Characterization of Host and Bacterial Contributions to Lung Barrier Dysfunction Following Co-infection with 2009 Pandemic Influenza and Methicillin Resistant Staphylococcus aureus.
Identifieur interne : 000165 ( PubMed/Checkpoint ); précédent : 000164; suivant : 000166Characterization 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 [Canada] ; Justine Ciric [Canada] ; Shane D. Falcinelli [États-Unis] ; Daniel S. Chertow [États-Unis] ; Jason Kindrachuk [Canada]Source :
- Viruses [ 1999-4915 ] ; 2019.
Descripteurs français
- KwdFr :
- Analyse par réseau de protéines, Barrière alvéolocapillaire (physiopathologie), Cellules A549, Co-infection (microbiologie), Co-infection (virologie), Facteurs de virulence, Grippe humaine (microbiologie), Grippe humaine (physiopathologie), Humains, Infections à staphylocoques (physiopathologie), Infections à staphylocoques (virologie), Pneumocytes (microbiologie), Pneumocytes (virologie), Poumon (anatomopathologie), Réplication virale, Sous-type H1N1 du virus de la grippe A, Staphylococcus aureus résistant à la méticilline.
- MESH :
- anatomopathologie : Poumon.
- microbiologie : Co-infection, Grippe humaine, Pneumocytes.
- physiopathologie : Barrière alvéolocapillaire, Grippe humaine, Infections à staphylocoques.
- virologie : Co-infection, Infections à staphylocoques, Pneumocytes.
- Analyse par réseau de protéines, Cellules A549, Facteurs de virulence, Humains, Réplication virale, Sous-type H1N1 du virus de la grippe A, Staphylococcus aureus résistant à la méticilline.
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
Affiliations:
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pubmed:30699912Le document en format XML
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<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>
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<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>
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<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>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nickol</LastName>
<ForeName>Michaela E</ForeName>
<Initials>ME</Initials>
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</AffiliationInfo>
<AffiliationInfo><Affiliation>Critical Care Medicine Department, National Institutes of Health Clinical Center, Bethesda, MD 20892, USA. chertowd@cc.nih.gov.</Affiliation>
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<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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<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>
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