Evidence map›Paper›PMID 27048452›Full record

ArticleDigestive diseases and sciences2016

The Gastric Mucosa from Patients Infected with CagA+ or VacA+ Helicobacter pylori Has a Lower Level of Dual Oxidase-2 Expression than Uninfected or Infected with CagA-/VacA- H. pylori.

Hongqian Li, Yunfeng Zhou, Yufeng Zheng, Hong Guo, Lei Gao, Pan Chen, Dandan Feng, Lijuan Wu, Moli Yang, Yanli Qi and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Digestive diseases and sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 13 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 2 countries.

Hongqian LiDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China.
Yunfeng ZhouShenzhen University Health Science Center, 3688 Nanhai Avenue, Nanshan District, Shenzhen, 518060, Guangdong, China.
Yufeng ZhengDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China.
Hong GuoDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China.
Lei GaoDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China.
Pan ChenDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China.
Dandan FengDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China.
Lijuan WuDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China.
Moli YangDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China.
Yanli QiDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China.
Hao GuoDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China.
Yongchao ChangDepartment of Clinical Laboratory, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China.
Fong-Fong ChuDepartment of Cancer Genetics and Epigenetics, Beckman Research Institute of City of Hope, Duarte, CA, 91010, USA.
Qiang GaoDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital and Clinical Medical College, Henan University of Science and Technology, 636 Guanlin Road, Luolong District, Luoyang, 471023, Henan Province, China. gaoq@mail.haust.edu.cn.
First Affiliated Hospital of Henan University of Science and Technology · CNHenan University of Science and Technology · CNCancer Genetics (United States) · USChina Rehabilitation Research Center · CNShenzhen University Health Science Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHelicobacter pylori (H. pylori) is a well-recognized gastroduodenal pathogen and class I carcinogen. Dual oxidase-2 (DUOX2), a member of NADPH oxidase family, has several critical physiological functions, including thyroid hormone biosynthesis and host mucosal defense.

aimTo investigate the effect of H. pylori infection on DUOX2 gene expression in human stomach. MATERIALS AND

methodsThe biopsies were obtained from patients who underwent endoscopic diagnosis. The patient serum was assayed for two virulence factors of H. pylori, CagA IgG and VacA. The inflammation in gastric mucosa was analyzed with histology. Real-time quantitative PCR was used to detect the expression of three members of NADPH oxidase, NOX1, NOX2, and DUOX2, as well as lactoperoxidase (LPO) in the gastric mucosa. NOX2, DUOX2, and myeloperoxidase (MPO) protein levels were quantified by Western blots or immunohistochemistry.

resultsThe H. pylori-infected gastric mucosa had more severe inflammation than uninfected samples. However, the expression of DUOX2 mRNA and protein was lower in gastric mucosa of patients with H. pylori infection compared to the uninfected. Among the H. pylori-infected patients, those having CagA IgG or VacA in the serum had lower DUOX2 expression levels than those infected with H. pylori without either virulence factor. The NOX2 and MPO levels were higher in those patients infected with H. pylori irrespective of the virulence factors than those uninfected patients. NOX1 and LPO mRNA were undetectable in the gastric mucosa.

conclusionCagA+ or VacA+ H. pylori in the stomach of patients may suppress DUOX2 expression to promote its own survival. Increased NOX2 could not eliminate H. pylori infection.

Indexed as

AdolescentAdultAgedAntibodies, BacterialAntigens, BacterialBacterial ProteinsBlotting, WesternDual OxidasesEnzyme-Linked Immunosorbent AssayFemaleGastric MucosaGastritisGastritis, AtrophicHelicobacter InfectionsHelicobacter pyloriHumansAntibodies, BacterialAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriCYBB protein, humanDual OxidasesDUOX2 protein, humanImmunoglobulin GLactoperoxidaseMembrane GlycoproteinsNADPH Oxidase 1NADPH Oxidase 2NADPH OxidasesNOX1 protein, humanPeroxidaseRNA, MessengerVacA protein, Helicobacter pyloriDual oxidase-2 (DUOX2)Gastric mucosaHelicobacter pylori (H. pylori)Lactoperoxidase (LPO)NOX2

Identifiers

PMID27048452
PMCPMC4943970
OpenAlexW2316405468

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.