Both cold stress and ambient fine particle particulate matter (PM2.5) has been reported to aggravate and induce respiratory problems like asthma, but the mechanism involved in that has not been fully understood. Therefore, the present study is to explore the mechanism involved in the increased susceptibility and severity of asthma caused by cold stress and PM2.5 exposure. Urban PM2.5 of Shanghai was concentrated to simulate a PM2.5‐polluted environment with an average concentration of 400 μg/m3, where 1‐month young C57BL/6J mice were exposed for 2 months under cold stress (2°C). Co‐exposure of cold stress and PM2.5 in childhood of mice led to significant infiltration of inflammatory cells in the peribronchial region or airspaces and the thickening or fibrosis of alveolar septum, increased OVA‐specific IgE in serum and total cells, eosinophil cells, and the levels of inflammatory cytokines including IL‐4, IL‐8, IL‐1β, IL‐5, IL‐13, and IFN‐γ in bronchoalveolar lavage fluid (BALF) of asthma mice. Moreover, mice in co‐exposure group presented a significantly high cough feature, reduced catalase (CAT), glutathione (GSH), superoxide dismutase (SOD), and elevated malonaldehyde (MDA) elevated in BALF; increased ratio of Th2/Th1 and the markable inhibition of Th17 differentiation toward Treg cells in the adulthood of asthma mice. Cold stress and PM2.5 co‐exposure in childhood may promote the deterioration of asthma symptoms in adulthood of mice by increasing inflammatory cytokines, ROS formation, Th2/Th1 imbalance, and suppressing the differentiation of Th17 toward Treg cells, which will help to provide experimental references when making some therapeutic strategies in allergic diseases through focusing on some natural solutions.

中文翻译：

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儿童期冷应激和 PM 2.5 共同暴露会加重小鼠成年期哮喘的易感性和严重性

据报道，冷应激和环境细颗粒物 (PM2.5) 都会加重和诱发哮喘等呼吸系统问题，但其中所涉及的机制尚未完全清楚。因此，本研究旨在探讨冷应激和 PM2.5 暴露导致哮喘易感性和严重程度增加的机制。上海城市 PM2.5 集中模拟平均浓度为 400 μg/m3 的 PM2.5 污染环境，其中 1 个月的幼龄 C57BL/6J 小鼠在冷应激（2°C）下暴露 2 个月。小鼠儿童期冷应激和 PM2.5 共同暴露导致支气管周围区域或气隙炎症细胞显着浸润，肺泡间隔增厚或纤维化，血清和总细胞、嗜酸性粒细胞中 OVA 特异性 IgE 升高，以及哮喘小鼠支气管肺泡灌洗液（BALF）中炎症细胞因子包括IL-4、IL-8、IL-1β、IL-5、IL-13和IFN-γ的水平。此外，共暴露组小鼠表现出明显的高咳嗽特征，过氧化氢酶（CAT）、谷胱甘肽（GSH）、超氧化物歧化酶（SOD）和BALF升高的丙二醛（MDA）升高；哮喘小鼠成年期 Th2/Th1 比值增加和 Th17 向 Treg 细胞分化的显着抑制。儿童期冷应激和 PM2.5 共同暴露可能通过增加炎性细胞因子、ROS 形成、Th2/Th1 失衡和抑制 Th17 向 Treg 细胞分化来促进小鼠成年期哮喘症状的恶化，