Dataset Information

The proteomic changes of GES1 infected by Helicobacter pylori

ABSTRACT: We explored the proteomic changes in GES1 cells induced by H.pylori. GES1 cells cocultured with increasing concentrations of H.pylori were subjected to quantitative proteomic analyses using label-free methods for relative quantitation.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Sisi Wei

LAB HEAD: Lianmei Zhao

PROVIDER: PXD025281 | Pride | 2022-02-14

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

Items per page:

1 - 5 of 24

Publications

Outer Membrane Vesicles Secreted by Helicobacter pylori Transmitting Gastric Pathogenic Virulence Factors.

Wei Sisi S Li Xiaoya X Wang Jingjing J Wang Yaojie Y Zhang Cong C Dai Suli S Wang Xian X Deng Xiaoqing X Zhao Lianmei L Shan Baoen B

ACS omega 20211228 1

Helicobacter pylori (H. pylori) is known to be a major pathogen causing gastric diseases through its direct localization in gastric epithelium cells. H. pylori releases outer membrane vesicles (OMVs) throughout the growth process. The content, function, and mechanism of H. pylori OMVs in gastric epithelial cells remain unclear. In this study, we extracted and characterized H. pylori OMVs of two strains (standard strain NCTC11637 and clinical strain Hp-400) and ...[more]

PMID: 35036696

Similar Datasets

Project description:Helicobacter pylori (H. pylori) classified as a class I carcinogen by the World Health Organization (WHO) plays an important role in the progression of chronic gastritis and the development of gastric cancer. A major bioactive component of Evodia rutaecarpa, evodiamine, has been known for its anti-bacterial effect and anti-cancer effects. However, the inhibitory effect of evodiamine against H. pylori is not yet known and the inhibitory mechanisms of evodiamine against gastric cancer cells are yet to be elucidated concretely. In this study, therefore, anti-bacterial effect of evodiamine on H. pylori growth and its inhibitory mechanisms as well as anti-inflammatory effects and its mechanisms of evodiamine on H. pylori-induced inflammation were investigated in vitr. Results of this study showed the growth of the H. pylori reference strains and clinical isolates were inhibited by evodiamine. It was considered one of the inhibitory mechanisms that evodiamine downregulated both gene expressions of replication and transcription machineries of H. pylori. Treatment of evodiamine also induced downregulation of urease and diminished translocation of cytotoxin-associated antigen A (CagA) and vacuolating cytotoxin A (VacA) proteins into gastric adenocarcinoma (AGS) cells. This may be resulted from the reduction of CagA and VacA expressions as well as the type IV secretion system (T4SS) components and secretion system subunit protein A (SecA) protein which are involved in translocation of CagA and VacA into host cells, respectively. In particular, evodiamine inhibited the activation of signaling proteins such as the nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) and the mitogen-activated protein kinase (MAPK) pathway induced by H. pylori infection. It consequently might contribute to reduction of interleukin (IL)-8 production in AGS cells. Collectively, these results suggest anti-bacterial and anti-inflammatory effects of evodiamine against H. pylori.

			Action	DRS
	GES1_11637_1_10_2.raw	Raw
	GES1_11637_1_10_3.raw	Raw
	GES1_11637_1_1_1.msf	Msf
	GES1_11637_1_1_1.raw	Raw
	GES1_11637_1_1_10.raw	Raw

Dataset Information

The proteomic changes of GES1 infected by Helicobacter pylori

Dataset's files

Publications

Outer Membrane Vesicles Secreted by <i>Helicobacter pylori</i> Transmitting Gastric Pathogenic Virulence Factors.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets