Inflammatory response in mouse lungs to haze episodes under different backgrounds of particulate matter exposure

被引:1
作者
Zhang, Yuanhang [1 ]
Zhang, Yuteng [1 ]
Liu, Kai [1 ]
Zhu, Ningning [2 ]
Pang, Jianfeng [2 ]
Qian, Xin [3 ]
Li, Huiming [1 ]
Liu, Xuemei [2 ]
机构
[1] Nanjing Normal Univ, Sch Environm, Nanjing, Peoples R China
[2] Huaiyin Inst Technol, Natl & Local Joint Engn Res Ctr Deep Utilizat Tech, Huaian, Peoples R China
[3] Nanjing Univ Informat Sci & Technol, Jiangsu Collaborat Innovat Ctr Atmospher Environm, Nanjing, Peoples R China
基金
中国国家自然科学基金;
关键词
AIR-POLLUTION; OXIDATIVE-STRESS; DNA-DAMAGE; HEALTH IMPACTS; EARLY-LIFE; SENESCENCE; RISK; DISEASE; PM2.5; ALZHEIMERS;
D O I
10.1038/s41598-023-49014-3
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Particulate matter (PM) toxicity has mostly been investigated through in vitro exposure or tracheal infusion in animal models. However, given the complexity of ambient conditions, most animal studies do not mimic real-life PM exposure. In this work, we established a novel integrated exposure model to study the dynamic inflammatory response and defense strategies in ambient PM-exposed mice. Three groups of male C57BL/6 mice were kept in three chambers with pre-exposure to filtered air (FA), unfiltered air (UFA), or the air with a low PM concentration (PM2.5 <= 75 mu g/m3) (LPM), respectively, for 37 days. Then all three groups of mice were exposed to haze challenge for 3 days, followed by exposure in filtered air for 7 days to allow recovery. Our results suggest that following a haze challenge, the defense strategies of mice of filtered air (FA) and low PM (LPM) groups comprised a form of "counterattack", whereas the response of the unfiltered air (UFA) group could be viewed as a "silence". While the latter strategy protected the lung tissues of mice from acute inflammatory damage, it also foreshadowed the development of chronic inflammatory diseases. These findings contribute to explaining previously documented PM-associated pathogenic mechanisms.
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页数:14
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