Evidence map›Paper›PMID 27672275›Full record

ArticleWorld journal of gastroenterology2016

Impact of Helicobacter pylori on the healing process of the gastric barrier.

Eliza Mnich, Magdalena Kowalewicz-Kulbat, Paulina Sicińska, Krzysztof Hinc, Michał Obuchowski, Adrian Gajewski, Anthony P Moran, Magdalena Chmiela

Open access · greenAbstract read
In one paragraph

Article in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 50 citations in OpenAlex.

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  11. Can Pyomelanin Produced byInternational journal of molecular sciences · 2023
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  13. In Vitro and In Vivo Biocompatibility of Natural and SyntheticInternational journal of molecular sciences · 2023
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  16. Equilibria of complexes in the aqueous cobalt(II)-Computational and structural biotechnology journal · 2023
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  20. Interference of LPSCells · 2021
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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

8 authors at 1 institution in 1 country.

Eliza MnichEliza Mnich, Magdalena Kowalewicz-Kulbat, Adrian Gajewski, Magdalena Chmiela, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Łódź, 90-237 Łódź, Poland.
Magdalena Kowalewicz-KulbatEliza Mnich, Magdalena Kowalewicz-Kulbat, Adrian Gajewski, Magdalena Chmiela, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Łódź, 90-237 Łódź, Poland.
Paulina SicińskaEliza Mnich, Magdalena Kowalewicz-Kulbat, Adrian Gajewski, Magdalena Chmiela, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Łódź, 90-237 Łódź, Poland.
Krzysztof HincEliza Mnich, Magdalena Kowalewicz-Kulbat, Adrian Gajewski, Magdalena Chmiela, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Łódź, 90-237 Łódź, Poland.
Michał ObuchowskiEliza Mnich, Magdalena Kowalewicz-Kulbat, Adrian Gajewski, Magdalena Chmiela, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Łódź, 90-237 Łódź, Poland.
Adrian GajewskiEliza Mnich, Magdalena Kowalewicz-Kulbat, Adrian Gajewski, Magdalena Chmiela, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Łódź, 90-237 Łódź, Poland.
Anthony P MoranEliza Mnich, Magdalena Kowalewicz-Kulbat, Adrian Gajewski, Magdalena Chmiela, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Łódź, 90-237 Łódź, Poland.
Magdalena ChmielaEliza Mnich, Magdalena Kowalewicz-Kulbat, Adrian Gajewski, Magdalena Chmiela, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Łódź, 90-237 Łódź, Poland.
University of Magdalena · CO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo determine the impact of selected well defined Helicobacter pylori (H. pylori) antigens on gastric barrier cell turnover.

methodsIn this study, using two cellular models of gastric epithelial cells and fibroblasts, we have focused on exploring the effects of well defined H. pylori soluble components such as glycine acid extract antigenic complex (GE), subunit A of urease (UreA), cytotoxin associated gene A protein (CagA) and lipopolysaccharide (LPS) on cell turnover by comparing the wound healing capacity of the cells in terms of their proliferative and metabolic activity as well as cell cycle distribution. Toxic effects of H. pylori components have been assessed in an association with damage to cell nuclei and inhibition of signal transducer and activator of transcription 3 (STAT3) phosphorylation.

resultsWe showed that H. pylori GE, CagA and UreA promoted regeneration of epithelial cells and fibroblasts, which is necessary for effective tissue healing. However, in vivo increased proliferative activity of these cells may constitute an increased risk of gastric neoplasia. In contrast, H. pylori LPS showed a dose-dependent influence on the process of wound healing. At a low concentration (1 ng/mL) H. pylori LPS accelerated of healing epithelial cells, which was linked to significantly enhanced cell proliferation and MTT reduction as well as lack of alterations in cell cycle and downregulation of epidermal growth factor (EGF) production as well as cell nuclei destruction. By comparison, H. pylori LPS at a high concentration (25 ng/mL) inhibited the process of wound repair, which was related to diminished proliferative activity of the cells, cell cycle arrest, destruction of cell nuclei and downregulation of the EGF/STAT3 signalling pathway.

conclusionIn vivo H. pylori LPS driven effects might lead to the maintenance of chronic inflammatory response and pathological disorders on the level of the gastric mucosal barrier.

Indexed as

Helicobacter pyloriAnimalsAntigens, BacterialBacterial ProteinsCell CycleCell DivisionCell Line, TumorCell MovementCell ProliferationCells, CulturedCell SurvivalEpithelial CellsGastric MucosaGlycineGuinea PigsHelicobacter InfectionsAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriGlycineLipopolysaccharidesUreaseGastric barrier dysfunctionHelicobacter pyloriWound healing

Identifiers

PMID27672275
PMCPMC5011668
OpenAlexW2515384064

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.