Basic Research
Copyright ©The Author(s) 2003. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 15, 2003; 9(5): 1038-1044
Published online May 15, 2003. doi: 10.3748/wjg.v9.i5.1038
The mRNA expression patterns of tumor necrosis factor-α and TNFR-I in some vital organs after thermal injury
Wen-Hui Fang, Yong-Ming Yao, Zhi-Guo Shi, Yan Yu, Ye Wu, Lian-Rong Lu, Zhi-Yong Sheng
Wen-Hui Fang, Yong-Ming Yao, Zhi-Guo Shi, Yan Yu, Ye Wu, Lian-Rong Lu, Zhi-Yong Sheng, Department of Microbiology and Immunology, Burns Institute, 304th Hospital of PLA, Beijing 100037, China
Author contributions: All authors contributed equally to the work.
Supported by the National Key Program for Fundamental Research and Development, No. G1999054203, the National Natural Science Outstanding Youth Foundation of China, No. 30125020, and the National Natural Science Foundation of China, No. 30200293
Correspondence to: Yong-Ming Yao, MD, Department of Microbiology and Immunology, Burns Institute, 304th Hospital of PLA, 51 Fu-Cheng Road, Beijing 100037, China. c_fanf@sina.com
Telephone: +86-10-66867394 Fax: +86-10-68429998
Received: October 30, 2002
Revised: November 14, 2002
Accepted: November 25, 2002
Published online: May 15, 2003
Abstract

AIM: To investigate changes of tumor necrosis factor-α (TNF-α) and TNFR-I expression in vital organs and their significance in the pathogenesis of multiple organ damage associated with endogenous endotoxin following major burns.

METHODS: Wistar rats subjected to a 35% full-thickness scald injury were sacrificed at 12 h, 24 h, 48 h, and 72 h postburn, respectively. Meanwhile, eight rats were taken as normal controls. Tissue samples from liver, spleen, kidney, lung and intestine were collected to assay tissue endotoxin levels and measure TNF-α and TNFR-I expression. In addition, blood samples were obtained for the determination of organ function parameters.

RESULTS: Endotoxin levels in liver, spleen and lung increased markedly after thermal injury, with the highest level in liver. The gene expression of TNF-α in liver, lung and kidney was up-regulated after thermal injury, while the TNFR-I mRNA expression in liver, lung, kidney and intestine was shown decreased throughout the observation period. Thus, the mRNA expression ratio of TNF-α to TNFR-I was significantly increased postburn, particularly in pulmonary tissue (67-fold). In addition, the significant correlations between the expression of TNFR-I or the expression ratio of TNF-α/TNFR mRNA in liver tissue and serum aspartate aminotransferase levels were noted (P < 0.05-0.01). Similar results were also obtained between pulmonary TNF-α mRNA expression and myeloperoxidase activities (P < 0.01), whereas there was a highly negative correlation between levels of renal TNFR-I mRNA expression and serum creatinine.

CONCLUSION: Burn injury could result in the translocation of gut-derived endotoxin that was mainly distributed in the liver, spleen and lung. The translocated endotoxin then made the expression of TNF-α and TNFR-I mRNA up-regulated and down-regulated respectively in various organs, which might be involved in the pathogenesis of multiple organ damage following burns.

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