Evidence map›Paper›PMID 27114422›Full record

ArticleGut and liver2016

Sensitization to and Challenge with Gliadin Induce Pancreatitis and Extrapancreatic Inflammation in HLA-DQ8 Mice: An Animal Model of Type 1 Autoimmune Pancreatitis.

Sung-Hoon Moon, Jihun Kim, Mi-Young Kim, Do Hyun Park, Tae Jun Song, Sun A Kim, Sang Soo Lee, Dong Wan Seo, Sung Koo Lee, Myung-Hwan Kim

Abstract read
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In one paragraph

Article in Gut and liver, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Autoimmune Pancreatitis and Immunoglobulin G4-related Sclerosing Cholangitis: Past, Present, and Future.The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi · 2022
    Review
  4. Pancreatic involvement in celiac disease.World journal of gastroenterology · 2022
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. 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

10 authors.

Sung-Hoon MoonDepartment of Internal Medicine, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Korea.
Jihun KimDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Mi-Young KimDepartment of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, Korea.
Do Hyun ParkDepartment of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Tae Jun SongDepartment of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Sun A KimDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Sang Soo LeeDepartment of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Dong Wan SeoDepartment of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Sung Koo LeeDepartment of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Myung-Hwan KimDepartment of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimsThe aim of this study was to establish a pathogenetic mechanism of pancreatitis in celiac disease and IgG4-related disease using gluten-sensitive human leukocyte antigen (HLA)-DQ8 transgenic mice.

methodsTransgenic mice expressing HLA-DQ8 genes were utilized. Control mice were not sensitized but were fed gliadin-free rice cereal. Experimental groups consisted of gliadin-sensitized and gliadin-challenged mice; nonsensitized mice with cerulein hyperstimulation; and gliadin-sensitized and gliadinchallenged mice with cerulein hyperstimulation.

resultsGliadin-sensitized and gliadin-challenged mice with cerulein hyperstimulation showed significant inflammatory cell infiltrates, fibrosis and acinar atrophy compared with the control mice and the other experimental groups. The immunohistochemical analysis showed greater IgG1-positive plasma cells in the inflammatory infiltrates of gliadin-sensitized and gliadin-challenged mice with cerulein hyperstimulation compared with the control mice and the other experimental groups. Gliadin-sensitized and gliadin-challenged mice with cerulein hyperstimulation or gliadin-sensitized and gliadinchallenged mice showed IgG1-stained inflammatory cell infiltrates in the extrapancreatic organs, including the bile ducts, salivary glands, kidneys, and lungs.

conclusionsGliadinsensitization and cerulein hyperstimulation of gluten-sensitive HLA-DQ8 transgenic mice resulted in pancreatitis and extrapancreatic inflammation. This animal model suggests that chronic gliadin ingestion in a susceptible individual with the HLA-DQ8 molecule may be associated with pancreatitis and extrapancreatic inflammation.

Indexed as

HypersensitivityAnimalsAutoimmune DiseasesCeruletideDisease Models, AnimalGliadinHLA-DQ AntigensImmunoglobulin GInflammationMiceMice, TransgenicPancreatitisCeruletideGliadinHLA-DQ8 antigenHLA-DQ AntigensImmunoglobulin GAutoimmune diseasesCeliac diseasePancreatitis

Identifiers

PMID27114422
PMCPMC5003210

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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.