Pulmonary inflammation induced by low-dose particulate matter exposure in mice | |
Chan, Yik Lung1,2; Wang, Baoming1,2; Chen, Hui1; Ho, Kin Fai3; Cao, Junji4; Hai, Guo5; Jalaludin, Bin6; Herbert, Cristan7,8; Thomas, Paul S.7,8; Saad, Sonia9; Oliver, Brian Gregory George1,2 | |
通讯作者 | Chan, Yik Lung(Yik.chan@uts.edu.au) |
2019-09-01 | |
发表期刊 | AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY |
ISSN | 1040-0605 |
卷号 | 317期号:3页码:L424-L430 |
摘要 | Air pollution is a ubiquitous problem and comprises gaseous and particulate matter (PM). Epidemiological studies have clearly shown that exposure to PM is associated with impaired lung function and the development of lung diseases, such as chronic obstructive pulmonary disease and asthma. To understand the mechanisms involved, animal models are often used. However, the majority of such models represent high levels of exposure and are not representative of the exposure levels in less polluted countries, such as Australia. Therefore, in this study, we aimed to determine whether low dose PM10 exposure has any detrimental effect on the lungs. Mice were intranasally exposed to saline or traffic-related PM10 (1 mu g or 5 mu g/day) for 3 wk. Bronchoalveolar lavage (BAL) and lung tissue were analyzed. PM10 at 1 mu g did not significantly affect inflammatory and mitochondrial markers. At 5 mu g, PM10 exposure increased lymphocytes and macrophages in BAL fluid. Increased NACHT, LRR and PYD domains-containing protein 3 (NLRP3) and IL-1 beta production occurred following PM10 exposure. PM10 (5 mu g) exposure reduced mitochondrial antioxidant manganese superoxide (antioxidant defense system) and mitochondrial fusion marker (OPA-1), while it increased fission marker (Drp-1). Autophagy marker light-chain 3 microtubule-associated protein (LC3)-II and phosphorylated-AMPK were reduced, and apoptosis marker (caspase 3) was increased. No significant change of remodeling markers was observed. In conclusion, a subchronic low-level exposure to PM can have an adverse effect on lung health, which should be taken into consideration for the planning of roads and residential buildings. |
DOI | 10.1152/ajplung.00232.2019 |
关键词[WOS] | NLRP3 INFLAMMASOME ; OXIDATIVE STRESS ; AUTOPHAGY ; PARTICLES ; RESPONSES |
收录类别 | SCI ; SCI |
语种 | 英语 |
资助项目 | SPHERE, RCG of the Hong Kong Special Administrative Region[CRF/C5004-15E] ; Strategic Focus Area scheme of The Research Institute for Sustainable Urban Development at The Hong Kong Polytechnic University[1-BBW9] ; National Natural Science Foundation of China[81750110554] ; National Health and Medical Research Council Australia[APP1110368] ; China Scholarship Council |
WOS研究方向 | Physiology ; Respiratory System |
项目资助者 | SPHERE, RCG of the Hong Kong Special Administrative Region ; Strategic Focus Area scheme of The Research Institute for Sustainable Urban Development at The Hong Kong Polytechnic University ; National Natural Science Foundation of China ; National Health and Medical Research Council Australia ; China Scholarship Council |
WOS类目 | Physiology ; Respiratory System |
WOS记录号 | WOS:000485282700011 |
出版者 | AMER PHYSIOLOGICAL SOC |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://ir.ieecas.cn/handle/361006/13476 |
专题 | 粉尘与环境研究室 |
通讯作者 | Chan, Yik Lung |
作者单位 | 1.Univ Technol Sydney, Sch Life Sci, Sydney, NSW, Australia 2.Woolcock Inst Med Res, Resp Cellular & Mol Biol, Sydney, NSW, Australia 3.Chinese Univ Hong Kong, Jockey Club Sch Publ Hlth & Primary, Hong Kong, Peoples R China 4.Chinese Acad Sci, Inst Earth Environm, Key Lab Aerosol Chem & Phys, Xian, Shaanxi, Peoples R China 5.Hong Kong Polytech Univ, Dept Civil & Environm Engn, Air Qual Studies, Hong Kong, Peoples R China 6.Univ New South Wales, Ingham Inst Appl Med Res, Sydney, NSW, Australia 7.Univ New South Wales, Fac Med, Dept Pathol, Sch Med Sci, Sydney, NSW, Australia 8.Univ New South Wales, Fac Med, Prince Wales Clin Sch, Sydney, NSW, Australia 9.Royal North Shore Hosp, Renal Grp Kolling Inst, St Leonards, NSW, Australia |
推荐引用方式 GB/T 7714 | Chan, Yik Lung,Wang, Baoming,Chen, Hui,et al. Pulmonary inflammation induced by low-dose particulate matter exposure in mice[J]. AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY,2019,317(3):L424-L430. |
APA | Chan, Yik Lung.,Wang, Baoming.,Chen, Hui.,Ho, Kin Fai.,Cao, Junji.,...&Oliver, Brian Gregory George.(2019).Pulmonary inflammation induced by low-dose particulate matter exposure in mice.AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY,317(3),L424-L430. |
MLA | Chan, Yik Lung,et al."Pulmonary inflammation induced by low-dose particulate matter exposure in mice".AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY 317.3(2019):L424-L430. |
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