Immunological Effects of Diesel Particles in a Murine Model of Healthy Mice.

Exposure to environmental pollutants such as diesel exhaust particles (DEP) increases the risk of respiratory disease exacerbation. However, the possible effects of these particles on the general population remain poorly understood. The present study aimed to assess the immunomodulatory and inflammatory effects of the inhalation of DEP in a model of healthy mice undergoing short-, mid- and long-term exposure. BALB/c ByJ mice were randomly divided into five experimental groups. The control group received three intranasal instillations of saline over 8 days while the other four groups received intranasal instillations of 150 µg of DEP 3 days per week for 8, 17, 26, and 53 days. Lung function assessment and flow cytometry were performed. In lung tissue, intranasal exposure to DEP decreased total monocytes ( < 0.015 in all groups). At 26 days, a reduction in inflammatory monocytes and an increase in resident monocytes were observed, = 0.001 and 0.0001, respectively. Eosinophils and neutrophils decreased at 26 days ( = 0.017 and = 0.041, respectively). The intranasal challenges of DEP increased the total population of dendritic cells (DC) at 26 and 53 days ( = 0.017 and = 0.022, respectively) and decreased the total and alveolar populations of macrophages ( < 0.003 for all groups compared to control), while interstitial macrophage populations increased over the time period ( = 0.0001 for all groups compared to control). Continuous DEP exposure triggers immune mechanisms that predispose healthy individuals to a pro-inflammatory and hyper-reactive microenvironment. This mouse model provides evidence of the capacity of DEP to increase DC, interstitial macrophages, and resident monocytes.