Interleukin-17 enhances the removal of respiratory syncytial virus in mice by promoting neutrophil migration and reducing interferon-gamma expression

Genet Mol Res. 2016 Mar 24;15(1). doi: 10.4238/gmr.15017002.

Abstract

The aim of this study was to observe the effect of interleukin (IL)-17 on early immune response and inflammation in the lungs of respiratory syncytial virus (RSV)-infected mice. Specific pathogen-free BALB/c mice were randomly assigned to control, RSV-infected, RSV-infected with phosphate-buffered saline, and RSV-infected + IL-17 intervention groups. The RSV infection model was set up by nasal mucosa immunization. The intervention group was provided with restructured IL-17 (intranasal). The viral load and cytokine concentrations in the lung tissues and broncho-alveolar lavage fluid (BALF) were determined by real-time-polymerase chain reaction and enzyme-linked immunosorbent assay. RSV caused acute lung inflammation in mice with a significantly higher number of neutrophils and cytokines such as interferon-gamma (IFN-γ), IL-1β, IL-6, and G-CSF in the BALF than that in the control group. IL-17 intervention led to a significant increase in the number of neutrophilic granulocytes in the BALF. Alternately, IL-17 intervention led to a significant decrease in the IFN-γ concentration and a significant increase in the IL-1β, IL-6 and G-CSF levels in the BALF. IL-17 induced a reduction in the viral load and an increase in the survival rate of mice on the third day of infection. IL- 17 mucosal immunity enhances the removal of RSV and strengthens the immune defense by promoting neutrophil migration and reducing the IFN-γ levels in mouse lungs.

MeSH terms

  • Animals
  • Granulocyte Colony-Stimulating Factor / metabolism
  • Interferon-gamma / metabolism*
  • Interleukin-17 / therapeutic use*
  • Interleukin-6 / metabolism
  • Lung / virology
  • Male
  • Mice
  • Mice, Inbred ICR
  • Neutrophils / cytology*
  • Neutrophils / drug effects*
  • Neutrophils / metabolism
  • Respiratory Syncytial Virus Infections / drug therapy*
  • Respiratory Syncytial Virus Infections / metabolism
  • Respiratory Syncytial Viruses / drug effects*
  • Respiratory Syncytial Viruses / pathogenicity*

Substances

  • Interleukin-17
  • Interleukin-6
  • Granulocyte Colony-Stimulating Factor
  • Interferon-gamma