The mRNA expression patterns of tumor necrosis factor-alpha and TNFR-I in some vital organs after thermal injury

• Published in: World journal of gastroenterology : WJG 2003-05, Vol.9 (5), p.1038-1044
• Main Authors: Fang, Wen-Hui, Yao, Yong-Ming, Shi, Zhi-Guo, Yu, Yan, Wu, Ye, Lu, Lian-Rong, Sheng, Zhi-Yong
• Format: Article
• Language: English
• Subjects: Animals; Antigens, CD - genetics; Base Sequence; Basic Research; Burns - complications; Burns - genetics; Burns - microbiology; Burns - physiopathology; DNA - genetics; Endotoxins - metabolism; Gene Expression; Gram-Negative Bacteria - isolation & purification; Gram-Negative Bacteria - pathogenicity; Gram-Negative Bacterial Infections - etiology; Gram-Negative Bacterial Infections - physiopathology; Intestines - physiopathology; Kidney - physiopathology; Liver - physiopathology; Lung - physiopathology; Male; Multiple Organ Failure - etiology; Multiple Organ Failure - genetics; Multiple Organ Failure - microbiology; Multiple Organ Failure - physiopathology; Rats; Rats, Wistar; Receptors, Tumor Necrosis Factor - genetics; Receptors, Tumor Necrosis Factor, Type I; RNA, Messenger - genetics; RNA, Messenger - metabolism; Sepsis - etiology; Sepsis - physiopathology; Tissue Distribution; Tumor Necrosis Factor-alpha - genetics
• ISSN: 1007-9327; 2219-2840
• DOI: 10.3748/wjg.v9.i5.1038

To investigate changes of tumor necrosis factor-alpha (TNF-alpha) and TNFR-I expression in vital organs and their significance in the pathogenesis of multiple organ damage associated with endogenous endotoxin following major burns. 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-alpha and TNFR-I expression. In addition, blood samples were obtained for the determination of organ function parameters. Endotoxin levels in liver, spleen and lung increased markedly after thermal injury, with the highest level in liver. The gene expression of TNF-alpha 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-alpha 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-alpha/TNFR mRNA in liver tissue and serum aspartate aminotransferase levels were noted (P