Suppr超能文献

多巴胺诱导的硫酸酯酶及其调节因子是沙门氏菌 Typhimurium 发病机制所必需的。

Dopamine-induced sulfatase and its regulator are required for Salmonella enterica serovar Typhimurium pathogenesis.

机构信息

Department of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI, USA.

出版信息

Microbiology (Reading). 2019 Mar;165(3):302-310. doi: 10.1099/mic.0.000769. Epub 2019 Jan 16.

Abstract

Catecholamine hormones enhance the virulence of pathogenic bacteria. Studies in the 1980s made intriguing observations that catecholamines were required for induction of sulfatase activity in many enteric pathogens, including Salmonella enterica serovar Typhimurium. In this report, we show that STM3122 and STM3124, part of horizontally acquired Salmonella pathogenesis island 13, encode a catecholamine-induced sulfatase and its regulator, respectively. Induction of sulfatase activity was independent of the well-studied QseBC and QseEF two-component regulatory systems. S. Typhimurium 14028S mutants lacking STM3122 or STM3124 showed reduced virulence in zebrafish. Because catecholamines are inactivated by sulfation in the mammalian gut, S. Typhimurium could utilize CA-induced sulfatase to access free catecholamines for growth and virulence.

摘要

儿茶酚胺激素增强了病原菌的毒力。20 世纪 80 年代的研究有一个有趣的发现,儿茶酚胺是许多肠道病原体(包括鼠伤寒沙门氏菌血清型 Typhimurium)诱导磺基转移酶活性所必需的。在本报告中,我们表明,水平获得的沙门氏菌致病岛 13 的一部分 STM3122 和 STM3124 分别编码儿茶酚胺诱导的磺基转移酶及其调节剂。磺基转移酶活性的诱导与研究充分的 QseBC 和 QseEF 双组分调控系统无关。缺乏 STM3122 或 STM3124 的鼠伤寒沙门氏菌 14028S 突变体在斑马鱼中表现出较低的毒力。因为儿茶酚胺在哺乳动物肠道中被磺化而失活,所以鼠伤寒沙门氏菌可以利用 CA 诱导的磺基转移酶来获取游离的儿茶酚胺以促进生长和毒力。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验