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DECREASED PRODUCTION OF SURFACTANT PROTEINS AFTER DIESEL EXHAUST EXPOSURE INCREASES SUSCEPTIBILITY TO INFLUENZA INFECTION
Citation:
GOWDY, K., J. CIENCEWICKI, I. JASPERS, M. IAN I. GILMOUR, AND E. BOYKIN. DECREASED PRODUCTION OF SURFACTANT PROTEINS AFTER DIESEL EXHAUST EXPOSURE INCREASES SUSCEPTIBILITY TO INFLUENZA INFECTION . Presented at American Thoracic Society Annual Meeting, San Diego, CA, May 19 - 24, 2006.
Description:
Pulmonary surfactant proteins A and D (SP-A and SP-D), termed collectins, enhance the opsonization of foreign particles and pathogens by phagocytic cells. Inhaled pollutants such as diesel exhaust (DE) have a possible role in suppressing the production of surfactant proteins which could increase susceptibility to respiratory infections. The purpose of this study was to evaluate various levels of DE exposure on the production of SP-A and SP-D and if it increases the severity of an influenza infection in vivo. BALB/c mice were exposed to air, 0.5 or 2 mg/m3 of DE for 5 days. One hour after the final exposure, mice were intratracheally instilled with 10 HA units of influenza A/Bangkok/1/79 virus. 18 and 96 hours post infection (p.i.) mice were sacrificed and BAL fluid was collected. SP-D, SP-A mRNA, and HA RNA, a marker of viral levels, were determined by real-time PCR in the lung tissue. Lung injury was assessed by the production of LDH, microalbumin, and protein in the BAL. Th1 cytokine mRNA production was assessed in the local lymph nodes. Exposure to 0.5 mg/m3 DE decreased the production of SP-D and SP-A 18 hours p.i. in the influenza and control exposed animals. This correlated with increased influenza-induced lung injury, as indicated by enhanced levels of protein, LDH and viral HA RNA, and greater IFN-¿ mRNA in the lymph nodes, suggestive of greater viral proliferation and by 96 hours p.i. this trend was no longer significant. The decrease of surfactant protein production was not seen in the 2.0 mg/m3 exposed groups. We conclude that mice exposed to moderate levels of DE (0.5 mg/m3) have a reduced expression of surfactant protein in the lung which could result in decreased viral clearance and increased viral induced lung injury. (Funded by EPA CT829470. This abstract does not reflect EPA policy).