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首页> 外文期刊>Genes and immunity. >Identification of genetic loci controlling bacterial clearance in experimental Salmonella enteritidis infection: an unexpected role of Nramp1 (Slc11a1) in the persistence of infection in mice.
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Identification of genetic loci controlling bacterial clearance in experimental Salmonella enteritidis infection: an unexpected role of Nramp1 (Slc11a1) in the persistence of infection in mice.

机译：鉴定控制实验性肠炎沙门氏菌感染中细菌清除的遗传基因座：Nramp1（Slc11a1）在小鼠感染持久性中的意外作用。

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The Gram-negative bacteria, Salmonella, cause a broad spectrum of clinical diseases in both animals and humans ranging from asymptomatic carriage to life-threatening sepsis. We have developed a model to study the contribution of genetic factors to the susceptibility of 129sv and C57BL/6J inbred mice to Salmonella enteritidis during the late phase of infection. C57BL/6J mice were able to eliminate completely sublethal inoculums of S. enteritidis from their reticuloendothelial system, whereas 129sv mice could not even after 60 days post inoculation. A genome scan performed on 302 (C57BL/6J x 129sv) F2 progeny identified three dominant loci (designated Ses1 to Ses3) that are associated with disease susceptibility in 129sv mice. Two highly significant linkages were identified on chromosomes 1 (Ses1) and 7 (Ses2) with respective LOD scores of 9.9 (P = 1.4 x 10(-11)) at D1Mcg5 and 4.0 (P = 1.9 x 10(-5)) at D7Mit62. One highly suggestive QTL was located on chromosomes15 (Ses3) with a LOD score 3.4 (P = 1.2 x 10(-4)). The estimated effects of Ses1, Ses2 and Ses3 on the bacterial clearance were greater in females. Using a model of three loci, with interaction between Ses1 and Ses2 and sex as a covariate, the three QTLs explained 32% of the phenotypic variance. The candidacy of Nramp1 as the gene for Ses1 was evaluated using mice carrying a null allele at Nramp1 (129sv-Nramp1(tm1Mcg)). These mice have a significantly lower spleen bacterial load compared to the wild-type 129sv mice, strongly suggesting the involvement of Nramp1 in controlling S. enteritidis clearance during the late phase of infection.
机译：革兰氏阴性细菌沙门氏菌在动物和人类中引起广泛的临床疾病，从无症状携带到威胁生命的败血症。我们已经开发了一个模型来研究遗传因素对感染后期阶段对129sv和C57BL / 6J近交小鼠对肠炎沙门氏菌的敏感性的影响。 C57BL / 6J小鼠能够从其网状内皮系统中完全消除肠炎链球菌的致死菌接种，而129sv小鼠甚至在接种后60天仍无法消除。对302（C57BL / 6J x 129sv）F2后代进行的基因组扫描确定了与129sv小鼠的疾病易感性相关的三个显性位点（称为Ses1至Ses3）。在1号染色体（Ses1）和7号染色体（Ses2）上鉴定到两个高度重要的连锁，D1Mcg5的LOD得分分别为9.9（P = 1.4 x 10（-11）），D1Mcg5的LOD得分为4.0（P = 1.9 x 10（-5））。 D7Mit62。一个高度提示性的QTL位于染色体15（Ses3）上，LOD得分为3.4（P = 1.2 x 10（-4））。女性中，Ses1，Ses2和Ses3对细菌清除的估计影响更大。使用三个基因座的模型，将Ses1和Ses2与性别之间的相互作用作为协变量，这三个QTL解释了32％的表型变异。使用在Nramp1（129sv-Nramp1（tm1Mcg））携带无效等位基因的小鼠评估了Nramp1作为Ses1基因的候选资格。与野生型129sv小鼠相比，这些小鼠的脾脏细菌载量显着降低，这强烈暗示了Nramp1在感染后期可参与控制肠炎沙门氏菌的清除。

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