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首页> 外文期刊>Infection and immunity >Intimin, Tir, and Shiga Toxin 1 Do Not Influence Enteropathogenic Responses to Shiga Toxin-Producing Escherichia coli in Bovine Ligated Intestinal Loops
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Intimin, Tir, and Shiga Toxin 1 Do Not Influence Enteropathogenic Responses to Shiga Toxin-Producing Escherichia coli in Bovine Ligated Intestinal Loops

机译:Intimin,Tir和志贺毒素1不影响牛结扎的肠to对产志贺毒素的大肠杆菌的肠致病反应。

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Shiga toxin-producing Escherchia coli (STEC) comprises a group of attaching and effacing (A/E) enteric pathogens of animals and humans. Natural and experimental infection of calves with STEC may result in acute enteritis or subclinical infection, depending on serotype- and host-specific factors. To quantify intestinal secretory and inflammatory responses to STEC in the bovine intestine, serotypes that are associated with human disease (O103:H2 and O157:H7) were introduced into ligated mid-ileal loops in gnotobiotic and conventional calves, and fluid accumulation and recruitment of radiolabeled neutrophils were measured after 12 h. STEC serotype O103:H2, but not serotype O157:H7, elicited strong enteropathogenic responses. To determine if the inflammatory response to STEC O103:H2 in calves requires Shiga toxin 1 or intimate bacterial attachment to the intestinal epithelium, defined mutations were made in the stx1, eae, and tir genes. Our data indicate that some STEC induce intestinal inflammatory responses in calves by a mechanism that is independent of A/E-lesion formation, intimin, or Shiga toxin 1. This may have implications for strategies to reduce STEC carriage in cattle.
机译:产生志贺毒素的大肠杆菌大肠杆菌(STEC)包括一组附着和消失的动物和人类肠道病原体(A / E)。根据血清型和宿主特异性因素,自然和实验感染STEC的小牛都可能导致急性肠炎或亚临床感染。为了量化牛肠道中对STEC的肠道分泌和炎性反应,将与人类疾病相关的血清型(O103:H2和O157:H7)引入结扎的回肠中肠回肠中和常规犊牛中,进行体液积聚和募集12小时后测量放射性标记的中性粒细胞。 STEC血清型O103:H2,但不是血清型O157:H7引起强烈的肠病原反应。为了确定小牛对STEC O103:H2的炎症反应是否需要志贺毒素1或紧密附着在肠上皮上的细菌,在 stx1 eae 中进行了明确的突变,和 tir 基因。我们的数据表明,某些STEC通过与A / E病灶形成,内膜素或志贺毒素1无关的机制诱导犊牛肠道炎症反应。这可能对减少牛STEC转运的策略有影响。

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