Evidence map›Paper›PMID 36877675›Full record

ArticlePloS one2023

Diisocyanates influence models of atopic dermatitis through direct activation of TRPA1.

Manoj Yadav, Prem Prashant Chaudhary, Brandon N D'Souza, Grace Ratley, Jacquelyn Spathies, Sundar Ganesan, Jordan Zeldin, Ian A Myles

2 registry-linked trialsOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.1field-weighted citation impact, top 5% 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.

NCT06096857 phase2recruitingnot on this mapstarted 2024, after this paper: background citation

A Phase 2b, Double-Blind, Randomized, Placebo-Controlled Trial of Cardamom and Topical Roseomonas in Atopic Dermatitis

TypeinterventionalSponsorNational Institute of Allergy and Infectious Diseases (NIAID)Ran2024 to 2027Enrolled120ConditionsAtopic Dermatitis, EczemaArmsRoseomonas mucosa (RSM2015) and Cardamom seeds, Placebo (sucrose)
NCT07271381 narecruitingnot on this mapstarted 2026, after this paper: background citation

THREAT: Testing Harms Related to Exposure to Allergenic and Epithelial Toxins

TypeinterventionalSponsorNational Institute of Allergy and Infectious Diseases (NIAID)Ran2026 to 2031Enrolled120ConditionsAllergic, InflammatoryArmsEnvironmental Exposures, Control Exposures
3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Targeting Pollutants in the Treatment and Prevention of Atopic Dermatitis.Immunology and allergy clinics of North America · 2025
    Review
  5. Review
  6. Topical Steroid Withdrawal Is a Targetable Excess of Mitochondrial NAD.The Journal of investigative dermatology · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. The circadian metabolome of atopic dermatitis.The Journal of allergy and clinical immunology · 2024
    Article
  12. Article
  13. Article
  14. 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

8 authors at 1 institution in 1 country.

Manoj YadavEpithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America.
Prem Prashant ChaudharyEpithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID 0000-0002-3467-8608
Brandon N D'SouzaEpithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America.
Grace RatleyEpithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America.
Jacquelyn SpathiesEpithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID 0000-0002-7731-1363
Sundar GanesanBiological Imaging Section, Research Technology Branch, NIAID, NIH, Bethesda, Maryland, United States of America.
Jordan ZeldinEpithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID 0000-0002-3259-1381
Ian A MylesEpithelial Therapeutics Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID 0000-0001-9316-3703
National Institutes of Health · US

Funding

Infectious Diseases Research Technologies Core - BethesdaZICAI001051 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CHERRY, JAMES · 2009 to 2025
$226.1M
Host Immunity Against BacteriaZIAAI001043 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MYLES, IAN · 2009 to 2025
$18.9M
6 · The paper itself

Abstract

We recently used EPA databases to identify that isocyanates, most notably toluene diisocyanate (TDI), were the pollutant class with the strongest spatiotemporal and epidemiologic association with atopic dermatitis (AD). Our findings demonstrated that isocyanates like TDI disrupted lipid homeostasis and modeled benefit in commensal bacteria like Roseomonas mucosa through disrupting nitrogen fixation. However, TDI has also been established to activate transient receptor potential ankyrin 1 (TRPA1) in mice and thus could directly contribute to AD through induction of itch, rash, and psychological stress. Using cell culture and mouse models, we now demonstrate that TDI induced skin inflammation in mice as well as calcium influx in human neurons; each of these findings were dependent on TRPA1. Furthermore, TRPA1 blockade synergized with R. mucosa treatment in mice to improve TDI-independent models of AD. Finally, we show that the cellular effects of TRPA1 are related to shifting the balance of the tyrosine metabolites epinephrine and dopamine. This work provides added insight into the potential role, and therapeutic potential, or TRPA1 in the pathogenesis of AD.

Indexed as

Dermatitis, AtopicExanthemaToluene 2,4-DiisocyanateAnimalsCytoskeletal ProteinsHumansIsocyanatesMicePruritusTRPA1 Cation ChannelCytoskeletal ProteinsIsocyanatesToluene 2,4-DiisocyanateTRPA1 Cation ChannelTRPA1 protein, humanTrpa1 protein, mouse

Identifiers

PMID36877675
PMCPMC9987805
OpenAlexW4323294971

What OpenQuestion holds

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LicenceCC0
Read underepoch 390

Registered trials

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.