Studies on biological modifier produced by bacteria

1)研究细菌肠毒素在肠组织中的信号转导机制是项目之一。在由产肠毒素大肠杆菌热稳定型肠毒素（ST）引起的水样腹泻中，发现环GMP依赖性蛋白激酶的激活是其信号转导的必要步骤，并且在暴露于霍乱肠毒素的肠细胞中，被环GMP依赖性蛋白激酶磷酸化的蛋白（81K-， 43K-和37K- dalfons）中的一个也被环amp依赖性蛋白激酶磷酸化。这一发现表明，ST和胆汁肠毒素通过其主要作用增加肠组织中环核苷酸含量，通过共同的机制起作用。假单胞菌杀白细胞素在溶酶体蛋白磷酸化后，激活多形核白细胞<Ca^(2+)>依赖性蛋白激酶的信号传导途径也与此类似。2)对多种产肠毒素病原菌产生的热稳定型肠毒素进行了详细的结构分析比较，发现了与热稳定性和生物活性相关的共同结构。对霍乱肠毒素结构的免疫学研究为开发新的有效的霍乱疫苗提供了依据。3)细菌脂多糖刺激T细胞释放白细胞介素，促进细胞生长，提示LPS在免疫应答中的重要作用。

1) The mechanism of signal trunsduction of bacterial enterotoxin in intestinal tissue was investigated as one of the projects. In watery diarrhea caused by heat-stable enterotoxin (ST) of Enterotoxigenic Escherichia coli, it was found that an activation of cyclic GMP dependent protein kinase is a necessary step in its signal transduction and that one of the proteins (81K-, 43K- and 37K- dalfons) phosphorylated by cyclic GMP-dependent protein kinase was also phosphorylated by cyclic AMP-dependent protein kinase in itestinal cells exposed to cholera enterotoxin. This finding suggests that ST and cholear enterotoxin work through a common mechanism after increase of cyclic nucleotide content in intestinal tissue by their primary actions. Similar signal trunsduction pathway was observed in the action of Pseudomonal leukocidin by which <Ca^(2+)> -dependent protein knase of polymorphonuclear leukocyte was activated, following phosphorylation of lysosomal protein.2) A detailed comparison of structural analysis of heat-stable enterotoxins produced by many enterotoxigenic pathogens indicated the common structure related to heat stability and biological activity. Immunological studies on the structure of cholera enterotoxin suggests the development of new effective vaccine against cholera.3) It was found that bacterial lipopolysaccharide stimulated the release of interleukin from T cell and enhanced the growth of the cell, indicating the significant role of LPS in immune response.