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宿主特异性差异改变了猪定植过程中某些沙门氏菌基因的需求。

Host specific differences alter the requirement for certain Salmonella genes during swine colonization.

机构信息

Agroecosystems Management Research Unit, National Laboratory for Agriculture and the Environment, ARS, USDA, NSRIC-2103, 2110 University Drive, Ames, IA 50011, USA.

出版信息

Vet Microbiol. 2011 Jun 2;150(3-4):215-9. doi: 10.1016/j.vetmic.2010.12.026. Epub 2011 Jan 11.

DOI:10.1016/j.vetmic.2010.12.026
PMID:21273009
Abstract

The pathogenic potential of Salmonella is determined during the complex interaction between pathogen and host, requiring optimal regulation of multiple bacterial genetic systems within variable in vivo environments. The mouse model of systemic disease has been an extremely productive model to investigate the pathogenesis of Salmonella enterica serovar Typhimurium (S. Typhimurium). Although the mouse model is a widely used paradigm for studying the pathogenesis of systemic disease caused by Salmonella, investigations concerning food safety interventions should employ natural hosts to examine gastrointestinal colonization by Salmonella. Recent research has demonstrated specific differences in the attenuation of certain S. Typhimurium mutants in mice compared to swine. This variation in pathogenesis between the mouse model and pigs for the S. Typhimurium mutants is presumably dependent upon either the requirements for specific gene products during systemic disease (mouse) versus gastrointestinal colonization (pig) or host specific differences. In addition, host specific diversity in Salmonella colonization of swine has also been described in comparison to other food-producing animals, including cattle and chickens. Differences in Salmonella colonization and pathogenesis across diverse animal species highlight the importance of species-specific studies of gastrointestinal colonization for the development of Salmonella interventions to enhance pork safety.

摘要

沙门氏菌的致病潜能是在病原体和宿主之间的复杂相互作用中确定的,这需要在不同的体内环境中对多个细菌遗传系统进行最佳调节。全身性疾病的小鼠模型一直是研究鼠伤寒沙门氏菌(S. Typhimurium)发病机制的极其有效的模型。尽管小鼠模型是研究沙门氏菌引起的全身性疾病发病机制的广泛使用范例,但有关食品安全干预措施的研究应使用天然宿主来检查沙门氏菌对胃肠道的定植。最近的研究表明,与猪相比,某些 S. Typhimurium 突变体在小鼠中的衰减存在特定差异。与猪相比,这种小鼠模型和猪中 S. Typhimurium 突变体发病机制的差异可能取决于全身性疾病(小鼠)与胃肠道定植(猪)过程中特定基因产物的需求,或者宿主的特异性差异。此外,与其他食用动物(包括牛和鸡)相比,猪中沙门氏菌定植的宿主特异性多样性也已被描述。不同动物物种中沙门氏菌定植和发病机制的差异突出了针对胃肠道定植进行特定物种研究对于开发增强猪肉安全性的沙门氏菌干预措施的重要性。

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