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DIESEL EXHAUST EXPOSURE INCREASES SEVERITY OF AN ONGOING INFLUENZA INFECTION
Citation:
GOWDY, K., J. CIENCEWICKI, I. JASPERS, Q. T. KRANTZ, E. BOYKIN, W. P. LINAK, AND M I. GILMOUR. DIESEL EXHAUST EXPOSURE INCREASES SEVERITY OF AN ONGOING INFLUENZA INFECTION. Presented at Keystone Symposium "Viral Immunity", Keystone, CO, January 20 - 25, 2008.
Impact/Purpose:
The purpose of this study was to evaluate the effects of DE exposure on the severity of an ongoing influenza infection in mice.
Description:
Numerous studies have shown that air pollutants including diesel exhaust (DE) alter host defense responses, resulting in decreased resistance to respiratory infection. The purpose of this study was to evaluate the effects of DE exposure on the severity of an ongoing influenza infection in mice. BALB/c mice were intra-tracheally instilled with 50 plaque forming units (PFUs) of influenza A/HongKong/8/68 and immediately exposed to air or 0.5 mg/m3 DE for 4 hrs/day, 14 days. Mice were necropsied at days 1, 4, 8 and 14 post-infection and lung tissue was assessed for virus titers by TCID50 and mRNA expression of antiviral cytokines. Lung injury was measured by differential cell counts and levels of LDH, microalbumin, and protein in bronchoalveolar lavage fluid (BALF). Inflammatory cytokines and chemokines were assessed in the BALF by immunoassay. Exposure to 0.5 mg/m3 DE during the course of infection caused an increase in viral titers at days 4 and 8 post-infection which was associated with a significant decrease in lymphocyte counts in the BALF. Production of RANTES, MIP-2, and GM-CSF were also significantly decreased in mice exposed to DE. Increase of virus load was not caused by decreased interferon production, since IFN-β levels were enhanced in these mice. We conclude that exposure to moderate levels of DE (0.5 mg/m3) during an influenza infection suppresses lymphocyte recruitment which could be responsible for delayed clearance of virus. (Funded by EPA CT829470. This abstract does not reflect EPA policy).