Microglial activation and inflammation caused by traffic-related particulate matter

Kuan-Jen Bai; Kai-Jen Chuang; Chia-Ling Chen; Ming-Kai Jhan; Ta-Chih Hsiao; Tsun-Jen Cheng; Li-Te Chang; Ta-Yuan Chang; Hsiao-Chi Chuang

doi:10.1016/j.cbi.2019.108762

Microglial activation and inflammation caused by traffic-related particulate matter

Chem Biol Interact. 2019 Sep 25:311:108762. doi: 10.1016/j.cbi.2019.108762. Epub 2019 Jul 23.

Authors

Kuan-Jen Bai¹, Kai-Jen Chuang², Chia-Ling Chen³, Ming-Kai Jhan⁴, Ta-Chih Hsiao⁵, Tsun-Jen Cheng⁶, Li-Te Chang⁷, Ta-Yuan Chang⁸, Hsiao-Chi Chuang⁹

Affiliations

¹ School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan; Division of Pulmonary Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
² School of Public Health, College of Public Health, Taipei Medical University, Taipei, Taiwan; Department of Public Health, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
³ School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan.
⁴ Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan; Department of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
⁵ Graduate Institute of Environmental Engineering, National Taiwan University, Taipei, Taiwan.
⁶ Institute of Occupational Medicine and Industrial Hygiene, College of Public Health, National Taiwan University, Taipei, Taiwan.
⁷ Department of Environmental Engineering and Science, Feng Chia University, Taichung, Taiwan.
⁸ Department of Occupational Safety and Health, College of Public Health, China Medical University, Taichung, Taiwan.
⁹ School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan; Cell Physiology and Molecular Image Research Center, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan; Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan. Electronic address: r92841005@ntu.edu.tw.

PMID: 31348917
DOI: 10.1016/j.cbi.2019.108762

Abstract

Neurotoxicity caused by particulate matter (PM) has been highlighted as being a potential risk factor for neurodegenerative diseases. However, the effects of brain inflammation in response to traffic-related PM remain unclear. The objective of this study was to investigate the effects of traffic-related PM on microglial responses. We determined the cytotoxicity, oxidative stress, lipid peroxidation, inflammation, activation, autophagy, and apoptosis due to exposure to carbon black (CB) and diesel exhaust particles (DEPs) in Bv2 microglial cells. Additionally, cells were pretreated with corticosteroid to determine alterations in microglial activation and inflammation. For in vivo confirmation, Sprague Dawley (SD) rats were whole-body exposed to traffic-related PM₁ (PM with an aerodynamic diameter of <1 μm) for 3 and 6 months. We observed that a decrease in cell viability and increases in dichlorodihydrofluorescein (DCFH), lactate dehydrogenase (LDH), and thiobarbituric acid-reactive substances (TBARSs) occurred due to CB and DEP. Production of interleukin (IL)-6 and soluble tumor necrosis factor (TNF)-α was significantly stimulated by CB and DEP, whereas production of cellular TNF-α was significantly stimulated by CB. Iba1 and prostaglandin E2 (PGE2) significantly increased due to CB and DEP. Consistently, we observed significant increases in Iba1 in the hippocampus of rats after 3 and 6 months of exposure to traffic-related PM₁. We found that the light chain 3II (LC3II)/LC3I ratio and caspase-3 activity increased due to CB and DEP exposure. Subsequently, LDH, TBARS, LC3II/I, and caspase-3 activities did not clearly respond to corticosteroid pretreatment followed by DEP exposure in BV2 cells. Results of the present study suggested that traffic-related PM induced cytotoxicity, lipid peroxidation, microglial activation, and inflammation as well as autophagy and caspase-3 regulation in microglia. We demonstrated that microglial activation and inflammation may play important roles in the response of the brain to traffic-related PM.

Keywords: Air pollution; Autophagy; Lipid peroxidation; Neurotoxicity; Particulate matter.

MeSH terms

Animals
Autophagy / drug effects
Brain / pathology
Calcium-Binding Proteins / analysis
Cell Line
Cell Survival / drug effects
Dinoprostone / analysis
Inflammation / etiology*
Interleukin-6 / metabolism
L-Lactate Dehydrogenase / metabolism
Male
Microfilament Proteins / analysis
Microglia / drug effects*
Microglia / metabolism
Microtubule-Associated Proteins / metabolism
Oxidative Stress / drug effects
Particulate Matter / toxicity*
Rats
Rats, Sprague-Dawley
Tumor Necrosis Factor-alpha / metabolism
Up-Regulation / drug effects
Vehicle Emissions / toxicity

Substances

Aif1 protein, rat
Calcium-Binding Proteins
Interleukin-6
LC3 protein, rat
Microfilament Proteins
Microtubule-Associated Proteins
Particulate Matter
Tumor Necrosis Factor-alpha
Vehicle Emissions
L-Lactate Dehydrogenase
Dinoprostone