Characterization of Host and Bacterial Contributions to Lung Barrier Dysfunction Following Co-infection with 2009 Pandemic Influenza and Methicillin Resistant Staphylococcus aureus.
Identifieur interne : 000176 ( PubMed/Corpus ); précédent : 000175; suivant : 000177Characterization of Host and Bacterial Contributions to Lung Barrier Dysfunction Following Co-infection with 2009 Pandemic Influenza and Methicillin Resistant Staphylococcus aureus.
Auteurs : Michaela E. Nickol ; Justine Ciric ; Shane D. Falcinelli ; Daniel S. Chertow ; Jason KindrachukSource :
- Viruses [ 1999-4915 ] ; 2019.
English descriptors
- KwdEn :
- A549 Cells, Alveolar Epithelial Cells (microbiology), Alveolar Epithelial Cells (virology), Blood-Air Barrier (physiopathology), Coinfection (microbiology), Coinfection (virology), Humans, Influenza A Virus, H1N1 Subtype, Influenza, Human (microbiology), Influenza, Human (physiopathology), Lung (pathology), Methicillin-Resistant Staphylococcus aureus, Protein Array Analysis, Staphylococcal Infections (physiopathology), Staphylococcal Infections (virology), Virulence Factors, Virus Replication.
- MESH :
- chemical : Virulence Factors.
- microbiology : Alveolar Epithelial Cells, Coinfection, Influenza, Human.
- pathology : Lung.
- physiopathology : Blood-Air Barrier, Influenza, Human, Staphylococcal Infections.
- virology : Alveolar Epithelial Cells, Coinfection, Staphylococcal Infections.
- A549 Cells, Humans, Influenza A Virus, H1N1 Subtype, Methicillin-Resistant Staphylococcus aureus, Protein Array Analysis, Virus Replication.
Abstract
Influenza viruses are a threat to global public health resulting in ~500,000 deaths each year. Despite an intensive vaccination program, influenza infections remain a recurrent, yet unsolved public health problem. Secondary bacterial infections frequently complicate influenza infections during seasonal outbreaks and pandemics, resulting in increased morbidity and mortality. Staphylococcus aureus, including methicillin-resistant S. aureus (MRSA), is frequently associated with these co-infections, including the 2009 influenza pandemic. Damage to alveolar epithelium is a major contributor to severe influenza-bacterial co-infections and can result in gas exchange abnormalities, fluid leakage, and respiratory insufficiency. These deleterious manifestations likely involve both pathogen- and host-mediated mechanisms. However, there is a paucity of information regarding the mechanisms (pathogen- and/or host-mediated) underlying influenza-bacterial co-infection pathogenesis. To address this, we characterized the contributions of viral-, bacterial-, and host-mediated factors to the altered structure and function of alveolar epithelial cells during co-infection with a focus on the 2009 pandemic influenza (pdm2009) and MRSA. Here, we characterized pdm2009 and MRSA replication kinetics, temporal host kinome responses, modulation of MRSA virulence factors, and disruption of alveolar barrier integrity in response to pdm2009-MRSA co-infection. Our results suggest that alveolar barrier disruption during co-infection is mediated primarily through host response dysregulation, resulting in loss of alveolar barrier integrity.
