高温对炎症性细胞因子释放的影响:一个体外和基于人群的研究
Xiaoxu Hu1,2, Hualing Fu1,2, Luou Zhang3
1State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China.
Environment & health (Washington, D.C.)
|October 30, 2024
概括
夏季的热浪和气温上升可能会损害炎症系统. 研究表明,即使是1.5°C的升温,也会通过烯碳水化合物受体 (AhR) 途径提升诸如白内素-6 (IL-6) 和白内素-8 (IL-8) 等炎症性细胞因子.
科学领域:
- 环境健康 环境健康
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 极端的夏季热浪是全球日益关注的问题.
- 高温对人类炎症系统的影响尚不清楚.
- 现有的研究往往侧重于死亡率,忽视其他健康风险.
研究的目的:
- 评估与夏季热浪相关的炎症风险.
- 为了研究将温度升高与细胞因子释放联系起来的细胞机制.
- 了解基碳化合物受体 (AhR) 途径在温度诱导的炎症中的作用.
主要方法:
- 在暴露于高高温和正常夏季温度的健康个体中,血清细胞因子水平的比较.
- 建立一个控制1.5°C温度升高的细胞模型.
- 通过AhR途径对细胞因子调节的分析,特别是通过AhR途径进行的介质素-6 (IL-6) 和介质素-8 (IL-8).
主要成果:
- 高温显著增加IL-6和IL-8的释放.
- 基碳化合物受体 (AhR) 途径介导温度诱导的细胞因子释放.
- 即使是适度的1.5°C温度升高也可以激活细胞中的炎症反应.
- 高温会增加其他因素的促炎作用.
结论:
- 高温对健康的影响,特别是对炎症系统的影响,可能被低估了.
- 温度升高,即使是看似微小的升高,也对细胞平衡构成重大挑战.
- 准AhR通路可能是缓解热相关炎症的潜在策略.
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