空肠弯曲杆菌调节人肠上皮细胞活性氧产生和NADPH氧化酶1表达

IF 2.6 2区 生物学 Q3 CELL BIOLOGY
Geunhye Hong, Cadi Davies, Zahra Omole, Janie Liaw, Anna D. Grabowska, Barbara Canonico, Nicolae Corcionivoschi, Brendan W. Wren, Nick Dorrell, Abdi Elmi, Ozan Gundogdu
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引用次数: 0

摘要

空肠弯曲杆菌是世界范围内食源性胃肠炎的主要细菌。在机制上,这种病原体如何与人类肠上皮细胞(IECs)的内在防御机制相互作用仍然是难以捉摸的。为了解决这个问题,我们研究了空肠梭菌如何抵消IECs细胞内和细胞外活性氧(ROS)。我们的研究表明,空肠梭菌对人T84和Caco-2细胞胞内和胞外ROS产生的调节存在差异。空肠梭菌下调IECs中产生活性氧的关键酶烟酰胺腺嘌呤二核苷酸磷酸(NAPDH)氧化酶(NOX1)和抗氧化防御基因CAT和SOD1的转录和翻译。此外,二苯基碘(DPI)和siRNA对NOX1的抑制降低了空肠C.在T84和Caco-2细胞内相互作用、侵袭和细胞内存活的能力。总的来说,这些发现为空肠梭菌如何调节IEC防御机制提供了机制上的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Campylobacter jejuni Modulates Reactive Oxygen Species Production and NADPH Oxidase 1 Expression in Human Intestinal Epithelial Cells
Campylobacter jejuni is the major bacterial cause of foodborne gastroenteritis worldwide. Mechanistically, how this pathogen interacts with intrinsic defence machinery of human intestinal epithelial cells (IECs) remains elusive. To address this, we investigated how C. jejuni counteracts the intracellular and extracellular reactive oxygen species (ROS) in IECs. Our work shows that C. jejuni differentially regulates intracellular and extracellular ROS production in human T84 and Caco-2 cells. C. jejuni downregulates the transcription and translation of nicotinamide adenine dinucleotide phosphate (NAPDH) oxidase (NOX1), a key ROS-generating enzyme in IECs and antioxidant defence genes CAT and SOD1. Furthermore, inhibition of NOX1 by diphenylene iodonium (DPI) and siRNA reduced C. jejuni ability to interact, invade, and intracellularly survive within T84 and Caco-2 cells. Collectively, these findings provide mechanistic insight into how C. jejuni modulates the IEC defence machinery.
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来源期刊
Cellular Microbiology
Cellular Microbiology 生物-微生物学
CiteScore
9.70
自引率
0.00%
发文量
26
审稿时长
3 months
期刊介绍: Cellular Microbiology aims to publish outstanding contributions to the understanding of interactions between microbes, prokaryotes and eukaryotes, and their host in the context of pathogenic or mutualistic relationships, including co-infections and microbiota. We welcome studies on single cells, animals and plants, and encourage the use of model hosts and organoid cultures. Submission on cell and molecular biological aspects of microbes, such as their intracellular organization or the establishment and maintenance of their architecture in relation to virulence and pathogenicity are also encouraged. Contributions must provide mechanistic insights supported by quantitative data obtained through imaging, cellular, biochemical, structural or genetic approaches.
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