研究动态
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CCL11/CCR3 依赖性嗜酸性粒细胞增多可减轻恶性胸腔积液并改善预后。

CCL11/CCR3-dependent eosinophilia alleviates malignant pleural effusions and improves prognosis.

发表日期:2024 Jun 29
作者: Min Zhang, Lixia Xia, Wenbei Peng, Guogang Xie, Fei Li, Chao Zhang, Madiha Zahra Syeda, Yue Hu, Fen Lan, Fugui Yan, Zhangchu Jin, Xufei Du, Yinling Han, Baihui Lv, Yuejue Wang, Miao Li, Xia Fei, Yun Zhao, Kaijun Chen, Yan Chen, Wen Li, Zhihua Chen, Qiong Zhou, Min Zhang, Songmin Ying, Huahao Shen
来源: npj Precision Oncology

摘要:

恶性胸腔积液(MPE)在晚期癌症中很常见,通常与不良预后有关。据报道,嗜酸性粒细胞参与 MPE 的发生。然而,嗜酸性粒细胞在 MPE 中的作用仍不清楚。为了研究这一点,我们使用人类样本和小鼠模型进行了研究。 MPE患者中嗜酸性粒细胞计数增加,表明嗜酸性粒细胞数量越高,LENT评分越低。在我们的动物模型中,发现嗜酸性粒细胞在暴露于肿瘤细胞后会主动迁移到胸膜腔。有趣的是,我们发现嗜酸性粒细胞的缺乏会加剧 MPE,这可能是由于嗜酸性粒细胞通过改变 MPE 的微环境而产生的抗肿瘤作用。此外,我们的实验探讨了 C-C 基序趋化因子配体 11 (CCL11) 及其受体 C-C 基序趋化因子受体 3 (CCR3) 在 MPE 病理学中的作用。总之,我们的研究强调了嗜酸性粒细胞对 MPE 发展的保护潜力,并且通过嗜酸性粒细胞过继转移或增加其数量来增加嗜酸性粒细胞可改善 MPE。© 2024。作者。
Malignant pleural effusion (MPE) is a common occurrence in advanced cancer and is often linked with a poor prognosis. Eosinophils were reported to involve in the development of MPE. However, the role of eosinophils in MPE remains unclear. To investigate this, we conducted studies using both human samples and mouse models. Increased eosinophil counts were observed in patients with MPE, indicating that the higher the number of eosinophils is, the lower the LENT score is. In our animal models, eosinophils were found to migrate to pleural cavity actively upon exposure to tumor cells. Intriguingly, we discovered that a deficiency in eosinophils exacerbated MPE, possibly due to their anti-tumor effects generated by modifying the microenvironment of MPE. Furthermore, our experiments explored the role of the C-C motif chemokine ligand 11 (CCL11) and its receptor C-C motif chemokine receptor 3 (CCR3) in MPE pathology. As a conclusion, our study underscores the protective potential of eosinophils against the development of MPE, and that an increase in eosinophils through adoptive transfer of eosinophils or increasing their numbers improved MPE.© 2024. The Author(s).