DOI: 10.3390/v11020116
PubMed: 30699912
Links to Exploration step
pubmed:30699912Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Characterization of Host and Bacterial Contributions to Lung Barrier Dysfunction Following Co-infection with 2009 Pandemic Influenza and Methicillin Resistant <i>Staphylococcus aureus</i>.</title><author><name sortKey="Nickol, Michaela E" sort="Nickol, Michaela E" uniqKey="Nickol M" first="Michaela E" last="Nickol">Michaela E. Nickol</name><affiliation><nlm:affiliation>Laboratory of Emerging and Re-Emerging Viruses, Department of Medical Microbiology, University of Manitoba, Winnipeg, MB R3E 0J9, Canada. nickolm@myumanitoba.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Ciric, Justine" sort="Ciric, Justine" uniqKey="Ciric J" first="Justine" last="Ciric">Justine Ciric</name><affiliation><nlm:affiliation>Laboratory of Emerging and Re-Emerging Viruses, Department of Medical Microbiology, University of Manitoba, Winnipeg, MB R3E 0J9, Canada. ciricj@myumanitoba.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Falcinelli, Shane D" sort="Falcinelli, Shane D" uniqKey="Falcinelli S" first="Shane D" last="Falcinelli">Shane D. 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Nickol</name><affiliation><nlm:affiliation>Laboratory of Emerging and Re-Emerging Viruses, Department of Medical Microbiology, University of Manitoba, Winnipeg, MB R3E 0J9, Canada. nickolm@myumanitoba.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Ciric, Justine" sort="Ciric, Justine" uniqKey="Ciric J" first="Justine" last="Ciric">Justine Ciric</name><affiliation><nlm:affiliation>Laboratory of Emerging and Re-Emerging Viruses, Department of Medical Microbiology, University of Manitoba, Winnipeg, MB R3E 0J9, Canada. ciricj@myumanitoba.ca.</nlm:affiliation></affiliation></author><author><name sortKey="Falcinelli, Shane D" sort="Falcinelli, Shane D" uniqKey="Falcinelli S" first="Shane D" last="Falcinelli">Shane D. Falcinelli</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, University of North Carolina Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA. shane_falcinelli@med.unc.edu.</nlm:affiliation></affiliation></author><author><name sortKey="Chertow, Daniel S" sort="Chertow, Daniel S" uniqKey="Chertow D" first="Daniel S" last="Chertow">Daniel S. Chertow</name><affiliation><nlm:affiliation>Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. chertowd@cc.nih.gov.</nlm:affiliation></affiliation></author><author><name sortKey="Kindrachuk, Jason" sort="Kindrachuk, Jason" uniqKey="Kindrachuk J" first="Jason" last="Kindrachuk">Jason Kindrachuk</name><affiliation><nlm:affiliation>Laboratory of Emerging and Re-Emerging Viruses, Department of Medical Microbiology, University of Manitoba, Winnipeg, MB R3E 0J9, Canada. Jason.Kindrachuk@umanitoba.ca.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Viruses</title><idno type="eISSN">1999-4915</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term><term>Alveolar Epithelial Cells (microbiology)</term><term>Alveolar Epithelial Cells (virology)</term><term>Blood-Air Barrier (physiopathology)</term><term>Coinfection (microbiology)</term><term>Coinfection (virology)</term><term>Humans</term><term>Influenza A Virus, H1N1 Subtype</term><term>Influenza, Human (microbiology)</term><term>Influenza, Human (physiopathology)</term><term>Lung (pathology)</term><term>Methicillin-Resistant Staphylococcus aureus</term><term>Protein Array Analysis</term><term>Staphylococcal Infections (physiopathology)</term><term>Staphylococcal Infections (virology)</term><term>Virulence Factors</term><term>Virus Replication</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Virulence Factors</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Alveolar Epithelial Cells</term><term>Coinfection</term><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Blood-Air Barrier</term><term>Influenza, Human</term><term>Staphylococcal Infections</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Alveolar Epithelial Cells</term><term>Coinfection</term><term>Staphylococcal Infections</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Humans</term><term>Influenza A Virus, H1N1 Subtype</term><term>Methicillin-Resistant Staphylococcus aureus</term><term>Protein Array Analysis</term><term>Virus Replication</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Influenza viruses are a threat to global public health resulting in ~500,000 deaths each year. Despite an intensive vaccination program, influenza infections remain a recurrent, yet unsolved public health problem. Secondary bacterial infections frequently complicate influenza infections during seasonal outbreaks and pandemics, resulting in increased morbidity and mortality. <i>Staphylococcus aureus</i>, including methicillin-resistant <i>S. aureus</i> (MRSA), is frequently associated with these co-infections, including the 2009 influenza pandemic. Damage to alveolar epithelium is a major contributor to severe influenza-bacterial co-infections and can result in gas exchange abnormalities, fluid leakage, and respiratory insufficiency. These deleterious manifestations likely involve both pathogen- and host-mediated mechanisms. However, there is a paucity of information regarding the mechanisms (pathogen- and/or host-mediated) underlying influenza-bacterial co-infection pathogenesis. To address this, we characterized the contributions of viral-, bacterial-, and host-mediated factors to the altered structure and function of alveolar epithelial cells during co-infection with a focus on the 2009 pandemic influenza (pdm2009) and MRSA. Here, we characterized pdm2009 and MRSA replication kinetics, temporal host kinome responses, modulation of MRSA virulence factors, and disruption of alveolar barrier integrity in response to pdm2009-MRSA co-infection. Our results suggest that alveolar barrier disruption during co-infection is mediated primarily through host response dysregulation, resulting in loss of alveolar barrier integrity.