放射治疗后的流感病毒扩大了肺损伤和单细胞衍生的巨细胞反应
Angela M Groves1, Carl J Johnston2, Nicole D Paris3
1University of Rochester Medical Center, Department of Radiation Oncology, Rochester, New York, United States; angela_groves@urmc.rochester.edu.
概括
呼吸道感染通过改变巨细胞的反应,显著加剧了放射治疗的肺毒性. 这种组合疗法被证明是致命的,即使在低辐射剂量下也是如此,这突出了癌症患者的关键研究不足的风险因素.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 肺部病理学 肺部病理学
背景情况:
- 胸部癌症的放射治疗 (RT) 提高了生存率,增加了预防肺部放射性毒性的重要性.
- 呼吸道感染是加剧RT毒性的肺部压力因素,但这种相互作用尚不清楚.
- 组织寄居的膜巨细胞被RT损坏,而被招募的单细胞衍生巨细胞 (MDMs) 促进肺纤维化.
研究的目的:
- 为了研究呼吸道感染对肺部辐射治疗后巨细胞群的影响.
- 为了评估慢性肺损伤和急性/慢性巨细胞反应后RT和流感A病毒 (IAV) 感染.
主要方法:
- 小鼠接受整体胸部RT (5-12.5 Gy),然后在1周或20周内感染IAV.
- 评估慢性肺损伤和急性/慢性巨细胞反应.
- 评估巨细胞动态,包括亲炎性和亲纤维性标记物.
主要成果:
- 在个人耐受良好剂量下,RT加IAV是致命的.
- IAV从低RT剂量 (5Gy) 中放大了慢性肺病理,即使感染延迟.
- 巨细胞的动态转向了亲炎性,亲纤维性MDM,成熟度和抗原呈现减少,但纤维性因素增加.
结论:
- 同时或连续的呼吸道感染和胸部RT显著增加肺损伤和死亡率.
- 相互作用将巨细胞群向亲纤维细胞表型转移,加剧肺损伤.
- 呼吸道感染对接受胸部放射治疗的患者来说是一个关键的,研究不足的危险因素.
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