Acute diesel exhaust particle exposure increases viral titre and inflammation associated with existing influenza infection, but does not exacerbate deficits in lung function.

BACKGROUND

Exposure to diesel exhaust particles (DEP) is thought to exacerbate many pre-existing respiratory diseases, including asthma, bronchitis and chronic obstructive pulmonary disease, however, there is a paucity of data on whether DEP exacerbates illness due to respiratory viral infection.

OBJECTIVES

To assess the physiological consequences of an acute DEP exposure during the peak of influenza-induced illness.

METHODS

We exposed adult female BALB/c mice to 100 μg DEP (or control) 3.75 days after infection with 10(4.5) plaque forming units of influenza A/Mem71 (or control). Six hours, 24 hours and 7 days after DEP exposure we measured thoracic gas volume and lung function at functional residual capacity. Bronchoalveolar lavage fluid was taken for analyses of cellular inflammation and cytokines, and whole lungs were taken for measurement of viral titre.

RESULTS

Influenza infection resulted in significantly increased inflammation, cytokine influx and impairment to lung function. DEP exposure alone resulted in less inflammation and cytokine influx, and no impairment to lung function. Mice infected with influenza and exposed to DEP had higher viral titres and neutrophilia compared with infected mice, yet they did not have more impaired lung mechanics than mice infected with influenza alone.

CONCLUSIONS

A single dose of DEP is not sufficient to physiologically exacerbate pre-existing respiratory disease caused by influenza infection in mice.