Evidence map›Paper›PMID 35111148›Full record

ArticleFrontiers in immunology2021

Neutrophil Extracellular Traps Caused by Gut Leakage Trigger the Autoimmune Response in Nonobese Diabetic Mice.

Qi You, Yiming Shen, Yiling Wu, Yuyan Li, Chang Liu, Fengjie Huang, Harvest F Gu, Jie Wu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  3. Review
  4. Article
  5. Review
  6. Review
  7. NETosis in hypersensitivity disorders.Molecular biology reports · 2025
    Review
  8. Article
  9. NETs: a new target for autoimmune disease.Frontiers in immunology · 2025
    Review
  10. Article
  11. Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
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  18. Review
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 1 institution in 1 country.

Qi YouCollege of Life Science and Technology, China Pharmaceutical University, Nanjing, China.
Yiming ShenCollege of Life Science and Technology, China Pharmaceutical University, Nanjing, China.
Yiling WuCollege of Life Science and Technology, China Pharmaceutical University, Nanjing, China.
Yuyan LiState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.
Chang LiuState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.
Fengjie HuangCollege of Life Science and Technology, China Pharmaceutical University, Nanjing, China.
Harvest F GuCenter for Pathophysiology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, China.
Jie WuCollege of Life Science and Technology, China Pharmaceutical University, Nanjing, China.
China Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased formation of neutrophil extracellular traps (NETs) is associated with gut leakage in type 1 diabetes (T1D). To explore the mechanism of how enteropathy exacerbated by NETs triggers pancreatic autoimmunity in T1D, we carried out a correlation analysis for NET formation with gut barrier functions and autoimmunity in nonobese diabetic (NOD) mice. Inducing chronic colitis or knocking out of peptidyl arginine deiminase type 4 (PAD4) in NOD mice were used to further study the effect of NET formation on the progression of T1D. Microbial alterations in Deferribacteres and Proteobacteria, along with the loss of gut barrier function, were found to be associated with increased endotoxin and abnormal formation of NETs in NOD mice. Both DSS-induced colitis and knockout of PAD4 in NOD mice indicated that PAD4-dependent NET formation was involved in the aggravation of gut barrier dysfunction, the production of autoantibodies, and the activation of enteric autoimmune T cells, which then migrated to pancreatic lymph nodes (PLNs) and caused self-damage. The current study thus provides evidence that PAD4-dependent NET formation is engaged in leaky gut triggering pancreatic autoimmunity and suggests that either degradation of NETs or inhibition of NET formation may be helpful for innovative therapeutic interventions in T1D.

Indexed as

AnimalsAutoantibodiesAutoimmunityColitisDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Disease Models, AnimalExtracellular TrapsFemaleMiceMice, Inbred BALB CMice, Inbred NODNeutrophilsProtein-Arginine Deiminase Type 4AutoantibodiesProtein-Arginine Deiminase Type 4autoimmunitygut barrier functionneutrophil extracellular trapspeptidyl arginine deiminase type 4type 1 diabetes

Identifiers

PMID35111148
PMCPMC8801438
OpenAlexW4205166130

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.