实验性自身免疫性脑脊髓炎
多发性硬化
FOXP3型
医学
免疫学
脑脊髓炎
烟草烟雾
被动吸烟
调节性T细胞
T细胞
病理
白细胞介素2受体
免疫系统
环境卫生
作者
Zhaowei Wang,Liping Wang,Fangfang Zhong,Chen Wu,Sheng T. Hou
标识
DOI:10.1016/j.neuint.2020.104892
摘要
Although substantial evidence supports smoking as a risk factor for the development of multiple sclerosis (MS) in adulthood, it remains controversial whether early-life exposure to environmental tobacco smoke (ETS) increases the risk of MS later in life. Here, using experimental autoimmune encephalomyelitis (EAE) as an animal model for MS, we show that exposing neonatal rats during the first week (ETS1-EAE), but not the second week (ETS2-EAE) and the third week (ETS3-EAE) after birth, increased the severity of EAE in adulthood in comparison to pups exposed to filtered compressed air (AIR-EAE). The ETS1-EAE rats showed a worse neurological deficit score and a significant increase in CD4+ cell infiltration, demyelination, and axonal injury in the spinal cord compared to AIR-EAE, ETS2-EAE, and ETS3-EAE groups. Flow cytometry analysis showed that the ETS1 group had decreased numbers of regulatory T (Treg) cells and increased effector T (Teff) cells in the brain and spinal cord. The expressions of Treg upstream regulator Foxp3 and downstream cytokines such as IL-10 were also altered accordingly. Together, these findings demonstrate that neonatal ETS exposure suppresses Treg functions and aggravates the severity of EAE, confirming early-life exposure to ETS as a potential risk factor for multiple sclerosis in adulthood.
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