Evidence map›Paper›PMID 35892679›Full record

ArticleBiomedicines2022

CCL4 Functions as a Biomarker of Type 2 Airway Inflammation.

Yoshiki Kobayashi, Hanh Hong Chu, Akira Kanda, Yasutaka Yun, Masami Shimono, Linh Manh Nguyen, Akitoshi Mitani, Kensuke Suzuki, Mikiya Asako, Hiroshi Iwai

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Novel insights intomSystems · 2026
    Article
  2. FPR1-dependent Pro-inflammatory Ccl4Respiratory research · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Age-specific Metabolomic profiles in children with food allergy.Clinical immunology (Orlando, Fla.) · 2024
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Olfactomedin 4 as a circulating biomarker for asthma.Annals of translational medicine · 2022
    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

10 authors at 1 institution in 1 country.

Yoshiki KobayashiAirway Disease Section, Department of Otorhinolaryngology, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0003-3755-3074
Hanh Hong ChuAirway Disease Section, Department of Otorhinolaryngology, Kansai Medical University, Osaka 573-1010, Japan.
Akira KandaAirway Disease Section, Department of Otorhinolaryngology, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0001-6324-721X
Yasutaka YunAirway Disease Section, Department of Otorhinolaryngology, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0002-6879-6303
Masami ShimonoAirway Disease Section, Department of Otorhinolaryngology, Kansai Medical University, Osaka 573-1010, Japan.
Linh Manh NguyenAirway Disease Section, Department of Otorhinolaryngology, Kansai Medical University, Osaka 573-1010, Japan.
Akitoshi MitaniAirway Disease Section, Department of Otorhinolaryngology, Kansai Medical University, Osaka 573-1010, Japan.
Kensuke SuzukiAirway Disease Section, Department of Otorhinolaryngology, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0003-1659-1549
Mikiya AsakoAirway Disease Section, Department of Otorhinolaryngology, Kansai Medical University, Osaka 573-1010, Japan.
Hiroshi IwaiAirway Disease Section, Department of Otorhinolaryngology, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0003-2646-8173
Kansai Medical University · JP

Funding

Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan 19K18823, 19K07949
6 · The paper itself

Abstract

Eosinophilic airway inflammatory disease is associated with bronchial asthma, with eosinophilic chronic rhinosinusitis (ECRS) typical of refractory type 2 airway inflammation. CCL4 produced at local inflammatory sites is involved in them via the accumulation and activation of type 2 inflammatory cells, including eosinophils. The detailed mechanism of CCL4 production remains unclear, and also the possibility it could function as a biomarker of type 2 airway inflammation remains unresolved. In this study, we evaluated CCL4 mRNA expression and production via the TSLP receptor (TSLPR) and toll-like receptors (TLRs) or proteinase-activated receptor-2 (PAR2) in BEAS-2B bronchial epithelial cells co-incubated with purified eosinophils or eosinophil peroxidase (EPX). We examined serum chemokine (CCL4, CCL11, CCL26, and CCL17) and total IgE serum levels, fractionated exhaled nitrogen oxide (FENO), and CCL4 expression in nasal polyps in patients with severe ECRS and asthma. CCL4 was induced by TSLP under eosinophilic inflammation. Furthermore, CCL4 was released via TLR3 signaling, which was enhanced by TSLP. CCL4 was mainly located in nasal polyp epithelial cells, while serum CCL4 levels were reduced after dupilumab treatment. Serum CCL4 levels were positively correlated with FENO, serum IgE, and CCL17 levels. Thus, CCL4 released from epithelial cells via the innate immune system during type 2 airway inflammation may function as a useful biomarker for the condition.

Indexed as

bronchial asthmaCCL4eosinophilic chronic rhinosinusitistype 2 airway inflammation

Identifiers

PMID35892679
PMCPMC9330411
OpenAlexW4287010199

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.