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首页> 外文期刊>Infection and immunity >Role for Neutrophils in Host Immune Responses and Genetic Factors That Modulate Resistance to Salmonella enterica Serovar Typhimurium in the Inbred Mouse Strain SPRET/Ei
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Role for Neutrophils in Host Immune Responses and Genetic Factors That Modulate Resistance to Salmonella enterica Serovar Typhimurium in the Inbred Mouse Strain SPRET/Ei

机译：中性粒细胞在自交系小鼠SPRET / Ei中对肠道沙门氏菌鼠伤寒沙门氏菌抗性的宿主免疫反应和遗传因素中的作用。

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Infection with Salmonella enterica serovar Typhimurium is a complex disease in which the host-bacterium interactions are strongly influenced by genetic factors of the host. We demonstrate that SPRET/Ei, an inbred mouse strain derived from Mus spretus, is resistant to S. Typhimurium infections. The kinetics of bacterial proliferation, as well as histological examinations of tissue sections, suggest that SPRET/Ei mice can control bacterial multiplication and spreading despite significant attenuation of the cytokine response. The resistance of SPRET/Ei mice to S. Typhimurium infection is associated with increased leukocyte counts in the circulation and enhanced neutrophil influx into the peritoneum during the course of infection. A critical role of neutrophils was confirmed by neutrophil depletion: neutropenic SPRET/Ei mice were sensitive to infection with S. Typhimurium and showed much higher bacterial loads. To identify genes that modulate the natural resistance of SPRET/Ei mice to S. Typhimurium infection, we performed a genome-wide study using an interspecific backcross between C3H/HeN and SPRET/Ei mice. The results of this analysis demonstrate that at least two loci, located on chromosomes 6 and 11, affect survival following lethal infection with S. Typhimurium. These two loci contain several interesting candidate genes which may have important implications for the search for genetic factors controlling Salmonella infections in humans and for our understanding of complex host-pathogen interactions in general.
机译：肠道沙门氏菌血清鼠伤寒沙门氏菌感染是一种复杂的疾病，其中宿主与细菌的相互作用受宿主遗传因素的强烈影响。我们证明SPRET / Ei，衍生自穆斯普勒斯的近交小鼠品系，对鼠伤寒沙门氏菌感染具有抗性。细菌增殖的动力学以及组织切片的组织学检查表明，尽管细胞因子反应显着减弱，SPRET / Ei小鼠仍可以控制细菌的繁殖和扩散。 SPRET / Ei小鼠对鼠伤寒沙门氏菌感染的抗性与感染过程中循环中白细胞计数增加和嗜中性白细胞向腹膜的流入增加有关。中性粒细胞耗竭证实了中性粒细胞的关键作用：中性白细胞减少症SPRET / Ei小鼠对鼠伤寒链球菌感染敏感，并显示出更高的细菌载量。为了鉴定调节SPRET / Ei小鼠对鼠伤寒沙门氏菌感染的天然抗性的基因，我们使用C3H / HeN和SPRET / Ei小鼠之间的种间回交进行了全基因组研究。该分析的结果表明，位于鼠伤寒沙门氏菌致死性感染后，位于染色体6和11上的至少两个基因座影响生存。这两个基因座包含几个有趣的候选基因，这些基因可能对寻找控制人类沙门氏菌感染的遗传因素以及我们对一般宿主-病原体相互作用的理解具有重要意义。

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