Evidence map›Paper›PMID 26197709›Full record

ArticleInternational journal of medical microbiology : IJMM2015

BH3-only protein Bim is associated with the degree of Helicobacter pylori-induced gastritis and is localized to the mitochondria of inflammatory cells in the gastric mucosa.

Yuko Akazawa, Katsuya Matsuda, Hajime Isomoto, Kayoko Matsushima, Yoko Kido, Shigetoshi Urabe, Naoyuki Yamaghchi, Ken Ohnita, Fuminao Takeshima, Hisayoshi Kondo and 5 more

Open access · greenAbstract read
In one paragraph

Article in International journal of medical microbiology : IJMM, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Mitochondria-Microbiota Interaction in Neurodegeneration.Frontiers in aging neuroscience · 2021
    Review
  2. Article
  3. Review
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

15 authors at 4 institutions in 2 countries.

Yuko AkazawaDepartment of Gastroenterology and Hepatology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki City, Nagasaki, 852-8501, Japan; Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, 1-12-4 Sakamoto, Nagasaki City, Nagasaki, 852-8523, Japan. Electronic address: akazaway@nagasaki-u.ac.jp.
Katsuya MatsudaDepartment of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, 1-12-4 Sakamoto, Nagasaki City, Nagasaki, 852-8523, Japan.
Hajime IsomotoDepartment of Gastroenterology and Hepatology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki City, Nagasaki, 852-8501, Japan.
Kayoko MatsushimaDepartment of Gastroenterology and Hepatology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki City, Nagasaki, 852-8501, Japan.
Yoko KidoDepartment of Gastroenterology and Hepatology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki City, Nagasaki, 852-8501, Japan.
Shigetoshi UrabeDepartment of Gastroenterology and Hepatology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki City, Nagasaki, 852-8501, Japan.
Naoyuki YamaghchiDepartment of Gastroenterology and Hepatology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki City, Nagasaki, 852-8501, Japan.
Ken OhnitaDepartment of Gastroenterology and Hepatology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki City, Nagasaki, 852-8501, Japan.
Fuminao TakeshimaDepartment of Gastroenterology and Hepatology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki City, Nagasaki, 852-8501, Japan.
Hisayoshi KondoBiostatistics Section, Division of Scientific Data Registry, Department of Radioisotope Medicine, Atomic Bomb Disease Institute, 1-12-4 Sakamoto, Nagasaki City, Nagasaki, 852-8523, Japan.
Hitoshi TsugawaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinano-cho, Shinjyuku-ku, Tokyo, 1600000, Japan.
Hidekazu SuzukiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinano-cho, Shinjyuku-ku, Tokyo, 1600000, Japan.
Joel MossCardiovascular and Pulmonary Branch, NHLBI, National Institutes of Health, Bethesda, Maryland, United States.
Kazuhiko NakaoDepartment of Gastroenterology and Hepatology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki City, Nagasaki, 852-8501, Japan.
Masahiro NakashimaDepartment of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, 1-12-4 Sakamoto, Nagasaki City, Nagasaki, 852-8523, Japan.
Nagasaki University Hospital · JPHiroshima Red Cross Hospital & Atomic-bomb Survivors Hospital · JPKeio University · JPNational Heart Lung and Blood Institute · US

Funding

ADP-ribosylation CyclesZIAHL000659 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MOSS, JOEL · 2009 to 2025
$29.8M
ADP-RIBOSYLATION CYCLESZ01HL000659 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MOSS, JOEL · 1993 to 2008
$2.1M
Intramural NIH HHS Z01 HL000659
6 · The paper itself

Abstract

BH3-only protein, Bim, is a pro-apoptotic protein that mediates mitochondria-dependent cell death. However, the role of Bim in Helicobacter pylori-associated gastritis remains unclear. This study aimed to assess the cellular localization of Bim and its possible role in H. pylori-induced gastritis. The study was conducted on biopsy specimens obtained from 80 patients who underwent upper gastrointestinal endoscopy (H. pylori-negative: n=30, positive: n=50). Association between Bim mRNA expression and severity of gastritis was evaluated and the localization of Bim was examined by immunofluorescence. Bim mRNA expression was positively correlated with the degree of gastritis, as defined by the Sydney system. Immunohistochemical analysis confirmed increased Bim expression in H. pylori-infected gastric mucosa compared with uninfected mucosa in both humans and mice. Bim localized in myeloperoxidase- and CD138-positive cells of H. pylori-infected lamina propria and submucosa of the gastric tract, indicating that this protein is predominantly expressed in neutrophils and plasma cells. In contrast, Bim did not localize in CD20-, CD3-, or CD68-positive cells. Bim was expressed in the mitochondria, where it was partially co-localized with activated Bax and cleaved-PARP. In conclusion, Bim is expressed in neutrophils and plasma cells in H. pylori-associated gastritis, where it may participate in the termination of inflammatory response by causing mitochondria-mediated apoptosis in specific leucocytes.

Indexed as

AdultAgedAnimalsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11FemaleGastric MucosaGastritisGene Expression RegulationHelicobacter InfectionsHelicobacter pyloriHumansMaleMembrane ProteinsMiceApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl2l11 protein, mouseBcl-2-Like Protein 11Membrane ProteinsProto-Oncogene ProteinsRNA, BacterialApoptosisBaxBcl-2BH3-only proteinBimGastritisHelicobacter pyloriMitochondria

Identifiers

PMID26197709
PMCPMC4556732
OpenAlexW805245881

What OpenQuestion holds

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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.