香烟烟雾维持了免疫抑制的微环境,诱导了M2巨细胞的两极分化和在肺癌环境中的活力
Francesca Bianchi1,2, Valentino Le Noci1, Giancarla Bernardo1
1Department of Biomedical Sciences for Health, University of Milan, Milan, Italy.
PloS one
|May 22, 2024
概括
香烟烟雾 (CS) 促进M2巨细胞的两极分化,这抵制了CS的毒性,并损害了M1-表型的变化. 这导致肺癌吸烟者的免疫抑制性肺微环境.
科学领域:
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
- 环境健康 环境健康
背景情况:
- 香烟烟雾 (CS) 对肺癌进展,患者预后和治疗反应产生负面影响.
- 吸烟者的肺部免疫细胞功能的改变与CS的有害影响有关.
- CS在制造炎症或免疫抑制性肺微环境中的确切作用需要进一步研究.
研究的目的:
- 为了研究体外吸烟抽出物 (CSE) 暴露对巨细胞的影响.
- 为了确定CSE如何影响巨细胞两极分化和功能在肺癌的背景下.
主要方法:
- 用CSE.培养的小鼠巨细胞系 (RAW 264.7) 进行培养.
- 通过实时PCR和cytofluorimetric分析评估巨细胞极化.
- 评估细胞活力 (SRB测定) 和激活 (聚I:C暴露).
- 使用共聚焦显微镜分析了巨细胞-路易斯肺癌 (LLC1) 相互作用.
主要成果:
- CSE诱导的巨细胞偏向于M2表型.
- M2巨细胞对CSE的毒性作用表现出抵抗力.
- CS暴露抑制了托尔样受体3 (TLR3) 介导的M2到M1表型转移.
- 这些机制有助于吸烟者的肺部M2巨细胞的丰富.
结论:
- 在吸烟者的肺癌微环境中,CS促进了M2类现象型巨细胞的流行.
- 这种患病率是由多种机制驱动的,包括受损的TLR3信号传输.
- 在肺癌吸烟者中,CS最终促进了抗炎和潜在的免疫抑制性肺微环境.
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