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J Infect Dis.: Protecting against post-influenza bacterial pneumonia by increasing phagocyte recruitment and ROS production

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  • J Infect Dis.: Protecting against post-influenza bacterial pneumonia by increasing phagocyte recruitment and ROS production

    J Infect Dis. (2013) doi: 10.1093/infdis/jit830 First published online: December 23, 2013



    Protecting against post-influenza bacterial pneumonia by increasing phagocyte recruitment and ROS production

    Renuka Subramaniam1,
    Peter F. Barnes1,
    Kalyn Fletcher1,
    Vijay Bogarram2,
    Zachary Hillberry1,
    Pierre Neuenschwander2 and
    Homayoun Shams*,1

    + Author Affiliations

    1Center for Pulmonary and Infectious Diseases Control (CPIDC)
    2Biomedical research, The University of Texas Health Science Center at Tyler 11937 U.S. Highway 271, Tyler, TX 75708-3154

    ↵*Corresponding author, Phone: 903-877-2837, Fax: 903-877-7989, E-mail: homayoun.shams@uthct.edu

    Abstract

    Seasonal and especially pandemic influenza predispose patients to secondary bacterial pneumonias, which are a major cause of deaths and morbidity. Staphylococcus aureus is a particularly common and deadly form of post-influenza pneumonia, and increasing staphylococcal drug resistance makes the development of new therapies urgent. We explored an innate immune-mediated model of the lung to define novel mechanisms by which the host can be protected against secondary staphylococcal pneumonia after sub-lethal influenza infection. We found that stimulating the innate immunity in the lung by overexpression of GM-CSF will result in resistance to S. aureus pneumonia after sublethal influenza infection. Resistance was mediated by alveolar macrophages and neutrophils, and was associated with increased production of reactive oxygen species (ROS) by alveolar macrophages. Resistance was abrogated by treatment with agents that scavenged ROS. We conclude that stimulating innate immunity in the lung markedly reduces susceptibility to post-influenza staphylococcal pneumonia and that this may represent a novel immunomodulatory strategy for prevention and treatment of secondary bacterial pneumonia after influenza.


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