Poly I:C enhances susceptibility to secondary pulmonary infections by gram-positive bacteria

Secondary bacterial pneumonias are a frequent complication of influenza and other respiratory viral infections, but the mechanisms underlying viral-induced susceptibility to bacterial infections are poorly understood. In particular, it is unclear whether the host's response against the viral in...

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Veröffentlicht in:PloS one 2012-09, Vol.7 (9), p.e41879
Hauptverfasser: Tian, Xiaoli, Xu, Feng, Lung, Wing Yi, Meyerson, Cherise, Ghaffari, Amir Ali, Cheng, Genhong, Deng, Jane C
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container_title PloS one
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Xu, Feng
Lung, Wing Yi
Meyerson, Cherise
Ghaffari, Amir Ali
Cheng, Genhong
Deng, Jane C
description Secondary bacterial pneumonias are a frequent complication of influenza and other respiratory viral infections, but the mechanisms underlying viral-induced susceptibility to bacterial infections are poorly understood. In particular, it is unclear whether the host's response against the viral infection, independent of the injury caused by the virus, results in impairment of antibacterial host defense. Here, we sought to determine whether the induction of an "antiviral" immune state using various viral recognition receptor ligands was sufficient to result in decreased ability to combat common bacterial pathogens of the lung. Using a mouse model, animals were administered polyinosine-polycytidylic acid (poly I:C) or Toll-like 7 ligand (imiquimod or gardiquimod) intranasally, followed by intratracheal challenge with Streptococcus pneumoniae. We found that animals pre-exposed to poly I:C displayed impaired bacterial clearance and increased mortality. Poly I:C-exposed animals also had decreased ability to clear methicillin-resistant Staphylococcus aureus. Furthermore, we showed that activation of Toll-like receptor (TLR)3 and Retinoic acid inducible gene (RIG-I)/Cardif pathways, which recognize viral nucleic acids in the form of dsRNA, both contribute to poly I:C mediated impairment of bacterial clearance. Finally, we determined that poly I:C administration resulted in significant induction of type I interferons (IFNs), whereas the elimination of type I IFN signaling improved clearance and survival following secondary bacterial pneumonia. Collectively, these results indicate that in the lung, poly I:C administration is sufficient to impair pulmonary host defense against clinically important gram-positive bacterial pathogens, which appears to be mediated by type I IFNs.
doi_str_mv 10.1371/journal.pone.0041879
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In particular, it is unclear whether the host's response against the viral infection, independent of the injury caused by the virus, results in impairment of antibacterial host defense. Here, we sought to determine whether the induction of an "antiviral" immune state using various viral recognition receptor ligands was sufficient to result in decreased ability to combat common bacterial pathogens of the lung. Using a mouse model, animals were administered polyinosine-polycytidylic acid (poly I:C) or Toll-like 7 ligand (imiquimod or gardiquimod) intranasally, followed by intratracheal challenge with Streptococcus pneumoniae. We found that animals pre-exposed to poly I:C displayed impaired bacterial clearance and increased mortality. Poly I:C-exposed animals also had decreased ability to clear methicillin-resistant Staphylococcus aureus. 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In particular, it is unclear whether the host's response against the viral infection, independent of the injury caused by the virus, results in impairment of antibacterial host defense. Here, we sought to determine whether the induction of an "antiviral" immune state using various viral recognition receptor ligands was sufficient to result in decreased ability to combat common bacterial pathogens of the lung. Using a mouse model, animals were administered polyinosine-polycytidylic acid (poly I:C) or Toll-like 7 ligand (imiquimod or gardiquimod) intranasally, followed by intratracheal challenge with Streptococcus pneumoniae. We found that animals pre-exposed to poly I:C displayed impaired bacterial clearance and increased mortality. Poly I:C-exposed animals also had decreased ability to clear methicillin-resistant Staphylococcus aureus. Furthermore, we showed that activation of Toll-like receptor (TLR)3 and Retinoic acid inducible gene (RIG-I)/Cardif pathways, which recognize viral nucleic acids in the form of dsRNA, both contribute to poly I:C mediated impairment of bacterial clearance. Finally, we determined that poly I:C administration resulted in significant induction of type I interferons (IFNs), whereas the elimination of type I IFN signaling improved clearance and survival following secondary bacterial pneumonia. Collectively, these results indicate that in the lung, poly I:C administration is sufficient to impair pulmonary host defense against clinically important gram-positive bacterial pathogens, which appears to be mediated by type I IFNs.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22962579</pmid><doi>10.1371/journal.pone.0041879</doi><tpages>e41879</tpages><oa>free_for_read</oa></addata></record>
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1932-6203
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subjects Aminoquinolines - pharmacology
Animals
Antibacterial agents
Antibodies - pharmacology
Antigens, Viral - administration & dosage
Antigens, Viral - immunology
Bacteria
Bacterial infections
Biology
Disease Susceptibility
Double-stranded RNA
Drug resistance
Gene Expression Regulation - drug effects
Gram-positive bacteria
Health aspects
Imidazoles - pharmacology
Imiquimod
Immune clearance
Immune system
Impairment
Indexing in process
Infections
Influenza
Interferon
Interferon Inducers - pharmacology
Interferon Type I - genetics
Interferon Type I - immunology
Ligands
Lungs
Medicine
Membrane Proteins - genetics
Membrane Proteins - immunology
Methicillin
Methicillin-Resistant Staphylococcus aureus - immunology
Mice
Nerve Tissue Proteins - genetics
Nerve Tissue Proteins - immunology
Nucleic acids
Pandemics
Pathogens
Pneumococcal Infections - genetics
Pneumococcal Infections - immunology
Pneumococcal Infections - microbiology
Pneumococcal Infections - mortality
Pneumonia
Pneumonia, Bacterial - genetics
Pneumonia, Bacterial - immunology
Pneumonia, Bacterial - microbiology
Pneumonia, Bacterial - mortality
Poly I-C - administration & dosage
Poly I-C - immunology
Polyinosinic:polycytidylic acid
Proteins
Receptor, Interferon alpha-beta - genetics
Receptor, Interferon alpha-beta - immunology
Retinoic acid
Signal Transduction - drug effects
Signaling
Staphylococcal Infections - genetics
Staphylococcal Infections - immunology
Staphylococcal Infections - microbiology
Staphylococcal Infections - mortality
Staphylococcus aureus
Staphylococcus aureus infections
Streptococcus infections
Streptococcus pneumoniae - immunology
Survival Rate
Toll-Like Receptor 3 - genetics
Toll-Like Receptor 3 - immunology
Toll-like receptors
Trachea
Viral infections
Viruses
title Poly I:C enhances susceptibility to secondary pulmonary infections by gram-positive bacteria
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