infections / pathology
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Pneumonia, Staphylococcal / genetics
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Pneumonia, Staphylococcal / immunology*
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Protein Kinases / genetics
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Protein Kinases / metabolism*
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Staphylococcus aureus / genetics
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Staphylococcus aureus / pathogenicity*
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Transcription Factors / genetics
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Transcription Factors / metabolism*
Substances
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Bacterial Proteins
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SaeR protein, Staphylococcus aureus
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Transcription Factors
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Protein Kinases
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SaeS protein, Staphylococcus aureus