Continuous exposure of PM2.5 exacerbates ovalbumin-induced asthma in mouse lung via a JAK-STAT6 signaling pathway.

BACKGROUND

Epidemiological studies and mice models have demonstrated that air pollution containing particulate matter smaller than 2.5 μm (PM2.5) exacerbates acute episodes of asthma in both children and adults.

OBJECTIVES

To investigate the effect of continuous PM2.5 treatment on asthma regulation mechanism behind this effect.

MATERIAL AND METHODS

In this study, the effects of continuous exposure to PM2.5 on asthma and eosinophil recruitment was compared to the effect of a single pre-ovalbumin (OVA)-sensitization exposure to PM2.5. Wild-type mice were either challenged once with PM2.5 + OVA before sensitization and asthma induction over a 27-day period, or with 5 times of PM2.5 + OVA treatment and sensitization/asthma induction over the same period.

RESULTS

Continuous exposure to PM2.5 significantly increased total plasma immunoglobulin E (IgE), bronchial alveolar lavage fluid (BALF) cell numbers, eosinophils, and macrophages, leading to increased lung injury. This effect was regulated through increased production of chemokines and cytokines, such as interleukin (IL)-1β, monocyte chemoattractant protein 1 (MCP-1), IL-12, IL-5, IL-13, and prostaglandin D2 (PGD2). Eosinophil recruitment during continuous PM2.5 treatment was regulated through phosphorylation of the JAK/STAT6 pathway. As this study shows, continuous PM2.5 treatment significantly worsens asthma as compared to single exposure to PM2.5 or OVA exposure alone.

CONCLUSIONS

Our findings reveal that continuous exposure of PM2.5 exacerbates OVA-induced asthma in mouse lung through JAK-STAT6 signaling pathway.