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KMID : 0383820090670010014
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Tuberculosis and Respiratory Diseases
2009 Volume.67 No. 1 p.14 ~ p.20
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Biphasic Increase of Pro-inflammatory Cytokines in Mice Lung after Irradiation
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Choi Yun-Jung
Kim Jae-Yeol
Rho Jin-Kyung
Jang Won-Suk
Lee Sun-Joo
Lee Seung-Sook
Koh Jae-Soo
Kim Hye-Ryoun
Kim Cheol-Hyeon
Lee Jae-Cheol
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Abstract
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Background: The pathophysiologic mechanisms of radiation-induced lung injury should be elucidated to enhance the therapeutic efficacy of radiotherapy and to manage patients exposed to serious radiation by accident. It has been suggested that pro-inflammatory cytokines play an important role in radiation-induced effect on the lung. This study was aimed to investigate changes in pro-inflammatory cytokines such as TNF-α, MIP-2, IL-1β and HMGB1, a newly recognized inflammatory mediator.
Methods: The chests of BALB/c mice were selectively irradiated with single fraction of 20 Gy and then sacrificed at indicated times. Pathologic changes in the lung were examined after H&E staining. The expression level of pro-inflammatory cytokines was evaluated by ELISA kits in lung homogenate and in serum.
Results: Radiation induced inflammatory changes and mild fibrosis in lung. Biphasic increase of TNF-α and IL-1β was found in lung homogenate at 4 hours and at 3 weeks after radiation. The elevation in the second phase tended to be more intense. However, there was no similar change in serum. MIP-2 level was slightly increased in lung homogenate at 4 hours, but not at 3 weeks. HMGB1 was increased at 3 weeks in serum while there was no significant change in lung homogenate.
Conclusion: Radiation induced a biphasic increase in TNF-α and IL-1β. The effective control of second phase cytokine elevation should contribute to preventing severe lung fibrosis caused by radiation.
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KEYWORD
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Radiation, Lung injury, Cytokines
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