You are here:
Exacerbation of allergic inflammation in mice exposed to diesel exhaust particles prior to viral infection.
Citation:
JASPERS, I., P. A. Sheridan, W. ZHANG, L. BRIGHTON, C. D. Kelly, X. Hua, AND S. Tilley. Exacerbation of allergic inflammation in mice exposed to diesel exhaust particles prior to viral infection. Particle and Fibre Toxicology. BioMed Central Ltd, London, Uk, 14:16-22, (2009).
Impact/Purpose:
These data demonstrate that exposure to diesel exhaust particles enhance virus-induced exacerbation of allergic inflammation
Description:
Background: Viral infections and exposure to oxidant air pollutants are two ofthe most important inducers ofasthma exacerbation. Our previous studies have demonstrated that exposure to diesel exhaust increases the susceptibility to influenza virus infections both in epithelial cells in vitro and in mice in vivo. Therefore, we examined whether in the setting of allergic asthma, exposure to oxidant air pollutants enhances the susceptibility to respiratory virus infections, which in turn leads to increased virus-induced exacerbation ofasthma. Ovalbuminsensitized (OVA) male C57BLl6 mice were instilled with diesel exhaust particles (DEP) or saline and 24 hours later infected with influenza A/PR/8. Animals were sacrificed 24 hours postinfection and analyzed for markers oflung injury, allergic inflammation, and pro-inflammatory cytokine production. Results: Exposure to DEP or infection with influenza alone had no significant effects on markers ofinjury or allergic inflammation. However, OVA-sensitized mice that were exposed to DEP and subsequently infected with influenza showed increased levels ofeosinophils in lung lavage and tissue. In addition Th2-type cytokines, such as IL-4 and IL-13, and markers ofeosinophil chemotaxis, such as CCLII and CCR3, were increased in OVA-sensitized mice exposed to DEP prior to infection with influenza. These mice also showed increased levels ofIL-Ia, but not IL10, RANTES, and MCP-I in lung homogenates. Conclusions: These data suggest that in the setting ofallergic asthma, exposure to diesel exhaust could enhance virus-induced exacerbation ofallergic inflammation.
