[推测的调节蛋白STM14_3514减少鼠伤寒沙门氏菌侵袭上皮细胞]。

微生物学报 Pub Date : 2017-04-04
Lingyan Jiang, Qixing Zhou, Peisheng Wang, Xiaohan Jiang, Lu Feng
{"title":"[推测的调节蛋白STM14_3514减少鼠伤寒沙门氏菌侵袭上皮细胞]。","authors":"Lingyan Jiang,&nbsp;Qixing Zhou,&nbsp;Peisheng Wang,&nbsp;Xiaohan Jiang,&nbsp;Lu Feng","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To study the function and mechanism of STM14_3514 gene that encoded in Salmonella pathogenicity island (SPI)-1 of Salmonella enterica serovar Typhimurium strain ATCC 14028.</p><p><strong>Methods: </strong>We constructed STM14_3514 mutant strain and a complemented strain of the mutant. Through mice experiment, attachment assays, invasion assays, macrophage replication assays, western blot, and Quantitative real-time PCR analysis (qRT-PCR), we compared the virulence of the mutant strain to that of the wild-type 14028.</p><p><strong>Results: </strong>STM14_3514 mutant shows increased virulence to mice, and the bacterial number of STM14_3514 mutant in liver, spleen, and ileum was more abundant than that of the wild-type strain. The increased virulence of STM14_3514 mutant is caused by its elevated invasion ability to epithelial cells (>2-fold and P<0.05). qRT-PCR and western blot results show that STM14_3514 reduced the expression of HilA and another SPI-1invasion locus. Moreover, the repression of HilA by STM14_3514 is mediated by HilC.</p><p><strong>Conclusion: </strong>STM14_3514 is a negative regulator in SPI-1, which can repress HilA and SPI-1invasion locus through HilC, and possibly contribute to the repression on SPI-1 after bacterial invasion.</p>","PeriodicalId":7120,"journal":{"name":"微生物学报","volume":"57 4","pages":"500-12"},"PeriodicalIF":0.0000,"publicationDate":"2017-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Putative regulatory protein STM14_3514 decreases Salmonella Typhimurium invasion of epithelial cells].\",\"authors\":\"Lingyan Jiang,&nbsp;Qixing Zhou,&nbsp;Peisheng Wang,&nbsp;Xiaohan Jiang,&nbsp;Lu Feng\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To study the function and mechanism of STM14_3514 gene that encoded in Salmonella pathogenicity island (SPI)-1 of Salmonella enterica serovar Typhimurium strain ATCC 14028.</p><p><strong>Methods: </strong>We constructed STM14_3514 mutant strain and a complemented strain of the mutant. Through mice experiment, attachment assays, invasion assays, macrophage replication assays, western blot, and Quantitative real-time PCR analysis (qRT-PCR), we compared the virulence of the mutant strain to that of the wild-type 14028.</p><p><strong>Results: </strong>STM14_3514 mutant shows increased virulence to mice, and the bacterial number of STM14_3514 mutant in liver, spleen, and ileum was more abundant than that of the wild-type strain. The increased virulence of STM14_3514 mutant is caused by its elevated invasion ability to epithelial cells (>2-fold and P<0.05). qRT-PCR and western blot results show that STM14_3514 reduced the expression of HilA and another SPI-1invasion locus. Moreover, the repression of HilA by STM14_3514 is mediated by HilC.</p><p><strong>Conclusion: </strong>STM14_3514 is a negative regulator in SPI-1, which can repress HilA and SPI-1invasion locus through HilC, and possibly contribute to the repression on SPI-1 after bacterial invasion.</p>\",\"PeriodicalId\":7120,\"journal\":{\"name\":\"微生物学报\",\"volume\":\"57 4\",\"pages\":\"500-12\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2017-04-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"微生物学报\",\"FirstCategoryId\":\"1089\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"微生物学报","FirstCategoryId":"1089","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

目的:研究肠沙门氏菌血清型鼠伤寒杆菌ATCC 14028沙门氏菌致病性岛(SPI)-1中编码的STM14_3514基因的功能及作用机制。方法:构建STM14_3514突变株及其互补株。通过小鼠实验、附着实验、侵袭实验、巨噬细胞复制实验、western blot和实时荧光定量PCR (Quantitative real-time PCR)分析,我们比较了突变株与野生型14028的毒力。结果:STM14_3514突变株对小鼠的毒力增强,其在肝脏、脾脏和回肠中的细菌数量比野生型菌株丰富。STM14_3514突变体毒力的增强是由于其对上皮细胞的侵袭能力提高(>2倍)所致。结论:STM14_3514是SPI-1的负调控因子,可通过HilC抑制HilA和SPI-1的侵袭位点,可能与细菌侵袭后SPI-1的抑制有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Putative regulatory protein STM14_3514 decreases Salmonella Typhimurium invasion of epithelial cells].

Objective: To study the function and mechanism of STM14_3514 gene that encoded in Salmonella pathogenicity island (SPI)-1 of Salmonella enterica serovar Typhimurium strain ATCC 14028.

Methods: We constructed STM14_3514 mutant strain and a complemented strain of the mutant. Through mice experiment, attachment assays, invasion assays, macrophage replication assays, western blot, and Quantitative real-time PCR analysis (qRT-PCR), we compared the virulence of the mutant strain to that of the wild-type 14028.

Results: STM14_3514 mutant shows increased virulence to mice, and the bacterial number of STM14_3514 mutant in liver, spleen, and ileum was more abundant than that of the wild-type strain. The increased virulence of STM14_3514 mutant is caused by its elevated invasion ability to epithelial cells (>2-fold and P<0.05). qRT-PCR and western blot results show that STM14_3514 reduced the expression of HilA and another SPI-1invasion locus. Moreover, the repression of HilA by STM14_3514 is mediated by HilC.

Conclusion: STM14_3514 is a negative regulator in SPI-1, which can repress HilA and SPI-1invasion locus through HilC, and possibly contribute to the repression on SPI-1 after bacterial invasion.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
7960
期刊介绍: Acta Microbiologica Sinica(AMS) is a peer-reviewed monthly (one volume per year)international journal,founded in 1953.It covers a wide range of topics in the areas of general and applied microbiology.The journal publishes original papers,reviews in microbiological science,and short communications describing unusual observations. Acta Microbiologica Sinica has been indexed in Index Copernicus (IC),Chemical Abstract (CA),Excerpt Medica Database (EMBASE),AJ of Viniti (Russia),Biological Abstracts (BA),Chinese Science Citation Database (CSCD),China National Knowledge Infrastructure(CNKI),Institute of Scientific and Technical Information of China(ISTIC),Chinese Journal Citation Report(CJCR),Chinese Biological Abstracts,Chinese Pharmaceutical Abstracts,Chinese Medical Abstracts and Chinese Science Abstracts.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信