Evidence map›Paper›PMID 26813347›Full record

ArticleMucosal immunology2016

Nucleotide-binding oligomerization domain 1 acts in concert with the cholecystokinin receptor agonist, cerulein, to induce IL-33-dependent chronic pancreatitis.

T Watanabe, Y Sadakane, N Yagama, T Sakurai, H Ezoe, M Kudo, T Chiba, W Strober

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

42 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. Article
  8. Circulating Markers of Necroptosis in Acute Pancreatitis.Digestive diseases and sciences · 2024
    Article
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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 4 institutions in 2 countries.

T WatanabeDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan.
Y SadakaneCenter for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan.
N YagamaCenter for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan.
T SakuraiDepartment of Gastroenterology and Hepatology, Kinki University Graduate School of Medicine, Osaka-sayama, Osaka, Japan.
H EzoeCenter for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan.
M KudoDepartment of Gastroenterology and Hepatology, Kinki University Graduate School of Medicine, Osaka-sayama, Osaka, Japan.
T ChibaDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan.
W StroberMucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Kyoto University · JPKindai University · JPNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Regulation of T cell DifferentiationZIAAI000872 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI STROBER, WARREN · 2009 to 2025
$9.6M
Immunoregulatory Defects In Inflammatory Bowel DiseaseZIAAI000354 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI STROBER, WARREN · 2009 to 2025
$8.7M
6 · The paper itself

Abstract

Nucleotide-binding oligomerization domain 1 (NOD1) fulfills important host-defense functions via its responses to a variety of gut pathogens. Recently, however, we showed that in acute pancreatitis caused by administration of cholecystokinin receptor (CCKR) agonist (cerulein) NOD1 also has a role in inflammation via its responses to gut commensal organisms. In the present study, we explored the long-term outcome of such NOD1 responsiveness in a new model of chronic pancreatitis induced by repeated administration of low doses of cerulein in combination with NOD1 ligand. We found that the development of chronic pancreatitis in this model requires intact NOD1 and type I IFN signaling and that such signaling mediates a macrophage-mediated inflammatory response that supports interleukin (IL)-33 production by acinar cells. The IL-33, in turn, has a necessary role in the induction of IL-13 and TGF-β1, factors causing the fibrotic reaction characteristic of chronic pancreatitis. Interestingly, the Th2 effects of IL-33 were attenuated by the concomitant type I IFN response since the inflammation was marked by clear increases in IFN-γ and TNF-α production but only marginal increases in IL-4 production. These studies establish chronic pancreatitis as an IL-33-dependent inflammation resulting from synergistic interactions between the NOD1 and CCKR signaling pathways.

Indexed as

Acinar CellsAnimalsCeruletideDiaminopimelic AcidDisease Models, AnimalGene Expression RegulationInterferon-gammaInterleukin-13Interleukin-33Interleukin-4MacrophagesMiceMice, Inbred C57BLMice, KnockoutNod1 Signaling Adaptor ProteinPancreatitis, ChronicCeruletideDiaminopimelic AcidFK 156Il33 protein, mouseInterferon-gammaInterleukin-13Interleukin-33Interleukin-4Nod1 protein, mouseNod1 Signaling Adaptor ProteinReceptors, CholecystokininTransforming Growth Factor beta1Tumor Necrosis Factor-alpha

Identifiers

PMID26813347
OpenAlexW2424811170

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.