Evidence map›Paper›PMID 22944599›Full record

ArticleThe American journal of pathology2012

On the etiology of type 1 diabetes: a new animal model signifying a decisive role for bacteria eliciting an adverse innate immunity response.

Stella Korsgren, Ylva Molin, Kaija Salmela, Torbjörn Lundgren, Asa Melhus, Olle Korsgren

Open access · bronzeAbstract readCase Reports
In one paragraph

Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Trial
  3. TLR5 influences the development of type 1 diabetes.BMJ open diabetes research & care · 2025
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
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  11. Type 1 diabetes mellitus: much progress, many opportunities.The Journal of clinical investigation · 2021
    Review
  12. Review
  13. Article
  14. Exocrine Pancreas Dysfunction in Type 1 Diabetes.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2020
    Review
  15. Article
  16. Review
  17. Review
  18. 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

6 authors at 3 institutions in 3 countries.

Stella KorsgrenDepartment of Immunology, Genetics, and Pathology, Rudbeck Laboratory, Uppsala University, Sweden.
Ylva Molin
Kaija Salmela
Torbjörn Lundgren
Asa Melhus
Olle Korsgren
Uppsala University · SEHospital District of Helsinki and Uusimaa · FIKarolinska Institutet · SE

Funding

Innate immunity in clinical islet transplantation: a clinical study (CIT0-01) in U01AI065192 · NIAID · UPPSALA UNIVERSITY · PI KORSGREN, OLLE · 2004 to 2012
$11.1M
NIAID NIH HHS 2U01AI065192-06NIAID NIH HHS U01 AI065192
6 · The paper itself

Abstract

The cause of type 1 diabetes (T1D) remains unknown; however, a decisive role for environmental factors is recognized. The increased incidence of T1D during the last decades, as well as regional differences, is paralleled by differences in the intestinal bacterial flora. A new animal model was established to test the hypothesis that bacteria entering the pancreatic ductal system could trigger β-cell destruction and to provide new insights to the immunopathology of the disease. Obtained findings were compared with those present in two patients dying at onset of T1D. Different bacterial species, present in the human duodenum, instilled into the ductal system of the pancreas in healthy rats rapidly induced cellular infiltration, consisting of mainly neutrophil polymorphonuclear cells and monocytes/macrophages, centered around the pancreatic ducts. Also, the islets of Langerhans attracted polymorphonuclear cells, possibly via release of IL-6, IL-8, and monocyte chemotactic protein 1. Small bleedings or large dilatations of the capillaries were frequently found within the islets, and several β-cells had severe hydropic degeneration (ie, swollen cytoplasm) but with preserved nuclei. A novel rat model for the initial events in T1D is presented, revealing marked similarities with the morphologic findings obtained in patients dying at onset of T1D and signifying a decisive role for bacteria in eliciting an adverse innate immunity response. The present findings support the hypothesis that T1D is an organ-specific inflammatory disease.

Indexed as

AdultAnimalsBacteriaCytokinesDiabetes Mellitus, Type 1Disease Models, AnimalFatal OutcomeHumansImmunity, InnateImmunohistochemistryInflammationIslets of LangerhansMaleModels, BiologicalRatsRats, WistarCytokines

Identifiers

PMID22944599
PMCPMC3483807
OpenAlexW1874055151

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.