Exploring the impact of ambient air PM2.5 on multiple sclerosis: an experimental dive into neuroinflammation

There is mounting evidence about the connection between particulate matter (PM) and neuroinflammation. This study aimed to evaluate the toxicological effects of PM2.5 associated with inflammatory factors in a mouse's multiple sclerosis (MS) model. Thirty C57BL/6 male mice were categorized into five groups: a group of healthy mice, a control cuprizone-induced MS group, and three MS-induced groups, intranasally exposed to three concentrations of ambient air PM2.5 (5, 10, and 20 mg/mL) from Tehran in a phosphate-buffered saline (PBS) solution. All mice were investigated by motor function, molecular, and histopathological assays. Moreover, the chemical content of the collected PM2.5 was assessed and reported. The cumulative exposure doses were equal to 0.025, 0.05, and 0.1 mg per gram of body weight of mice, which were approximately 3.52, 7.04, and 14.08 times higher than the human daily dose in Tehran. The PM2.5-exposed groups showed a high inflammatory response characterized by a significant increase in the mRNA expression of tumor necrosis alpha (TNF-alpha), NLRP3, and interleukin 18 (IL-18). In addition, the PM2.5-exposed groups exhibited a notably lower velocity level, total traveled distance (TD), and duration traveled in the central zone (DC) than the control group. The histopathological assays revealed significant pathological alterations and demyelination in the PM2.5-exposed groups compared to the control group. Identifying the risks and reducing the likelihood of exposure through preventive measures and regulations can result in financial savings and improve the quality of life for MS patients.