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Intestinal mucosal protection against F4+ ETEC in pigs by oral immunisation with purified F4 fimbriae

机译:用纯化的F4 FIMBRIAE口服免疫,对猪的F4 + etec肠道粘膜保护

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Enterotoxigenie Escherichia coli (ETEC) are an important cause of diarrhoea and mortality in neonatal and recently weaned piglets. Some of these ETEC strains bear F4 fimbriae, by which they adhere to specific receptors (F4R), present on brush borders of villous enlerocytes, and consequently colonise the small intestine. Neonatal infections can be prevented effectively by passive colostral and lactogenic immunity which can be obtained and increased by vaccination of the sow. After weaning however, the piglets become susceptible again to ETEC infections. At that moment, the induction of an active mucosal immune response is required to evoke a protective immunity. It has recently been demonstrated that oral F4 administration in pigs induces a mucosalimmune response. In the present study it is shown that F4R are a prerequisite for an immune response following oral immunisation. Furthermore, indications were obtained that oral F4 immunisation can induce mucosal protection. Fifteen F4 seronegative piglets (6-week-old) were used. All animals were killed at the end of the experiment to determine the presence of F4R on their villous enterocytes.
机译:Enterotoxigenie大肠杆菌(ETEC)是新生儿和最近断奶仔猪腹泻和死亡率的重要原因。其中一些ETEC菌株承载F4 FIMBRIAE,它们粘附在绒毛肌细胞的刷子边界上的特定受体(F4R),并因此殖民化小肠。通过被动脱牛肉和肠外脱离泌乳可有效地防止新生儿感染,并通过母猪接种疫苗来获得和增加。然而,断奶后,仔猪再次变得易感到​​ETEC感染。此时,需要活跃的粘膜免疫应答所需的诱导来引起保护性免疫力。最近已经证明,猪中的口腔F4给药诱导粘滞可影响。在本研究中,表明F4R是口服免疫后免疫应答的先决条件。此外,获得了口腔F4免疫可以诱导粘膜保护的适应症。使用十五个F4血清猪肉(6周龄)。在实验结束时杀死所有动物,以确定绒毛肠细胞上的F4R的存在。

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