Defective innate immune responses to respiratory syncytial virus infection in ovalbumin-sensitized mice

Shen Hao Lai, Sui Ling Liao, Kin Sun Wong, Tzou Yien Lin

研究成果: 雜誌貢獻文章

3 引文 (Scopus)

摘要

Background/Purpose Respiratory viral infections have frequently been reported to closely correlate with asthma exacerbations. Distinctive expression of cytokine/chemokine and anomalous responses of innate immunity induced by respiratory viral infections were suggested to play a key role. This study further evaluates the effects of airway sensitization on innate immunity in response to different viruses. Methods Murine sensitization was established using an ovalbumin (OVA) sensitization model. Mice were subsequently infected with either respiratory syncytial virus (RSV) or human metapneumovirus (hMPV). Type I interferon (IFN), cytokines, and chemokines were measured in bronchoalveolar lavage (BAL) fluid. Pulmonary tissue samples were collected for the analysis of viral titers and type I IFN signal transcriptors. Results Distinct expressions of cytokine/chemokine responses after viral infection were also found in mice with OVA sensitization. A significant increase of virus replication was found in lungs of RSV-infected sensitized mice. The increment of RSV titer was associated with the decreased levels of type I IFN. Although Toll-like receptor 3 (TLR3) expression was significantly increased in the lungs, the key signal transcriptor, IFN regulatory factor 3, was significantly suppressed in the RSV-infected sensitized mice. Conclusion A defective antiviral innate response was observed in the murine respiratory allergy model. Suppressed expression of IFN signal transcriptor contributes to decreased production of type I IFN. The defective innate immune response might result in acute viral exacerbations of allergic airway diseases.
原文英語
頁(從 - 到)17-25
頁數9
期刊Journal of Microbiology, Immunology and Infection
50
發行號1
DOIs
出版狀態已發佈 - 二月 1 2017
對外發佈Yes

指紋

Respiratory Syncytial Virus Infections
Interferon Type I
Respiratory Syncytial Viruses
Ovalbumin
Innate Immunity
Virus Diseases
Chemokines
Cytokines
Respiratory Tract Infections
Lung
Interferon Regulatory Factor-3
Toll-Like Receptor 3
Metapneumovirus
Bronchoalveolar Lavage Fluid
Virus Replication
Viral Load
Interferons
Antiviral Agents
Hypersensitivity
Asthma

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology and Microbiology(all)
  • Microbiology (medical)
  • Infectious Diseases

引用此文

Defective innate immune responses to respiratory syncytial virus infection in ovalbumin-sensitized mice. / Lai, Shen Hao; Liao, Sui Ling; Wong, Kin Sun; Lin, Tzou Yien.

於: Journal of Microbiology, Immunology and Infection, 卷 50, 編號 1, 01.02.2017, p. 17-25.

研究成果: 雜誌貢獻文章

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abstract = "Background/Purpose Respiratory viral infections have frequently been reported to closely correlate with asthma exacerbations. Distinctive expression of cytokine/chemokine and anomalous responses of innate immunity induced by respiratory viral infections were suggested to play a key role. This study further evaluates the effects of airway sensitization on innate immunity in response to different viruses. Methods Murine sensitization was established using an ovalbumin (OVA) sensitization model. Mice were subsequently infected with either respiratory syncytial virus (RSV) or human metapneumovirus (hMPV). Type I interferon (IFN), cytokines, and chemokines were measured in bronchoalveolar lavage (BAL) fluid. Pulmonary tissue samples were collected for the analysis of viral titers and type I IFN signal transcriptors. Results Distinct expressions of cytokine/chemokine responses after viral infection were also found in mice with OVA sensitization. A significant increase of virus replication was found in lungs of RSV-infected sensitized mice. The increment of RSV titer was associated with the decreased levels of type I IFN. Although Toll-like receptor 3 (TLR3) expression was significantly increased in the lungs, the key signal transcriptor, IFN regulatory factor 3, was significantly suppressed in the RSV-infected sensitized mice. Conclusion A defective antiviral innate response was observed in the murine respiratory allergy model. Suppressed expression of IFN signal transcriptor contributes to decreased production of type I IFN. The defective innate immune response might result in acute viral exacerbations of allergic airway diseases.",
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N2 - Background/Purpose Respiratory viral infections have frequently been reported to closely correlate with asthma exacerbations. Distinctive expression of cytokine/chemokine and anomalous responses of innate immunity induced by respiratory viral infections were suggested to play a key role. This study further evaluates the effects of airway sensitization on innate immunity in response to different viruses. Methods Murine sensitization was established using an ovalbumin (OVA) sensitization model. Mice were subsequently infected with either respiratory syncytial virus (RSV) or human metapneumovirus (hMPV). Type I interferon (IFN), cytokines, and chemokines were measured in bronchoalveolar lavage (BAL) fluid. Pulmonary tissue samples were collected for the analysis of viral titers and type I IFN signal transcriptors. Results Distinct expressions of cytokine/chemokine responses after viral infection were also found in mice with OVA sensitization. A significant increase of virus replication was found in lungs of RSV-infected sensitized mice. The increment of RSV titer was associated with the decreased levels of type I IFN. Although Toll-like receptor 3 (TLR3) expression was significantly increased in the lungs, the key signal transcriptor, IFN regulatory factor 3, was significantly suppressed in the RSV-infected sensitized mice. Conclusion A defective antiviral innate response was observed in the murine respiratory allergy model. Suppressed expression of IFN signal transcriptor contributes to decreased production of type I IFN. The defective innate immune response might result in acute viral exacerbations of allergic airway diseases.

AB - Background/Purpose Respiratory viral infections have frequently been reported to closely correlate with asthma exacerbations. Distinctive expression of cytokine/chemokine and anomalous responses of innate immunity induced by respiratory viral infections were suggested to play a key role. This study further evaluates the effects of airway sensitization on innate immunity in response to different viruses. Methods Murine sensitization was established using an ovalbumin (OVA) sensitization model. Mice were subsequently infected with either respiratory syncytial virus (RSV) or human metapneumovirus (hMPV). Type I interferon (IFN), cytokines, and chemokines were measured in bronchoalveolar lavage (BAL) fluid. Pulmonary tissue samples were collected for the analysis of viral titers and type I IFN signal transcriptors. Results Distinct expressions of cytokine/chemokine responses after viral infection were also found in mice with OVA sensitization. A significant increase of virus replication was found in lungs of RSV-infected sensitized mice. The increment of RSV titer was associated with the decreased levels of type I IFN. Although Toll-like receptor 3 (TLR3) expression was significantly increased in the lungs, the key signal transcriptor, IFN regulatory factor 3, was significantly suppressed in the RSV-infected sensitized mice. Conclusion A defective antiviral innate response was observed in the murine respiratory allergy model. Suppressed expression of IFN signal transcriptor contributes to decreased production of type I IFN. The defective innate immune response might result in acute viral exacerbations of allergic airway diseases.

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