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30699912</PMID><DateCompleted><Year>2019</Year><Month>06</Month><Day>19</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>09</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1999-4915</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>2</Issue><PubDate><Year>2019</Year><Month>01</Month><Day>29</Day></PubDate></JournalIssue><Title>Viruses</Title><ISOAbbreviation>Viruses</ISOAbbreviation></Journal><ArticleTitle>Characterization of Host and Bacterial Contributions to Lung Barrier Dysfunction Following Co-infection with 2009 Pandemic Influenza and Methicillin Resistant <i>Staphylococcus aureus</i>.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">E116</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/v11020116</ELocationID><Abstract><AbstractText>Influenza viruses are a threat to global public health resulting in ~500,000 deaths each year. Despite an intensive vaccination program, influenza infections remain a recurrent, yet unsolved public health problem. Secondary bacterial infections frequently complicate influenza infections during seasonal outbreaks and pandemics, resulting in increased morbidity and mortality. <i>Staphylococcus aureus</i>, including methicillin-resistant <i>S. aureus</i> (MRSA), is frequently associated with these co-infections, including the 2009 influenza pandemic. Damage to alveolar epithelium is a major contributor to severe influenza-bacterial co-infections and can result in gas exchange abnormalities, fluid leakage, and respiratory insufficiency. These deleterious manifestations likely involve both pathogen- and host-mediated mechanisms. However, there is a paucity of information regarding the mechanisms (pathogen- and/or host-mediated) underlying influenza-bacterial co-infection pathogenesis. To address this, we characterized the contributions of viral-, bacterial-, and host-mediated factors to the altered structure and function of alveolar epithelial cells during co-infection with a focus on the 2009 pandemic influenza (pdm2009) and MRSA. Here, we characterized pdm2009 and MRSA replication kinetics, temporal host kinome responses, modulation of MRSA virulence factors, and disruption of alveolar barrier integrity in response to pdm2009-MRSA co-infection. Our results suggest that alveolar barrier disruption during co-infection is mediated primarily through host response dysregulation, resulting in loss of alveolar barrier integrity.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nickol</LastName><ForeName>Michaela E</ForeName><Initials>ME</Initials><AffiliationInfo><Affiliation>Laboratory of Emerging and Re-Emerging Viruses, Department of Medical Microbiology, University of Manitoba, Winnipeg, MB R3E 0J9, Canada. nickolm@myumanitoba.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ciric</LastName><ForeName>Justine</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Laboratory of Emerging and Re-Emerging Viruses, Department of Medical Microbiology, University of Manitoba, Winnipeg, MB R3E 0J9, Canada. ciricj@myumanitoba.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Falcinelli</LastName><ForeName>Shane D</ForeName><Initials>SD</Initials><Identifier Source="ORCID">0000-0002-3554-226X</Identifier><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of North Carolina Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA. shane_falcinelli@med.unc.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chertow</LastName><ForeName>Daniel S</ForeName><Initials>DS</Initials><Identifier Source="ORCID">0000-0002-1675-1728</Identifier><AffiliationInfo><Affiliation>Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. chertowd@cc.nih.gov.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Critical Care Medicine Department, National Institutes of Health Clinical Center, Bethesda, MD 20892, USA. chertowd@cc.nih.gov.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kindrachuk</LastName><ForeName>Jason</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0002-3305-7084</Identifier><AffiliationInfo><Affiliation>Laboratory of Emerging and Re-Emerging Viruses, Department of Medical Microbiology, University of Manitoba, Winnipeg, MB R3E 0J9, Canada. Jason.Kindrachuk@umanitoba.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>01</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Viruses</MedlineTA><NlmUniqueID>101509722</NlmUniqueID><ISSNLinking>1999-4915</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D037521">Virulence Factors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000072283" MajorTopicYN="N">A549 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056809" MajorTopicYN="N">Alveolar Epithelial Cells</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015824" MajorTopicYN="N">Blood-Air Barrier</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D060085" MajorTopicYN="N">Coinfection</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053118" MajorTopicYN="N">Influenza A Virus, H1N1 Subtype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055624" MajorTopicYN="N">Methicillin-Resistant Staphylococcus aureus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D040081" MajorTopicYN="N">Protein Array Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013203" MajorTopicYN="N">Staphylococcal Infections</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D037521" MajorTopicYN="N">Virulence Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">2009 pandemic</Keyword><Keyword MajorTopicYN="Y">Staphylococcus aureus</Keyword><Keyword MajorTopicYN="Y">alveolar epithelial cells</Keyword><Keyword MajorTopicYN="Y">barrier function</Keyword><Keyword MajorTopicYN="Y">co-infection</Keyword><Keyword MajorTopicYN="Y">influenza</Keyword><Keyword MajorTopicYN="Y">kinome</Keyword><Keyword MajorTopicYN="Y">virulence factors</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>01</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>01</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>2</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>2</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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