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幼鼠对F5(K99)大肠杆菌感染的易感性:近交系CBA和DBA/2品系小鼠肠黏膜中糖基转移酶活性的差异

Susceptibility of infant mice to F5 (K99) E. coli infection: differences in glycosyltransferase activities in intestinal mucosa of inbred CBA and DBA/2 strains.

作者信息

Grange P A, Mouricout M

机构信息

Laboratoire de Biochimie, UER des Sciences, Limoges, France.

出版信息

Glycoconj J. 1996 Feb;13(1):45-52. doi: 10.1007/BF01049678.

Abstract

Enterotoxigenic Escherichia coli (ETEC) strains expressing F5 (K99) fimbriae cause diarrhoea in the young animal through adhesion to specific sialoglycolipids of the small intestine surface. We studied here an infant mouse diarrhoea model, as CBA infant mice are susceptible to F5-positive ETEC infection, whereas DBA/2 ones are resistant. In an attempt to determine an enzymatic basis for susceptibility and resistance, we investigated the intestine ganglioside pattern in relation to the activity of glycosyltransferases responsible for the globo- and ganglio-series. We observed that the intestine of susceptible CBA infant mice displayed a characteristic sialoglycolipid pattern containing mainly the F5 receptors. The two murine strains differed in the relative activities of galactosyltransferases (GbOse3Cer and GM1 synthases), N-acetylgalactosylaminyltransferases (GA2 and GM2 synthases) and sialytransferases (GM3 and GD3 synthases). An elevated GM3-synthase activity was observed in the intestine of susceptible CBA infant mice, at the age of high susceptibility. Hence, we conclude that the marked specificity of mouse type correlated with susceptibility and resistance to F5-positive ETEC infection which could be controlled through the regulation of glycosyltransferase activities.

摘要

表达F5(K99)菌毛的产肠毒素大肠杆菌(ETEC)菌株通过粘附于小肠表面的特定唾液酸糖脂而导致幼龄动物腹泻。我们在此研究了一种幼鼠腹泻模型,因为CBA幼鼠易受F5阳性ETEC感染,而DBA/2幼鼠则具有抗性。为了确定易感性和抗性的酶学基础,我们研究了与负责球系列和神经节系列的糖基转移酶活性相关的肠道神经节苷脂模式。我们观察到,易感的CBA幼鼠的肠道呈现出一种特征性的唾液酸糖脂模式,主要包含F5受体。这两种小鼠品系在半乳糖基转移酶(GbOse3Cer和GM1合酶)、N-乙酰半乳糖胺基转移酶(GA2和GM2合酶)和唾液酸转移酶(GM3和GD3合酶)的相对活性上存在差异。在高易感性年龄阶段的易感CBA幼鼠的肠道中观察到GM3合酶活性升高。因此,我们得出结论,小鼠类型的显著特异性与对F5阳性ETEC感染的易感性和抗性相关,这可以通过调节糖基转移酶活性来控制。

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