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An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
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Surfactant protein C-deficient mice are susceptible to respiratory syncytial virus infection

Stephan W Glasser1, Teah L Witt, Albert P Senft

  • 1Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039, USA. steve.glasser@cchmc.org

American Journal of Physiology. Lung Cellular and Molecular Physiology
|March 24, 2009
PubMed

Insights

Pulmonary surfactant protein C (SP-C) deficiency worsens respiratory syncytial virus (RSV) lung inflammation by increasing Toll-like receptor 3 (TLR3) signaling. This leads to more severe lung damage and slower recovery in SP-C deficient mice.

Area of Science:

  • Pulmonary medicine
  • Immunology
  • Genetics

Background:

  • Mutations in the pulmonary surfactant protein C (SP-C) gene are linked to interstitial lung disease and severe respiratory infections.
  • Respiratory syncytial virus (RSV) infections can cause significant pulmonary complications in individuals with SP-C gene mutations.

Purpose of the Study:

  • To investigate the impact of SP-C deficiency on the severity and resolution of RSV-induced lung inflammation.
  • To explore the role of Toll-like receptor 3 (TLR3) signaling in SP-C deficient mice during RSV infection.

Main Methods:

  • Comparison of RSV-induced lung pathology in SP-C deficient (Sftpc(-/-)) and wild-type (Sftpc(+/+)) mice.
  • Analysis of bronchoalveolar lavage (BAL) fluid for inflammatory cell counts and viral loads.
  • Measurement of viral F and G protein mRNA and Toll-like receptor 3 (TLR3) mRNA expression in lung tissue.
  • In vitro experiments assessing the effect of SP-C on poly(I:C)-induced TLR3 signaling.

Main Results:

  • SP-C deficient mice exhibited more severe interstitial thickening, air space consolidation, and goblet cell hyperplasia after RSV infection.
  • RSV-induced lung pathology resolved more slowly in SP-C deficient mice, with persistent inflammation.
  • Increased viral titers and viral F and G protein mRNA were observed in SP-C deficient and heterozygous mice.
  • Upregulated TLR3 mRNA expression and heightened inflammatory cell response to TLR3 ligand were noted in SP-C deficient mice.
  • Purified SP-C and synthetic phospholipids inhibited poly(I:C)-induced TLR3 signaling in vitro.

Conclusions:

  • SP-C deficiency exacerbates RSV-induced pulmonary inflammation and pathology.
  • The mechanism involves the dysregulation of TLR3 signaling pathways.
  • SP-C plays a protective role in modulating the innate immune response to viral lung infections.

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