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

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.

• Publication year

  2017

• Venue

  Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi

• Publication date

  2017-02-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/j.jmii.2014.09.001PMID 25708602
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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