Wenting Tang1, Suran Huang2, Lili Du3, Wen Sun3, Zhiqiang Yu4, Yanmei Zhou3, Jingsi Chen3, Xiuying Li3, Xiaomei Li3, Bolan Yu3, Dunjin Chen5. 1. Department of Obstetrics and Gynecology, Third Affiliated Hospital of Guangzhou Medical University, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Guangzhou, 510150, China; Department of Obstetrics and Gynecology, Dongguan People's Hospital, Dongguan, 523000 China. 2. Department of Obstetrics and Gynecology, Dongguan People's Hospital, Dongguan, 523000 China. 3. Department of Obstetrics and Gynecology, Third Affiliated Hospital of Guangzhou Medical University, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Guangzhou, 510150, China. 4. State Key Laboratory of Organic Geochemistry, Guangdong Key Laboratory of Environment and Resources, Guangzhou Institute of Geochemistry Chinese Academy of Sciences, Guangzhou, 510150 China. 5. Department of Obstetrics and Gynecology, Third Affiliated Hospital of Guangzhou Medical University, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Guangzhou, 510150, China. Electronic address: gzdrchen@gzhmu.edu.cn.
Abstract
OBJECTIVES: Maternal particulate matter with less than 2.5 μm in diameter (PM2.5) is associated with an increased risk for acute lower respiratory infections and allergic airway inflammation; however, its effect on the developing lung remains unclear. The aim of this study is to determine the effect of maternal PM2.5 during pregnancy on lung development in offspring. METHODS: Timed pregnant Sprague-Dawley rats were treated with PM2.5 (0.1, 0.5, 2.5, or 7.5 mg/kg) once every 3 days from day 0-18 of pregnancy and delivered at term. Lungs were obtained on postnatal day 0, the structure of the lung was analyzed by quantitative micro-computed tomography (CT) and the levels of proinflammatory cytokines were analyzed using enzyme-linked immunosorbent assay (ELISA). The expression of high mobility group box-1 (HMGB1) was also detected by immunohistochemistry, Western blotting, and quantitative RT-PCR. RESULTS: Ground-glass opacity and high-density volumes in CT slice images of maternal PM2.5-exposure rats were observed. The concentrations of IL-1, IL-6 and TNF-α were significantly increased by 2.36-, 3.91- and 4.36-fold, respectively, in the rats of the PM-7.5 group compared with the rats in the control group. The PM2.5-treated rats showed a significant upregulated expression of HMGB1 in lungs. CONCLUSIONS: PM2.5 exposure during pregnancy results in lung inflammation in offspring mediated by increased HMGB1 expression, followed by upregulated IL-1, IL-6 and TNF-α secretions, which may contribute to the development of inflammatory lung diseases in later life.
OBJECTIVES: Maternal particulate matter with less than 2.5 μm in diameter (PM2.5) is associated with an increased risk for acute lower respiratory infections and allergic airway inflammation; however, its effect on the developing lung remains unclear. The aim of this study is to determine the effect of maternal PM2.5 during pregnancy on lung development in offspring. METHODS: Timed pregnant Sprague-Dawley rats were treated with PM2.5 (0.1, 0.5, 2.5, or 7.5 mg/kg) once every 3 days from day 0-18 of pregnancy and delivered at term. Lungs were obtained on postnatal day 0, the structure of the lung was analyzed by quantitative micro-computed tomography (CT) and the levels of proinflammatory cytokines were analyzed using enzyme-linked immunosorbent assay (ELISA). The expression of high mobility group box-1 (HMGB1) was also detected by immunohistochemistry, Western blotting, and quantitative RT-PCR. RESULTS: Ground-glass opacity and high-density volumes in CT slice images of maternal PM2.5-exposure rats were observed. The concentrations of IL-1, IL-6 and TNF-α were significantly increased by 2.36-, 3.91- and 4.36-fold, respectively, in the rats of the PM-7.5 group compared with the rats in the control group. The PM2.5-treated rats showed a significant upregulated expression of HMGB1 in lungs. CONCLUSIONS: PM2.5 exposure during pregnancy results in lung inflammation in offspring mediated by increased HMGB1 expression, followed by upregulated IL-1, IL-6 and TNF-α secretions, which may contribute to the development of inflammatory lung diseases in later life.
Authors: Natalie M Johnson; Aline Rodrigues Hoffmann; Jonathan C Behlen; Carmen Lau; Drew Pendleton; Navada Harvey; Ross Shore; Yixin Li; Jingshu Chen; Yanan Tian; Renyi Zhang Journal: Environ Health Prev Med Date: 2021-07-12 Impact factor: 3.674
Authors: Jung-Hyun Kim; Jeeyoung Kim; Woo Jin Kim; Yung Hyun Choi; Se-Ran Yang; Seok-Ho Hong Journal: Int J Environ Res Public Health Date: 2020-11-13 Impact factor: 3.390