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首页> 外文期刊>Applied Microbiology and Biotechnology >Intestinal receptors for adhesive fimbriae of enterotoxigenic Escherichia coli (ETEC) K88 in swine - a review [Review]
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Intestinal receptors for adhesive fimbriae of enterotoxigenic Escherichia coli (ETEC) K88 in swine - a review [Review]

机译:猪肠毒素性大肠杆菌(ETEC)K88黏附菌毛的肠道受体-综述[综述]

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Determining the structure of the intestinal receptor for enterotoxigenic Escherichia coli (ETEC) K88 fimbriae will make it possible to develop new strategies to prevent K88+ ETEC-induced disease in pigs. Putative K88 adhesin receptors have been identified in both intestinal brush border and mucus preparations as either glycoproteins or glycolipids. Proteins with sizes of 25, 35, 40-42, 60, and 80 kDa in the intestinal mucus and 16, 23, 35, 40-70, 74, 210, and 240 kDa in brush border membranes were reported to bind specifically to K88ab and K88ac fimbriae. The factors accounting for these variable results may include the variants of K88, ages, breeds, and phenotypes of pigs, and even the sampling sites in the small intestine. Of the reported K88 receptors, only three brush border receptors, i.e., a pair of mucin-type sialoglycoproteins (210 kDa or 240 kDa), an intestinal neutral glycosphingolipid (IGLad), and a 74-kDa transferrin glycoprotein (GP74), have fulfilled the criteria as phenotype-specific K88 fimbrial receptors. Inhibiting the attachment of ETEC to intestine by modifying the receptor attachment sites has been the key for developing novel approaches to preventing ETEC-induced diarrhea in pigs. These include: (1) receptor analogs from a variety of biological sources, (2) an enteric protected protease, (3) chicken egg-yolk containing anti-K88 fimbrial antibodies, and (4) some Lactobacillus isolates producing proteinaceous components or carbohydrates interacting with mucus components. Future studies should be directed to further characterize the carbohydrate and protein moieties of receptors recognized by the K88 adhesin variants and to identify the genes responsible for susceptibility to K88 + infections. [References: 63]
机译:确定肠毒素性大肠杆菌(ETEC)K88菌毛的肠受体的结构,将有可能开发出预防K88 + ETEC诱导的猪疾病的新策略。在肠刷缘和粘液制剂中均已鉴定出推定的K88粘附素受体为糖蛋白或糖脂。据报道,在肠粘液中大小分别为25、35、40-42、60和80 kDa的蛋白质,在刷状缘膜中大小分别为16、23、35、40-70、74、210和240 kDa的蛋白质与K88ab特异性结合。和K88ac菌毛。造成这些可变结果的因素可能包括猪的K88变体,年龄,品种和表型,甚至包括小肠的采样部位。在已报道的K88受体中,只有三个刷状边界受体,即一对粘蛋白型唾液酸糖蛋白(210 kDa或240 kDa),肠中性糖鞘脂(IGLad)和74 kDa转铁蛋白糖蛋白(GP74)已实现。作为表型特异性K88纤维受体的标准。通过修饰受体附着位点抑制ETEC与肠道的附着一直是开发预防ETEC引起的猪腹泻新方法的关键。其中包括:(1)来自多种生物学来源的受体类似物,(2)肠保护性蛋白酶,(3)含有抗K88纤维抗体的鸡卵黄,以及(4)一些产生蛋白质成分或碳水化合物相互作用的乳杆菌分离株与粘液成分。未来的研究应针对进一步表征K88粘附素变体识别的受体的碳水化合物和蛋白质部分,并鉴定导致K88 +感染易感性的基因。 [参考:63]

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