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首页> 外文期刊>Infection and immunity >Immune response to the iron-deprivation-induced proteins of Salmonella typhi in typhoid fever.
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Immune response to the iron-deprivation-induced proteins of Salmonella typhi in typhoid fever.

机译：伤寒中对伤寒沙门氏菌的铁剥夺诱导蛋白的免疫反应。

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摘要

Iron starvation conditions limited the growth of Salmonella typhi, as evidenced by an increase in the lag phase of a culture and a decrease in the number of bacteria reached in the stationary phase. The analysis of the outer membrane of bacteria grown under these conditions identified new protein components with apparent molecular weights of 83,000, 78,000, and 69,000. The extent of induction of these proteins was regulated by increased iron deprivation. Immunoblot analysis showed that the serum of patients with typhoid fever exhibited an immunoglobulin G response to these iron-deprivation-induced proteins. The results of bioassays and DNA-DNA hybridization experiments indicated that pathogenic strains of S. typhi produced enterochelin but not aerobactin. Immunodetection with an anti-FepA antiserum confirmed that one of the induced proteins is the S. typhi analog of the Escherichia coli fepA gene product. These studies suggest a role for iron uptake in the pathogenesis of typhoid fever and confirm the immunogenicity of some of the outer membrane proteins of this pathogen.
机译：铁饥饿条件限制了伤寒沙门氏菌的生长，这可以通过培养物的迟滞期增加和静止期达到的细菌数量减少来证明。在这些条件下生长的细菌的外膜的分析确定了表观分子量分别为83,000、78,000和69,000的新蛋白质成分。这些蛋白质的诱导程度通过增加铁剥夺来调节。免疫印迹分析表明，伤寒患者的血清对这些铁剥夺诱导的蛋白表现出免疫球蛋白G的反应。生物测定和DNA-DNA杂交实验的结果表明，伤寒沙门氏菌的致病菌株产生肠螯合素而不产生气杆菌素。用抗FepA​​抗血清进行免疫检测证实，诱导的蛋白质之一是大肠杆菌fepA基因产物的伤寒沙门氏菌类似物。这些研究表明铁在伤寒发病机理中的作用，并证实了该病原体某些外膜蛋白的免疫原性。

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