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首页> 外文期刊>Berliner und Munchener Tierarztliche Wochenschrift >Murine infection models for the investigation of Campylobacter jejuni - host interactions and pathogenicity
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Murine infection models for the investigation of Campylobacter jejuni - host interactions and pathogenicity

机译:空肠弯曲菌-宿主相互作用和致病性研究的小鼠感染模型

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摘要

Despite the socioeconomic burden of campylobacteriosis, our insights into the molecular mechanisms underlying Campylobacter (C.) jejuni-induced intestinal immunopathogenesis are limited. The absence and the ban of convenient murine infection models caused fundamental restrictions in Campylobacter research. The development of novel and modified murine infection models in the last years has greatly contributed to our knowledge in C. jejuni host interactions and pathogenicity. Novel findings revealed that the colonization resistance of mice against C. jejuni infection can be overcome by modification of the intestinal microbiota. In particular C. jejuni infected infant mice harbouring a conventional microbiota and Interleukin-10-deficient mice rendered gnotobiotic by antibiotic treatment develop lipooligosaccharide mediated inflammation and specific T-cell responses both key features of campylobacteriosis in humans. This short review focuses on the major progress in this growing research field and intends to summarize some of the most important findings.
机译:尽管存在弯曲杆菌病的社会经济负担,但我们对空肠弯曲杆菌(C.)空肠诱导的肠道免疫发病机理的分子机制的见解仍然有限。方便的鼠类感染模型的缺失和禁止导致弯曲杆菌研究的基本限制。近年来,新型和改良的鼠类感染模型的发展极大地促进了我们对空肠弯曲杆菌宿主相互作用和致病性的了解。新发现表明,通过改变肠道菌群可以克服小鼠对空肠弯曲杆菌感染的定植性。特别地,具有常规微生物群的空肠弯曲杆菌感染的婴儿小鼠和通过抗生素治疗成为致病菌的白介素10缺陷小鼠发展脂环寡糖介导的炎症和特异性T细胞应答,这都是人弯曲杆菌病的关键特征。这篇简短的评论着重于这个不断发展的研究领域的主要进展,并打算总结一些最重要的发现。

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