Acid-regulated gene expression of Helicobacter pylori: Insight into acid protection and gastric colonization.

Acid-regulated gene expression of Helicobacter pylori: Insight into acid protection and gastric colonization.
复制标题

DOI:
10.1111/hel.12490
复制
发表时间:
2018-06
期刊:
影响因子:
4.4
通讯作者:
Scott DR
Scott DR
中科院分区:
医学2区
文献类型:
--
作者:
Marcus EA;Sachs G;Scott DR

文献摘要

参考文献

被引文献

相似文献

病原体幽门螺杆菌遇到许多压力,因为它的过境和感染胃上皮。胃酸是细菌在初始感染和建立持续感染期间遇到的主要应激源。H.幽门螺杆菌启动对酸的快速反应,以维持细胞内pH和适合嗜中性粒细胞的质子动力。但H.幽门螺杆菌也可以作为转录触发因子,以增加破坏宿主防御所需的其他致病因子的水平,如酸适应、抗氧化剂、鞭毛合成和组装以及CagA分泌。H. pylori在尿素存在下在pH 3.0、4.5、6.0与非酸性pH下进行酸攻击4小时,然后进行RNAseq分析和qPCR。在相同条件下监测细胞质pH。大约250个基因被诱导,在酸性pH值下,相同数量的基因被抑制。编码抗氧化蛋白,鞭毛结构蛋白,特别是2类基因,T4 SS/CagPAI,FoF 1-ATP酶和蛋白质参与酸驯化的高表达在酸性pH值。细胞质pH值从7.8在pHout的8.0下降到6.0在pHout的3.0。这些结果表明,增加细胞外或细胞内酸度或两者都被细菌检测到,并作为一个信号,启动增加生产的保护性和致病性因子所需的对抗宿主防御持续感染。这些变化取决于酸度和酸暴露的时间,引发对定植所需环境的协调反应。
The pathogen Helicobacter pylori encounters many stressors as it transits to and infects the gastric epithelium. Gastric acidity is the predominate stressor encountered by the bacterium during initial infection and establishment of persistent infection. H. pylori initiates a rapid response to acid to maintain intracellular pH and proton motive force appropriate for a neutralophile. However, acid sensing by H. pylori may also serve as a transcriptional trigger to increase the levels of other pathogenic factors needed to subvert host defenses such as acid acclimation, antioxidants, flagellar synthesis and assembly, and CagA secretion. H. pylori were acid-challenged at pH 3.0, 4.5, 6.0 vs non-acidic pH for four hours in the presence of urea, followed by RNAseq analysis and qPCR. Cytoplasmic pH was monitored under the same conditions. About 250 genes were induced and an equal number were repressed at acidic pHs. Genes encoding for antioxidant proteins, flagellar structural proteins, particularly class 2 genes, T4SS/CagPAI, FoF1-ATPase and proteins involved in acid acclimation were highly expressed at acidic pH. Cytoplasmic pH decreased from 7.8 at pHout of 8.0 to 6.0 at pHout of 3.0. These results suggest that increasing extracellular or intracellular acidity or both are detected by the bacterium and serve as a signal to initiate increased production of protective and pathogenic factors needed to counter host defenses for persistent infection. These changes are dependent on degree of acidity and time of acid exposure, triggering a coordinated response to the environment required for colonization.
DOI: 10.1128/jb.184.17.4775-4782.2002
发表时间: 2002-09-01
影响因子: 3.2
作者:
Chiba, S;Akiyama, Y;Ito, K
通讯作者: Ito, K
DOI: 10.1371/journal.ppat.0020110
发表时间: 2006-10
期刊: PLOS PATHOGENS
影响因子: 6.7
作者:
Aspholm, Marina;Olfat, Farzad O.;Norden, Jenny;Sonden, Berit;Lundberg, Carina;Sjostrom, Rolf;Altraja, Siiri;Odenbreit, Stefan;Haas, Rainer;Wadstrom, Torkel;Engstrand, Lars;Semino-Mora, Cristina;Liu, Hui;Dubois, Andre;Teneberg, Susann;Arnqvist, Anna;Boren, Thomas
通讯作者: Boren, Thomas
DOI: 10.1073/pnas.90.12.5791
发表时间: 1993-06-15
影响因子: 11.1
作者:
COVACCI, A;CENSINI, S;RAPPUOLI, R
通讯作者: RAPPUOLI, R
DOI: 10.1128/jb.172.2.771-778.1990
发表时间: 1990-02-01
影响因子: 3.2
作者:
FOSTER, JW;HALL, HK
通讯作者: HALL, HK
DOI: 10.1128/jb.01001-13
发表时间: 2013-12-01
影响因子: 3.2
作者:
Benoit, Stephane L.;Bayyareddy, Krishnareddy;Maier, Robert J.
通讯作者: Maier, Robert J.