Evidence map›Paper›PMID 26644382›Full record

ArticleInfection and immunity2016

Gastric Metaplasia Induced by Helicobacter pylori Is Associated with Enhanced SOX9 Expression via Interleukin-1 Signaling.

Takako Serizawa, Yoshihiro Hirata, Yoku Hayakawa, Nobumi Suzuki, Kosuke Sakitani, Yohko Hikiba, Sozaburo Ihara, Hiroto Kinoshita, Hayato Nakagawa, Keisuke Tateishi and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
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  5. NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025
    Review
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  20. Mature gastric chief cells are not required for the development of metaplasia.American journal of physiology. Gastrointestinal and liver physiology · 2018
    Article
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

11 authors at 2 institutions in 1 country.

Takako SerizawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yoshihiro HirataDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan hiratay-int@h.u-tokyo.ac.jp.
Yoku HayakawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Nobumi SuzukiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kosuke SakitaniDivision of Gastroenterology, Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan.
Yohko HikibaDivision of Gastroenterology, Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan.
Sozaburo IharaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hiroto KinoshitaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hayato NakagawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Keisuke TateishiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kazuhiko KoikeDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
The University of Tokyo · JPInstitute for Adult Diseases Asahi Life Foundation · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histopathological changes of the gastric mucosa after Helicobacter pylori infection, such as atrophy, metaplasia, and dysplasia, are considered to be precursors of gastric cancer, yet the mechanisms of histological progression are unknown. The aim of this study was to analyze the histopathological features of the gastric mucosa in mice infected with H. pylori strain PMSS1 in relation to gastric stem cell marker expression. C57BL/6J mice infected with PMSS1 were examined for histopathological changes, levels of proinflammatory cytokines, and expression of stem cell markers. Histopathological gastritis scores, such as atrophy and metaplasia, and levels of proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-α) and interleukin-1β (IL-1β), were increased after PMSS1 infection. Expression levels of the cell proliferation and stem cell markers CD44 and SOX9 were also significantly increased in PMSS1-infected mice. Importantly, almost all metaplastic cells induced by PMSS1 infection expressed SOX9. When IL-1 receptor (IL-1R) knockout mice were infected with PMSS1, metaplastic changes and expression levels of stem cell markers were significantly decreased compared with those in wild-type (WT) mice. In conclusion, H. pylori infection induced the expression of cytokines and stem cell markers and histopathological metaplasia in the mouse gastric mucosa. SOX9 expression, in particular, was strongly associated with metaplastic changes, and these changes were dependent on IL-1 signaling. The results suggested the importance of SOX9 in gastric carcinogenesis.

Indexed as

AnimalsCytokinesGastric MucosaGastritisHelicobacter InfectionsHelicobacter pyloriHyaluronan ReceptorsInterleukin-1MetaplasiaMice, Inbred C57BLMice, KnockoutSignal TransductionSOX9 Transcription FactorCytokinesHyaluronan ReceptorsInterleukin-1Sox9 protein, mouseSOX9 Transcription Factor

Identifiers

PMID26644382
PMCPMC4730566
OpenAlexW2189796606

What OpenQuestion holds

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Registered trials

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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.