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Diesel Exhaust Exposure Increases Susceptibility to Influenza Infection and Induces Dendritic Cell Migration and Maturation.
Citation:
GOWDY, K., R. Wilson, W. ZHU, Q. T. KRANTZ, W. P. LINAK, AND M. I. GILMOUR. Diesel Exhaust Exposure Increases Susceptibility to Influenza Infection and Induces Dendritic Cell Migration and Maturation. . Presented at American Thoracic Society 2008 International Conference, Toronto, ON, CANADA, May 16 - 21, 2008.
Impact/Purpose:
Numerous studies have shown that diesel exhaust (DE) decreases resistance to respiratory infection and can alter the maturation and migration of dendritic cells (DCs). The purpose of this study was to evaluate the effects of DE exposure on susceptibilty to influenza infection in mice and to determine if this correlated with changes in the pulmonary DC populations. BALB/c mice were exposed to air or 0.5 mg/m3 DE from a diesel-powered generator (4 hrs/day, 5 days) and after the final diesel exposure, were intra-nasally instilled with 10-3 LD50 of influenza A/PR/8/34 virus.
Description:
Mice were necropsied at day 1, 4, 8 and 14 post-infection and lung tissue was assessed for virus titers by TCID50, lung injury and inflammation. Lung and lymph node DC populations (CD11c+, MHCII, CD45+, CD80+ and CD86+) were identified by flow cytometry. Prior exposure to DE significantly increased viral titers in the lung at 4 and 8 days post infection in association with increased neutrophil influx and lung injury. Pro-inflammatory cytokines including IP-10, MCP-1, GM-CSF, and IL-1β, and the antiviral cytokine IFN-β were also increased at days 1, 4 and 8 post infection compared to air/flu controls. The number of DCs in the lung was not affected with previous exposure to DE, however the lymph nodes had increased number of mature DCs at 1, 4, and 8 days post infection compared to the air/flu controls. We conclude that exposure to DE prior to an influenza infection increases pulmonary inflammation, viral titers, and stimulates more DCs to migrate to the lymph nodes and mature as a consequence of the DE-enhanced influenza infection.