Fernandez-Beros M E, Gonzalez C, McIntosh M A, Cabello F C
Department of Microbiology and Immunology, New York Medical College, Valhalla 10595.
Infect Immun. 1989 Apr;57(4):1271-5. doi: 10.1128/iai.57.4.1271-1275.1989.
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.
缺铁条件限制了伤寒沙门氏菌的生长，培养物延滞期的延长以及稳定期细菌数量的减少证明了这一点。对在这些条件下生长的细菌外膜进行分析，鉴定出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受缺铁加剧的调节。免疫印迹分析表明，伤寒热患者的血清对这些缺铁诱导蛋白表现出免疫球蛋白G反应。生物测定和DNA-DNA杂交实验结果表明，伤寒沙门氏菌的致病菌株产生肠螯合素但不产生气杆菌素。用抗FepA抗血清进行免疫检测证实，其中一种诱导蛋白是大肠杆菌fepA基因产物的伤寒沙门氏菌类似物。这些研究表明铁摄取在伤寒热发病机制中起作用，并证实了该病原体一些外膜蛋白的免疫原性。
