Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 1.736
5-Year Impact Factor – 2.135
Index Copernicus  – 168.52
MEiN – 70 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

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Advances in Clinical and Experimental Medicine

2020, vol. 29, nr 7, July, p. 825–832

doi: 10.17219/acem/121009

Publication type: original article

Language: English

License: Creative Commons Attribution 3.0 Unported (CC BY 3.0)

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

Yonghui Yang1,A,B,C, Xiaoxia Li1,B,C, Xiaoying An2,B,C,D, Ling Zhang3,B,C, Xingbin Li3,B,C, Liang Wang3,B,C, Guiyun Zhu1,D,E,F

1 Department of Pathology, Hebei Province Chest Hospital, Lung Cancer Prevention and Control Center of Hebei Province, Shijiazhuang, China

2 Laboratory of Molecular Biology, Hebei Province Chest Hospital, Lung Cancer Prevention and Control Center of Hebei Province, Shijiazhuang, China

3 Department of Pneumology, Hebei Province Chest Hospital, Lung Cancer Prevention and Control Center of Hebei Province, Shijiazhuang, China

Abstract

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

Key words

inflammation, asthma, PM2.5, JAK-STAT6 pathway

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