ESTRO 2025 - Abstract Book

S3936

Radiobiology - Normal tissue radiobiology

ESTRO 2025

staining, Immunofluorescence, western blotting, real-time PCR and flow cytometry were employed to analyze the effect of LXA4 on radiation damage.

Results: In our customized radiation-induced lung injury model, macrophage infiltration into alveolar spaces significantly increase. The CD206/iNOS ratio, indicative of M2 versus M1 macrophage, varied with radiation dose and post-IR time. LXA4 treatment mitigates inflammation and fibrosis, promoting M2 polarization with CD206 expression at early stages of injury and reducing fibrotic region at late stages. In vitro, LXA4 enhances M2 polarization and downregulates TNF-α, IL-1β, and IL-6 expression. LXA4 also regulates the NF-κB and ALK signaling pathway in radiation induced injury. Conclusion: LXA4 modulates macrophage polarization, initially promoting M2 macrophage polarization to reduce inflammation and supporting early tissue repair while preventing fibrotic process in the later stages. These findings suggest LXA4`s therapeutic potential in managing radiation-induced pneumonitis and fibrosis, offering a novel approach in radiation-induced lung injury. References: 1. Zhou BW, Liu HM, Xu F, Jia XH. The role of macrophage polarization and cellular crosstalk in the pulmonary fibrotic microenvironment: a review. Cell Commun Signal. 2024 Mar 9;22(1):172. 2. Ni J, Guo T, Zhou Y, Jiang S, Zhang L, Zhu Z. STING signaling activation modulates acrophage polarization via CCL2 in radiation-induced lung injury. J Transl Med. 2023 Sep 4;21(1):590. 3. Zhang L, Wang Y, Wu G, Xiong W, Gu W, Wang CY. Macrophages: friend or foe in idiopathic pulmonary fibrosis? Respir Res. 2018 Sep 6;19(1):170. 4. Li QQ, Ding DH, Wang XY, Sun YY, Wu J. Lipoxin A4 regulates microglial M1/M2 polarization after cerebral ischemia-reperfusion injury via the Notch signaling pathway. Exp Neurol. 2021 May;339:113645. Keywords: RILI, macrophage, lipoxin A4 Proffered Paper Spatial analysis of microglia activation and proliferation on individual cell level following partial brain proton irradiation in mice Sindi Nexhipi 1,2 , Suckert Theresa 1,2 , Johannes Richard Soltwedel 2,3 , Elke Beyreuther 2,4 , Max Noßol 2 , Laura Pecht 2 , Moritz Schneider 2,4 , Felix Horst 2 , Steffen Löck 2,5,6 , Mechthild Krause 5,1,2 , Armin Lühr 7 , Antje Dietrich 1,2 1 German Cancer Consortium (DKTK), Partner Site Dresden, German Cancer Research Center (DKFZ), Heidelberg, Germany. 2 OncoRay - National Center for Radiation Research in Oncology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Helmholtz-Zentrum Dresden - Rossendorf, Germany, Dresden, Germany. 3 DFG Cluster of Excellence ‘Physics of Life’, TU Dresden, Dresden, Germany. 4 Institute of Radiation Physics, e. Helmholtz-Zentrum Dresden - Rossendorf (HZDR), Dresden, Germany. 5 Department of Radiotherapy and Radiation Oncology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany. 6 National Center for Tumor Diseases (NCT), Partner Site Dresden, German Cancer Research Center (DKFZ), Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Helmholtz Association / Helmholtz-Zentrum Dresden - Rossendorf (HZDR), Dresden, Germany. 7 Department of Physics, TU Dortmund University, Dortmund, Germany 2837