Abstract
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. To investigate the effect of continuous PM2.5 treatment on asthma regulation mechanism behind this effect. 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. 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. Our findings reveal that continuous exposure of PM2.5 exacerbates OVA-induced asthma in mouse lung through JAK-STAT6 signaling pathway.
Highlights
A combination of enormous population growth, rapid urbanization and industrialization in China has led to a massive increase of air pollution, a phenomenon previously observed in developed countries.[1–3] A detrimental effect from increased air pollution is that the general population is exposed to harmful air pollutants containing particulate matter (PM)
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)
Our findings reveal that continuous exposure of PM2.5 exacerbates OVA-induced asthma in mouse lung through JAK-STAT6 signaling pathway
Summary
A combination of enormous population growth, rapid urbanization and industrialization in China has led to a massive increase of air pollution, a phenomenon previously observed in developed countries.[1–3] A detrimental effect from increased air pollution is that the general population is exposed to harmful air pollutants containing particulate matter (PM). Depending on the city where the pollutant is collected, PM can contain varying amounts of fossil fuel combustion remains, such as polycyclic aromatic hydrocarbons, sulfates (SO42−), nitrates (NO3−), microbial material, and chemical elements such as iron, zinc, silica, sodium, and aluminium.[4–6]. These PMs can remain in the atmosphere for a lengthy amount of time, transverse great distances and trigger lung disease.[7]. 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
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