Evidence map›Paper›PMID 22890997›Full record

ArticleInfection and immunity2012

Role of interleukin-32 in Helicobacter pylori-induced gastric inflammation.

Kosuke Sakitani, Yoshihiro Hirata, Yoku Hayakawa, Takako Serizawa, Wachiko Nakata, Ryota Takahashi, Hiroto Kinoshita, Kei Sakamoto, Hayato Nakagawa, Masao Akanuma and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.6field-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

33 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Frontiers in cell and developmental biology · 2023
    Review
  7. Clinical implications of interleukins-31, 32, and 33 in gastric cancer.World journal of gastrointestinal oncology · 2022
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Metaplasia in the Stomach-Precursor of Gastric Cancer?International journal of molecular sciences · 2017
    Review
  17. Article
  18. Review
  19. Article
  20. 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

13 authors at 3 institutions in 1 country.

Kosuke SakitaniDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yoshihiro Hirata
Yoku Hayakawa
Takako Serizawa
Wachiko Nakata
Ryota Takahashi
Hiroto Kinoshita
Kei Sakamoto
Hayato Nakagawa
Masao Akanuma
Haruhiko Yoshida
Shin Maeda
Kazuhiko Koike
The University of Tokyo · JPInstitute for Adult Diseases Asahi Life Foundation · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Helicobacter pylori infection is associated with gastritis and gastric cancer. An H. pylori virulence factor, the cag pathogenicity island (PAI), is related to host cell cytokine induction and gastric inflammation. Since elucidation of the mechanisms of inflammation is important for therapy, the associations between cytokines and inflammatory diseases have been investigated vigorously. Levels of interleukin-32 (IL-32), a recently described inflammatory cytokine, are increased in various inflammatory diseases, such as rheumatoid arthritis and Crohn's disease, and in malignancies, including gastric cancer. In this report, we examined IL-32 expression in human gastric disease. We also investigated the function of IL-32 in activation of the inflammatory cytokines in gastritis. IL-32 expression paralleled human gastric tissue pathology, with low IL-32 expression in H. pylori-uninfected gastric mucosa and higher expression levels in gastritis and gastric cancer tissues. H. pylori infection increased IL-32 expression in human gastric epithelial cell lines. H. pylori-induced IL-32 expression was dependent on the bacterial cagPAI genes and on activation of nuclear factor κB (NF-κB). IL-32 expression induced by H. pylori was not detected in the supernatant of AGS cells but was found in the cytosol. Expression of the H. pylori-induced cytokines CXCL1, CXCL2, and IL-8 was decreased in IL-32-knockdown AGS cell lines compared to a control AGS cell line. We also found that NF-κB activation was decreased in H. pylori-infected IL-32-knockdown cells. These results suggest that IL-32 has important functions in the regulation of cytokine expression in H. pylori-infected gastric mucosa.

Indexed as

Cell LineCloning, OrganismCytokinesEnzyme-Linked Immunosorbent AssayGastric MucosaGastritisHelicobacter InfectionsHelicobacter pyloriHumansInterleukinsReal-Time Polymerase Chain ReactionRNA, MessengerCytokinesIL32 protein, humanInterleukinsRNA, Messenger

Identifiers

PMID22890997
PMCPMC3486038
OpenAlexW2151997025

What OpenQuestion holds

Textmetadata
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.