Wang Chenlin, Wu Yanan, Liu Chao, Li Yang, Mi Song, Yang Xiaofan, Liu Tong, Tian Yuanjing, Zhang YingYing, Hu Pingping, Qiao Lili, Deng Guodong, Liang Ning, Sun Jinyue, Zhang Yan, Zhang Jiandong
Department of Oncology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Lung Cancer Institute, Jinan, China.
School of Clinical Medicine, Shandong Second Medical University, Weifang, China.
Front Immunol. 2024 Dec 11;15:1405020. doi: 10.3389/fimmu.2024.1405020. eCollection 2024.
Patients receiving chest radiation therapy, or exposed to high radiation levels due to accidental nuclear leakage are at risk of radiation-induced lung injury (RILI). In innate immunity, macrophages not only exhibit certain radiation tolerance but also play an important regulatory role in the whole pathological process. Nervonic acid (NA), a long-chain unsaturated fatty acid found in nerve tissue, plays a pivotal role in maintaining normal tissue growth and repair. However, the influence of NA on RILI progression has yet to be examined.
This study aimed to assess the role of macrophage subtypes in RILI and whether NA can alleviate RILI. Specifically, whether NA can alleviate RILI by targeting macrophages and reducing the levels of inflammatory mediators in mouse models was assessed.
Mice RILI model was employed with 13 Gy whole thoracic radiation with or without administration of NA. Various assays were performed to evaluate lung tissue histological changes, cytokine expression, IκB-α expression and the number and proportion of macrophages.
Radiation can lead to the release of inflammatory mediators, thereby exacerbating RILI. The specific radiation dose and duration of exposure can lead to different dynamic changes in the number of subpopulations of lung macrophages. NA can affect the changes of macrophages after irradiation and reduce inflammatory responses to alleviate RILI.
Macrophages play a significant role in the integrated pathological process of lung injury after irradiation which shows a dynamic change with different times. NA can protect lung tissues against the toxic effects of ionizing radiation and is a new potential functional component for targeting macrophages.
接受胸部放射治疗的患者，或因意外核泄漏而暴露于高辐射水平下的患者，有发生放射性肺损伤（RILI）的风险。在固有免疫中，巨噬细胞不仅表现出一定的辐射耐受性，而且在整个病理过程中发挥重要的调节作用。神经酸（NA）是一种在神经组织中发现的长链不饱和脂肪酸，在维持正常组织生长和修复中起关键作用。然而，NA对RILI进展的影响尚未得到研究。
本研究旨在评估巨噬细胞亚型在RILI中的作用，以及NA是否可以减轻RILI。具体而言，评估NA是否可以通过靶向巨噬细胞并降低小鼠模型中炎症介质的水平来减轻RILI。
采用小鼠RILI模型，给予13 Gy全胸照射，同时给予或不给予NA。进行各种检测以评估肺组织的组织学变化、细胞因子表达、IκB-α表达以及巨噬细胞的数量和比例。
辐射可导致炎症介质的释放，从而加重RILI。特定的辐射剂量和暴露持续时间可导致肺巨噬细胞亚群数量的不同动态变化。NA可以影响照射后巨噬细胞的变化，并减少炎症反应以减轻RILI。
巨噬细胞在照射后肺损伤的综合病理过程中起重要作用，且随时间呈现动态变化。NA可以保护肺组织免受电离辐射的毒性作用，是一种靶向巨噬细胞的新的潜在功能成分。
