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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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. |
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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.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0041879</identifier><identifier>PMID: 22962579</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>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</subject><ispartof>PloS one, 2012-09, Vol.7 (9), p.e41879</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>Tian et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Tian et al 2012 Tian et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c791t-f341d0ece8f093cb8a04b08b3aab1b12744c1d60ddbd1ed01205cb297367bb4f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3433467/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3433467/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,2104,2930,23873,27931,27932,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22962579$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Jeyaseelan, Samithamby</contributor><creatorcontrib>Tian, Xiaoli</creatorcontrib><creatorcontrib>Xu, Feng</creatorcontrib><creatorcontrib>Lung, Wing Yi</creatorcontrib><creatorcontrib>Meyerson, Cherise</creatorcontrib><creatorcontrib>Ghaffari, Amir Ali</creatorcontrib><creatorcontrib>Cheng, Genhong</creatorcontrib><creatorcontrib>Deng, Jane C</creatorcontrib><title>Poly I:C enhances susceptibility to secondary pulmonary infections by gram-positive bacteria</title><title>PloS one</title><addtitle>PLoS One</addtitle><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.</description><subject>Aminoquinolines - pharmacology</subject><subject>Animals</subject><subject>Antibacterial agents</subject><subject>Antibodies - pharmacology</subject><subject>Antigens, Viral - administration & dosage</subject><subject>Antigens, Viral - immunology</subject><subject>Bacteria</subject><subject>Bacterial infections</subject><subject>Biology</subject><subject>Disease Susceptibility</subject><subject>Double-stranded RNA</subject><subject>Drug resistance</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gram-positive bacteria</subject><subject>Health aspects</subject><subject>Imidazoles - pharmacology</subject><subject>Imiquimod</subject><subject>Immune clearance</subject><subject>Immune system</subject><subject>Impairment</subject><subject>Indexing in process</subject><subject>Infections</subject><subject>Influenza</subject><subject>Interferon</subject><subject>Interferon Inducers - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tian, Xiaoli</au><au>Xu, Feng</au><au>Lung, Wing Yi</au><au>Meyerson, Cherise</au><au>Ghaffari, Amir Ali</au><au>Cheng, Genhong</au><au>Deng, Jane C</au><au>Jeyaseelan, Samithamby</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Poly I:C enhances susceptibility to secondary pulmonary infections by gram-positive bacteria</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-09-04</date><risdate>2012</risdate><volume>7</volume><issue>9</issue><spage>e41879</spage><pages>e41879-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>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.</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> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2012-09, Vol.7 (9), p.e41879 |
issn | 1932-6203 1932-6203 |
language | eng |
recordid | cdi_plos_journals_1326544973 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
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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