Department of Immunology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Inflammation. 2015 Apr;38(2):465-75. doi: 10.1007/s10753-014-9952-8.
Radiation-induced lung injury is a kind of sterile inflammation, which may lead to morbidity and mortality. The mechanism by which ionizing radiation activate the immune system is not well understood. In the present study, we have investigated the immunological responses induced by local irradiation-induced damage in mouse lung. The left lungs of C57BL/6 mice were irradiated at a high dose of 100 Gy. The histology of the lungs and spleen showed evidences of alveolar inflammation and congestion at 2 weeks after X-ray treatment. Also, prominent increase in cells expressing the cell surface markers, Gr(+)CD11b(+)F4/80(+) and Ly6C(+) Ly6G(+) were observed 2 weeks after X-ray treatment (100 Gy). Gr1(+)CD11b(+)F4/80(+) cell depletion by clodronate treatment reversed the histological effects and also failed to recruit Gr(+)CD11b(+) cells or F4/80(+) cells caused by irradiation. The origin of recruited Gr1(+)CD11b(+) cells was found to be a mixed resident and recruited phenotype.
放射性肺损伤是一种无菌性炎症，可能导致发病率和死亡率。电离辐射激活免疫系统的机制尚不清楚。在本研究中，我们研究了局部照射损伤诱导的小鼠肺中的免疫反应。用高剂量 100Gy 对 C57BL/6 小鼠的左肺进行照射。X 射线治疗 2 周后，肺和脾脏的组织学显示出肺泡炎症和充血的证据。此外，在 X 射线治疗（100Gy）后 2 周观察到表达细胞表面标记物 Gr(+)CD11b(+)F4/80(+)和 Ly6C(+)Ly6G(+)的细胞明显增加。用氯膦酸盐处理耗尽 Gr1(+)CD11b(+)F4/80(+)细胞可逆转组织学效应，并且不能募集照射引起的 Gr(+)CD11b(+)细胞或 F4/80(+)细胞。发现募集的 Gr1(+)CD11b(+)细胞的来源是混合的常驻和募集表型。
