Evidence map›Paper›PMID 41322401›Full record

ArticleFrontiers in immunology2025

Cold temperature enhances innate eosinophilic airway inflammation via transient receptor potential ankyrin1.

Yoichi Dotake, Takahiro Matsuyama, Kentaro Machida, Hiromi Matsuyama, Koichi Takagi, Keiko Mizuno, Keiko Kan-O, Tomoyuki Kuwaki, Hiromasa Inoue, Kentaro Tanaka

Abstract read
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In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

10 authors.

Yoichi Dotake *Department of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Takahiro Matsuyama *Department of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Kentaro MachidaDepartment of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Hiromi MatsuyamaDepartment of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Koichi TakagiDepartment of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Keiko MizunoDepartment of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Keiko Kan-ODepartment of Respiratory Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Tomoyuki KuwakiDepartment of Physiology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Hiromasa InoueDepartment of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Kentaro TanakaDepartment of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and objective: Asthma exacerbations due to cold air exposure are well recognized; however, the underlying mechanisms remain unclear. We investigate the role of the transient receptor potential ankyrin1 (TRPA1) channel in cold air-induced aggravation of innate airway inflammation using a murine model of papain stimulation combined with cold air exposure. Methods: Wild-type (WT) and Results: Papain treatment increased eosinophils in BALF, and the number of eosinophils was similar in WT and Conclusions: These findings suggest that TRPA1 channels expressed in airway epithelial cells play a critical role in producing TSLP, contributing to the enhancement of eosinophilic airway inflammation mediated by innate immunity upon cold air exposure, providing valuable insights into the mechanisms underlying asthma exacerbation triggered by cold temperatures.

Indexed as

AsthmaCold TemperatureEosinophilsImmunity, InnateTRPA1 Cation ChannelAnimalsBronchoalveolar Lavage FluidCytokinesDisease Models, AnimalHumansInflammationIsothiocyanatesMiceMice, Inbred C57BLMice, KnockoutPapainCytokinesIsothiocyanatesPapainTRPA1 Cation ChannelTrpa1 protein, mouseairway inflammationasthmagroup 2 innate lymphoid cellthymic stromal lymphopoietintransient receptor potential A1

Identifiers

PMID41322401
PMCPMC12657488

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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.