Biphasic Increase of Pro-inflammatory Cytokines in Mice Lung after Irradiation / 결핵및호흡기질환
Tuberculosis and Respiratory Diseases
;
: 14-20, 2009.
Article
in Korean
| WPRIM
| ID: wpr-74000
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Thorax
/
Fibrosis
/
Enzyme-Linked Immunosorbent Assay
/
Cytokines
/
Tumor Necrosis Factor-alpha
/
HMGB1 Protein
/
Lung Injury
/
Lung
Limits:
Animals
/
Humans
Language:
Korean
Journal:
Tuberculosis and Respiratory Diseases
Year:
2009
Type:
Article
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