Evidence map›Paper›PMID 22214844›Full record

ArticleThe Journal of clinical investigation2012

Severe dermatitis with loss of epidermal Langerhans cells in human and mouse zinc deficiency.

Tatsuyoshi Kawamura, Youichi Ogawa, Yuumi Nakamura, Satoshi Nakamizo, Yoshihiro Ohta, Hajime Nakano, Kenji Kabashima, Ichiro Katayama, Schuichi Koizumi, Tatsuhiko Kodama and 2 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.1field-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

34 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Special Issue "Molecular Studies of Dermatitis: From Mechanism to Therapy".International journal of molecular sciences · 2024
    Article
  8. Article
  9. Metalation and activation of ZnBiophysics reviews · 2023
    Review
  10. Article
  11. Review
  12. Zinc: an undervalued microelement in research and treatment.Postepy dermatologii i alergologii · 2023
    Review
  13. Zinc and Zinc Transporters in Dermatology.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

12 authors at 6 institutions in 1 country.

Tatsuyoshi KawamuraDepartment of Dermatology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan. tkawa@yamanashi.ac.jp
Youichi Ogawa
Yuumi Nakamura
Satoshi Nakamizo
Yoshihiro Ohta
Hajime Nakano
Kenji Kabashima
Ichiro Katayama
Schuichi Koizumi
Tatsuhiko Kodama
Atsuhito Nakao
Shinji Shimada
University of Yamanashi · JPKyoto University · JPThe University of Tokyo · JPHirosaki University · JPOsaka University · JPUniversity of Yamanashi Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zinc deficiency can be an inherited disorder, in which case it is known as acrodermatitis enteropathica (AE), or an acquired disorder caused by low dietary intake of zinc. Even though zinc deficiency diminishes cellular and humoral immunity, patients develop immunostimulating skin inflammation. Here, we have demonstrated that despite diminished allergic contact dermatitis in mice fed a zinc-deficient (ZD) diet, irritant contact dermatitis (ICD) in these mice was more severe and prolonged than that in controls. Further, histological examination of ICD lesions in ZD mice revealed subcorneal vacuolization and epidermal pallor, histological features of AE. Consistent with the fact that ATP release from chemically injured keratinocytes serves as a causative mediator of ICD, we found that the severe ICD response in ZD mice was attenuated by local injection of soluble nucleoside triphosphate diphosphohydrolase. In addition, skin tissue from ZD mice with ICD showed increased levels of ATP, as did cultured wild-type keratinocytes treated with chemical irritants and the zinc-chelating reagent TPEN. Interestingly, numbers of epidermal Langerhans cells (LCs), which play a protective role against ATP-mediated inflammatory signals, were decreased in ZD mice as well as samples from ZD patients. These findings suggest that upon exposure to irritants, aberrant ATP release from keratinocytes and impaired LC-dependent hydrolysis of nucleotides may be important in the pathogenesis of AE.

Indexed as

AcrodermatitisAdenosine TriphosphateAnimalsCells, CulturedChemokinesDermatitis, Allergic ContactDietary SupplementsFemaleHumansKeratinocytesLangerhans CellsMiceMice, Inbred BALB CSkinTransforming Growth Factor beta1ZincAdenosine TriphosphateChemokinesTransforming Growth Factor beta1Zinc

Identifiers

PMID22214844
PMCPMC3266781
OpenAlexW2156905475

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.