Evidence map›Paper›PMID 27965774›Full record

ArticleAsthma research and practice2016

CXC chemokine superfamily induced by Interferon-γ in asthma: a cross-sectional observational study.

Yotaro Takaku, Tomoyuki Soma, Yoshitaka Uchida, Takehito Kobayashi, Kazuyuki Nakagome, Makoto Nagata

Open access · goldAbstract read
In one paragraph

Article in Asthma research and practice, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Observational
  2. Article
  3. Influence of serum IL-36 subfamily cytokines on clinical manifestations of asthma.The journal of allergy and clinical immunology. Global · 2025
    Article
  4. Review
  5. Article
  6. