Abstract
Radiation therapy (RT) is one of the major cancer treatment modalities. However, normal tissues surrounding tumor are inevitably exposed to radiation during radiation therapy. In particular, all patients receiving external beam radiation therapy are at risk of skin damage, which can result from harmful immune change. In this study, we investigated effects of radiation on skin damage, Th2 response and its underlying mechanism. The dorsal skin of a mini pig was divided into two paraspinal sections, with 18 small irradiation fields (2 cm × 2 cm) in each section, and each section was irradiated with 30 Gy single fraction or 30 Gy in 5 fraction by a 6 MeV electron beam. Biopsy specimens of each radiation field these were harvested for histology, eosinophil counting, immunostaining with anti-CD31, TGF-β1, IL-6 at 1st, 2nd, 4th, 6th, 8th, 10th and 12th weeks. In addition, IL-4, IL-5, CCL11 and IL-33 were evaluated to study on underlying mechanism of eosinophil recruitment by radiation. IL-6, TGF- β1 and CD-31 were produced after 30 Gy more in single fraction than in five fractions. Irradiation enhanced eosinophil infiltration into irradiated sites, which was also pronounced more after 30 Gy in single fraction compared with in 5 fractions. The number of eosinophils began rising sharply at 4 weeks and it was peak 6-8 weeks after radiation, and then normalized. 30 Gy single-fraction radiation increased IL-5, CCL-11 and IL-4 in the irradiated skin of a mini pig compared to 30 Gy in 5 fractions. In addition, 30 Gy single fraction-irradiated skins showed the strong vascular damage in compared with 30 Gy in 5 fractions during 1-4 weeks. Especially, IL-33 was secreted by vascular endothelial cells receiving injury that induced Th2 responses such as IL-4 production and degranulation of mast cells in irradiated skin. Our results suggest that high-dose single fraction irradiation enhances more Th2 immune responses via recruitment of eosinophils in skin comparing to fractionated radiation. In particular, IL-33 seems to be the key molecule operating eosinophil recruitment and radiation-induced Th2 response.
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