Critical role of constitutive type I interferon response in bronchial epithelial cell to influenza infection

Innate antiviral responses in bronchial epithelial cells (BECs) provide the first line of defense against respiratory viral infection and the effectiveness of this response is critically dependent on the type I interferons (IFNs). However the importance of the antiviral responses in BECs during infl...

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Published inPloS one Vol. 7; no. 3; p. e32947
Main Authors Hsu, Alan C-Y, Parsons, Kristy, Barr, Ian, Lowther, Sue, Middleton, Deborah, Hansbro, Philip M, Wark, Peter A B
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 02.03.2012
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Abstract Innate antiviral responses in bronchial epithelial cells (BECs) provide the first line of defense against respiratory viral infection and the effectiveness of this response is critically dependent on the type I interferons (IFNs). However the importance of the antiviral responses in BECs during influenza infection is not well understood. We profiled the innate immune response to infection with H3N2 and H5N1 virus using Calu-3 cells and primary BECs to model proximal airway cells. The susceptibility of BECs to influenza infection was not solely dependent on the sialic acid-bearing glycoprotein, and antiviral responses that occurred after viral endocytosis was more important in limiting viral replication. The early antiviral response and apoptosis correlated with the ability to limit viral replication. Both viruses reduced RIG-I associated antiviral responses and subsequent induction of IFN-β. However it was found that there was constitutive release of IFN-β by BECs and this was critical in inducing late antiviral signaling via type I IFN receptors, and was crucial in limiting viral infection. This study characterizes anti-influenza virus responses in airway epithelial cells and shows that constitutive IFN-β release plays a more important role in initiating protective late IFN-stimulated responses during human influenza infection in bronchial epithelial cells.
AbstractList Innate antiviral responses in bronchial epithelial cells (BECs) provide the first line of defense against respiratory viral infection and the effectiveness of this response is critically dependent on the type I interferons (IFNs). However the importance of the antiviral responses in BECs during influenza infection is not well understood. We profiled the innate immune response to infection with H3N2 and H5N1 virus using Calu-3 cells and primary BECs to model proximal airway cells. The susceptibility of BECs to influenza infection was not solely dependent on the sialic acid-bearing glycoprotein, and antiviral responses that occurred after viral endocytosis was more important in limiting viral replication. The early antiviral response and apoptosis correlated with the ability to limit viral replication. Both viruses reduced RIG-I associated antiviral responses and subsequent induction of IFN-[beta]. However it was found that there was constitutive release of IFN-[beta] by BECs and this was critical in inducing late antiviral signaling via type I IFN receptors, and was crucial in limiting viral infection. This study characterizes anti-influenza virus responses in airway epithelial cells and shows that constitutive IFN-[beta] release plays a more important role in initiating protective late IFN-stimulated responses during human influenza infection in bronchial epithelial cells.
Innate antiviral responses in bronchial epithelial cells (BECs) provide the first line of defense against respiratory viral infection and the effectiveness of this response is critically dependent on the type I interferons (IFNs). However the importance of the antiviral responses in BECs during influenza infection is not well understood. We profiled the innate immune response to infection with H3N2 and H5N1 virus using Calu-3 cells and primary BECs to model proximal airway cells. The susceptibility of BECs to influenza infection was not solely dependent on the sialic acid-bearing glycoprotein, and antiviral responses that occurred after viral endocytosis was more important in limiting viral replication. The early antiviral response and apoptosis correlated with the ability to limit viral replication. Both viruses reduced RIG-I associated antiviral responses and subsequent induction of IFN-β. However it was found that there was constitutive release of IFN-β by BECs and this was critical in inducing late antiviral signaling via type I IFN receptors, and was crucial in limiting viral infection. This study characterizes anti-influenza virus responses in airway epithelial cells and shows that constitutive IFN-β release plays a more important role in initiating protective late IFN-stimulated responses during human influenza infection in bronchial epithelial cells.Innate antiviral responses in bronchial epithelial cells (BECs) provide the first line of defense against respiratory viral infection and the effectiveness of this response is critically dependent on the type I interferons (IFNs). However the importance of the antiviral responses in BECs during influenza infection is not well understood. We profiled the innate immune response to infection with H3N2 and H5N1 virus using Calu-3 cells and primary BECs to model proximal airway cells. The susceptibility of BECs to influenza infection was not solely dependent on the sialic acid-bearing glycoprotein, and antiviral responses that occurred after viral endocytosis was more important in limiting viral replication. The early antiviral response and apoptosis correlated with the ability to limit viral replication. Both viruses reduced RIG-I associated antiviral responses and subsequent induction of IFN-β. However it was found that there was constitutive release of IFN-β by BECs and this was critical in inducing late antiviral signaling via type I IFN receptors, and was crucial in limiting viral infection. This study characterizes anti-influenza virus responses in airway epithelial cells and shows that constitutive IFN-β release plays a more important role in initiating protective late IFN-stimulated responses during human influenza infection in bronchial epithelial cells.
