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Host Susceptibility to the Attaching and Effacing Bacterial Pathogen Citrobacter rodentium

机译：宿主对细菌病原体柠檬酸杆菌的附着和脱落的敏感性

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Many studies have shown that genetic susceptibility plays a key role in determining whether bacterial pathogens successfully infect and cause disease in potential hosts. Surprisingly, whether host genetics influence the pathogenesis of attaching and effacing (A/E) bacteria such as enteropathogenic and enterohemorrhagic Escherichia coli has not been examined. To address this issue, we infected various mouse strains with Citrobacter rodentium, a member of the A/E pathogen family. Of the strains tested, the lipopolysaccharide (LPS) nonresponder C3H/HeJ mouse strain experienced more rapid and extensive bacterial colonization than did other strains. Moreover, the high bacterial load in these mice was associated with accelerated crypt hyperplasia, mucosal ulceration, and bleeding, together with very high mortality rates. Interestingly, the basis for the increased susceptibility was not due to LPS hyporesponsiveness, as the genetically related but LPS-responsive C3H/HeOuJ and C3H/HeN mouse strains were also susceptible to infection. Analysis of the intestinal pathology in these susceptible strains revealed significant crypt epithelial cell apoptosis (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end label staining) as well as bacterial translocation to the mesenteric lymph nodes. Further studies with infection of SCID (T- and B-lymphocyte-deficient) C3H/HeJ mice demonstrated that loss of lymphocytes had no effect on bacterial numbers but did reduce crypt cell apoptosis and delayed mortality. These studies thus identify the adaptive immune system, crypt cell apoptosis, and bacterial translocation but not LPS responsiveness as contributing to the tissue pathology and mortality seen during C. rodentium infection of highly susceptible mouse strains. Determining the basis for these strains' susceptibility to intestinal colonization by an A/E pathogen will be the focus of future studies.
机译：许多研究表明，遗传易感性在确定细菌病原体是否成功感染并在潜在宿主中引起疾病​​方面起着关键作用。令人惊讶的是，尚未检查宿主遗传学是否影响附着和消失的细菌（A / E）的发病机理，例如肠致病性和肠出血性大肠杆菌。为解决此问题，我们用A / E病原体家族成员 Centrobacter rodentium 感染了多种小鼠品系。在测试的菌株中，脂多糖（LPS）无应答C3H / HeJ小鼠菌株比其他菌株经历了更快，更广泛的细菌定植。而且，这些小鼠中的高细菌负荷与加速的隐窝增生，粘膜溃疡和出血有关，并且死亡率很高。有趣的是，易感性增加的基础不是由于LPS反应低下，因为与基因相关，但LPS反应性C3H / HeOuJ和C3H / HeN小鼠品系也容易感染。对这些易感菌株的肠道病理学分析表明，隐窝上皮细胞凋亡显着（末端脱氧核苷酸转移酶介导的dUTP-生物素缺口末端标记染色），以及细菌易位至肠系膜淋巴结。对SCID（T和B淋巴细胞缺陷型）C3H / HeJ小鼠感染的进一步研究表明，淋巴细胞的丢失对细菌数量没有影响，但确实减少了隐窝细胞凋亡并延迟了死亡率。因此，这些研究确定了适应性免疫系统，隐窝细胞凋亡和细菌易位，但不是LPS反应性导致了 C 期间的组织病理学和死亡率。高度易感小鼠品系的 rodentium 感染。确定这些菌株对A / E病原菌对肠道菌落的敏感性的基础将是未来研究的重点。

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