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首页> 外文期刊>Infection and immunity >Pathogenesis of defined invasion mutants of Yersinia enterocolitica in a BALB/c mouse model of infection.
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Pathogenesis of defined invasion mutants of Yersinia enterocolitica in a BALB/c mouse model of infection.

机译：在感染的BALB / c小鼠模型中确定的小肠结肠炎耶尔森菌侵袭突变体的发病机理。

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It has been hypothesized for many years that the ability of Yersinia spp. to invade tissue culture cells is reflective of their ability to penetrate the intestinal epithelium and that this capacity is an important aspect of the disease process. Three different genes from Yersinia spp. that are involved in the tissue culture invasion phenotype have been identified: inv, ail, and yadA. It was previously shown that inv is necessary for efficient penetration of the intestinal epithelium by Yersinia enterocolitica. The present study was initiated to determine whether other known Yersinia invasion factors could promote uptake of the bacteria by mice in the absence of invasion. In addition, the roles of these three invasion factors in the survival of the bacteria, lethality for mice, and development of pathology were compared. We found that YadA is necessary for persistence of Y. enterocolitica in Peyer's patches, and consistent with this observation, the yadA mutant was avirulent for mice infected either orally or intraperitoneally. In addition, the inv yadA double mutant was avirulent. Histological and immunohistological examination of the Peyer's patches of infected mice indicated that despite the presence of large numbers of CFU at 24 h the yadA and ail yadA mutants cause only minimal pathology and recruitment of macrophages. At 42 h postinfection, Peyer's patches from mice infected with the inv mutant showed no pathology, despite the prediction that some of the mice by this time would be colonized. However, at 72 h, inflammation and necrosis were evident in some Peyer's patches. Together, these observations suggest that for visible pathology to develop, a threshold number of bacteria (> 10(5)) is needed and the bacteria need to persist for more than 24 h. Lastly, YadA but not Ail may play a role in the less efficient, delayed invasion of the intestinal epithelium observed for the inv mutant.
机译：多年以来一直假设耶尔森菌属的能力。侵袭组织培养细胞反映了它们穿透肠道上皮的能力，并且这种能力是疾病过程的重要方面。耶尔森氏菌的三种不同基因。已经鉴定出与组织培养物侵袭表型有关的那些：inv，ail和yadA。先前已经表明，肠球菌耶尔森氏菌有效渗透inv对于肠上皮是必需的。开始本研究以确定在没有侵袭的情况下其他已知的耶尔森氏菌侵袭因子是否可以促进小鼠对细菌的吸收。此外，还比较了这三种入侵因子在细菌存活，小鼠致死率和病理发展中的作用。我们发现YadA对于在淋巴集结中持续存在小肠结肠炎耶尔森菌是必要的，并且与该观察结果一致，yadA突变体对口服或腹膜内感染的小鼠无毒。另外，inv yadA双突变体是无毒的。对感染小鼠的派伊尔氏斑的组织学和免疫组织学检查表明，尽管在24小时存在大量CFU，但yadA和ail yadA突变体仅引起最小的病理学和巨噬细胞募集。感染后42小时，尽管有人预测到此时某些小鼠会被定殖，但感染inv突变体的小鼠的Peyer斑块未显示任何病理。但是，在72小时时，在一些Peyer斑块中明显出现了炎症和坏死。总之，这些观察结果表明，要发展可见的病理学，就需要一定数量的细菌（> 10（5）），并且细菌必须持续存在24小时以上。最后，YadA而不是Ail可能在inv突变体观察到的肠上皮的低效，延迟侵袭中起作用。

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