Innate antiviral responses in bronchial epithelial cells (BECs) provide the first line of defense against respiratory viral infection and the effectiveness of this response is critically dependent on the type I interferons (IFNs). However the importance of the antiviral responses in BECs during influenza infection is not well understood. We profiled the innate immune response to infection with H3N2 and H5N1 virus using Calu-3 cells and primary BECs to model proximal airway cells. The susceptibility of BECs to influenza infection was not solely dependent on the sialic acid-bearing glycoprotein, and antiviral responses that occurred after viral endocytosis was more important in limiting viral replication. The early antiviral response and apoptosis correlated with the ability to limit viral replication. Both viruses reduced RIG-I associated antiviral responses and subsequent induction of IFN-β. However it was found that there was constitutive release of IFN-β by BECs and this was critical in inducing late antiviral signaling via type I IFN receptors, and was crucial in limiting viral infection. This study characterizes anti-influenza virus responses in airway epithelial cells and shows that constitutive IFN-β release plays a more important role in initiating protective late IFN-stimulated responses during human influenza infection in bronchial epithelial cells.
Audience Academic
Author Middleton, Deborah
Hansbro, Philip M
Barr, Ian
Wark, Peter A B
Parsons, Kristy
Lowther, Sue
Hsu, Alan C-Y
AuthorAffiliation 3 The Commonwealth Scientific and Industrial Research Organization (CSIRO) - Australian Animal Health Laboratory, Geelong, Victoria, Australia
4 Department of Respiratory and Sleep Medicine, John Hunter Hospital, Newcastle, New South Wales, Australia
2 World Health Organization Collaborating Centre for Reference and Research on Influenza, Melbourne, Victoria, Australia
1 Centre for Asthma and Respiratory Disease, The University of Newcastle, Newcastle, New South Wales, Australia
Kantonal Hospital St. Gallen, Switzerland
AuthorAffiliation_xml – name: 1 Centre for Asthma and Respiratory Disease, The University of Newcastle, Newcastle, New South Wales, Australia
– name: 4 Department of Respiratory and Sleep Medicine, John Hunter Hospital, Newcastle, New South Wales, Australia
– name: Kantonal Hospital St. Gallen, Switzerland
– name: 3 The Commonwealth Scientific and Industrial Research Organization (CSIRO) - Australian Animal Health Laboratory, Geelong, Victoria, Australia
– name: 2 World Health Organization Collaborating Centre for Reference and Research on Influenza, Melbourne, Victoria, Australia
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  givenname: Alan C-Y
  surname: Hsu
  fullname: Hsu, Alan C-Y
  email: Alan.Hsu@uon.edu.au
  organization: Centre for Asthma and Respiratory Disease, The University of Newcastle, Newcastle, New South Wales, Australia. Alan.Hsu@uon.edu.au
– sequence: 2
  givenname: Kristy
  surname: Parsons
  fullname: Parsons, Kristy
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  givenname: Ian
  surname: Barr
  fullname: Barr, Ian
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  givenname: Sue
  surname: Lowther
  fullname: Lowther, Sue
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– sequence: 7
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/22396801$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright COPYRIGHT 2012 Public Library of Science
2012 Hsu 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.
Hsu et al. 2012
Copyright_xml – notice: COPYRIGHT 2012 Public Library of Science
– notice: 2012 Hsu 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.
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Conceived and designed the experiments: AH PMH PAW. Performed the experiments: AH KP SL. Analyzed the data: AH PMH PAW. Contributed reagents/materials/analysis tools: IB DM. Wrote the paper: AH PMH PAW.
OpenAccessLink https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292582/
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PublicationDate 2012-03-02
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Snippet Innate antiviral responses in bronchial epithelial cells (BECs) provide the first line of defense against respiratory viral infection and the effectiveness of...
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SubjectTerms Analysis
Animals
Apoptosis
Avian influenza
Avian influenza viruses
Biological response modifiers
Biology
Bronchi - cytology
Bronchi - virology
Cell Line
Constraining
Cycloheximide - pharmacology
Disease susceptibility
Dogs
Endocytosis
Epithelial cells
Epithelial Cells - metabolism
Epithelial Cells - virology
Glycoproteins
Health aspects
Human behavior
Humans
Immune response
Immune system
Infection
Infections
Influenza
Influenza A Virus, H3N2 Subtype - metabolism
Influenza A Virus, H5N1 Subtype - metabolism
Influenza, Human - metabolism
Innate immunity
Interferon
Interferon Type I - metabolism
Interferon-beta - metabolism
Kinases
Medicine
Models, Biological
N-Acetylneuraminic Acid - chemistry
Organic acids
Pandemics
Protein Synthesis Inhibitors - pharmacology
Receptors
Replication
Respiratory tract
Signaling
Virus diseases
Virus replication
Viruses
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Title Critical role of constitutive type I interferon response in bronchial epithelial cell to influenza infection
URI https://www.ncbi.nlm.nih.gov/pubmed/22396801
https://www.proquest.com/docview/1323982804
https://www.proquest.com/docview/926879622
https://pubmed.ncbi.nlm.nih.gov/PMC3292582
https://doaj.org/article/0eef907b001041e69763837f978366c0
http://dx.doi.org/10.1371/journal.pone.0032947
Volume 7
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