- Author:
Yun Jung CHOI
1
;
Jin Kyung RHO
;
Won Seok JANG
;
Seon Joo LEE
;
Seung Sook LEE
;
Jae Soo KOH
;
Jae Yeol KIM
;
Hye Ryoun KIM
;
Cheol Hyeon KIM
;
Jae Cheol LEE
Author Information
- Publication Type:Original Article
- Keywords: Radiation; Lung injury; Cytokines
- MeSH: Animals; Cytokines; Enzyme-Linked Immunosorbent Assay; Fibrosis; HMGB1 Protein; Humans; Lung; Lung Injury; Mice; Thorax; Tumor Necrosis Factor-alpha
- From:Tuberculosis and Respiratory Diseases 2009;67(1):14-20
- CountryRepublic of Korea
- Language:Korean
- Abstract: 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-alpha, MIP-2, IL-1beta 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-alpha and IL-1beta 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-alpha and IL-1beta. The effective control of second phase cytokine elevation should contribute to preventing severe lung fibrosis caused by radiation.