AIM:To investigate changes of tumor necrosis factor-α (TNF-α) and TNFR-I expression in vital organs and their significancein the pathogenesis of multiple organ damage associated withendogenous endotoxin following major burns.METHODS:Wistar rats subjected to a 35% full-thicknessscald injury were sacrificed at 12 h,24 h,48 h,and 72 hpostburn,respectively.Meanwhile,eight rats were taken asnormal controls.Tissue samples from liver,spleen,kidney,lung and intestine were collected to assay tissue endotoxinlevels and measure TNF-α and TNFR-I expression.Inaddition,blood samples were obtained for the determinationof organ function parameters.RESULTS:Endotoxin levels in liver,spleen and lungincreased markedly after thermal injury,with the highestlevel in liver.The gene expression of TNF-α in liver,lungand kidney was up-regulated after thermal injury,whilethe TNFR-I mRNA expression in liver,lung,kidney andintestine was shown decreased throughout the observationperiod.Thus,the mRNA expression ratio of TNF-α to TNFR-I was significantly increased postburn,particularly inpulmonary tissue (67-fold).In addition,the significantcorrelations between the expression of TNFR-I or theexpression ratio of TNF-α/TNFR mRNA in liver tissue andserum aspartate aminotransferase levels were noted (P<0.05-0.01).Similar results were also obtained betweenpulmonary TNF-α mRNA expression and myeloperoxidaseactivities (P<0.01),whereas there was a highly negativecorrelation between levels of renal TNFR-I mRNA expressionand serum creatinine.CONCLUSION:Burn injury could result in the translocationof gut-derived endotoxin that was mainly distributed in theliver,spleen and lung.The translocated endotoxin then madethe expression of TNF-α and TNFR-I mRNA up-regulatedand down-regulated respectively in various organs,whichmight be involved in the pathogenesis of multiple organdamage following burns. 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 withendogenous endotoxin following major burns. METHODS: Wistar rats subjected to a 35% full -thicknessscald injury were sacrificed at 12 h, 24 h, 48 h, and 72 hpostburn, 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. 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 highestlevel 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 markedly throughout the observation period. atio of TNF-α to TNFR-I was significantly increased postburn, particularly in pulmonary tissue (67-fold). In addition, the significant relationships between the expression of TNFR-I or the expression ratio of TNF-α / TNFR mRNA in liver tissue and serum aspartate The results of 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), 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, whichmight be involved in the pathogenesis of multiple organdamage following burns.