Exacerbation of allergic inflammation in mice exposed to diesel exhaust particles prior to viral infection

• Main Authors: Chason Kelly D, Brighton Luisa E, Zhang Wenli, Sheridan Patricia A, Jaspers Ilona, Hua Xiaoyang, Tilley Stephen L
• Format: Article
• Language: English
• Published: BMC 2009-08-01
• Series: Particle and Fibre Toxicology
• Online Access: http://www.particleandfibretoxicology.com/content/6/1/22

<p>Abstract</p> <p>Background</p> <p>Viral infections and exposure to oxidant air pollutants are two of the most important inducers of asthma exacerbation. Our previous studies have demonstrated that exposure to diesel exhaust increases the susceptibility to influenza virus infections both in epithelial cells <it>in vitro </it>and in mice <it>in vivo</it>. 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 of asthma. Ovalbumin-sensitized (OVA) male C57BL/6 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 post-infection and analyzed for markers of lung injury, allergic inflammation, and pro-inflammatory cytokine production.</p> <p>Results</p> <p>Exposure to DEP or infection with influenza alone had no significant effects on markers of injury or allergic inflammation. However, OVA-sensitized mice that were exposed to DEP and subsequently infected with influenza showed increased levels of eosinophils in lung lavage and tissue. In addition Th2-type cytokines, such as IL-4 and IL-13, and markers of eosinophil chemotaxis, such as CCL11 and CCR3, were increased in OVA-sensitized mice exposed to DEP prior to infection with influenza. These mice also showed increased levels of IL-1α, but not IL-10, RANTES, and MCP-1 in lung homogenates.</p> <p>Conclusion</p> <p>These data suggest that in the setting of allergic asthma, exposure to diesel exhaust could enhance virus-induced exacerbation of allergic inflammation.</p>