Published online May 15, 2003. doi: 10.3748/wjg.v9.i5.1038
Revised: November 14, 2002
Accepted: November 25, 2002
Published online: May 15, 2003
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.