The manuscript “In ovo very early-in-life exposure to diesel exhaust induced cardiopulmonary toxicity in a hatchling chick model” had been published on international scientific journal Environmental Pollution (Impact factor 5.714) by Dr. Qixiao Jiang (Ph.D., associate professor) and Dr. Yuxin Zheng (Ph.D., professor) from School of Public Health. In the manuscript, it had been discovered that
1. Chicken embryo may serve as an ideal model for diesel exhaust very early-in-life inhalation toxicity model
2. Persistent cardiopulmonary toxicities in hatchling chickens were observed following diesel exhaust very early-in-life inhalation exposure.
3. AhR/TGFβ1/MAPK signaling are associated with observed effects.
A novel inhalation model had been established, based on the unique characteristic of chicken embryo development, during which air inside the air-cell will be firstly inhaled when internal piping occured. With this model, the very early-in-life exposure towards “first breath in life” was achieved. Subsequent observations at 0-, 1-, and 2-weeks post hatch revealed persistent elevation of heart rate, thickening of right ventricular wall, enhanced expression of alpha-actin in pulmonary arterial wall and decreased cavity/vascular ratio, suggesting presence of cardiopulmonary toxicities. On the other hand, while no fibrosis were observed in 0-week animal myocardium or lung tissues, remarkable fibrotic changes were observed in both myocardium and lung tissues starting from 1-week post hatch and became more prominent at 2-week post hatch, suggesting that delayed fibrosis may be one of the toxicological endpoints following very early-in-life diesel exhaust exposure. Further mechanistic studies revealed that the classical AhR signaling was activated remarkably at 0-week time point but recovered over time. TGFβ1 signaling was also activated at 0-week and recovered by 1-week, but a suppression was observed at 2-week time point. Meanwhile, no significant changes were observed in MAPK signaling at 0- or 1-week, but elevated activation was observed at 2-week. These results suggested that different signaling molecules participated in different time points in the observed cardiopulmonary toxicities. This work indicated that neonatal exposure to diesel exhaust may affect cardiopulmonary health during childhood or even adulthood, thus provided evidence for better protection for human developmental cardiopulmonary health.
Dr. Qixiao Jiang is the first author of this manuscript and Dr. Yuxin Zheng is the corresponding author. This work is supported by National Natural Science Foundation of China (Grant No. 91643203, 91543208, 81872591).
2020年5月3日，国际学术期刊Environmental Pollution (影响因子：5.714) 在线发表了亚搏登录姜启晓副教授与郑玉新教授题为“In ovo very early-in-life exposure to diesel exhaust induced cardiopulmonary toxicity in a hatchling chick model”的研究论文。该研究发现：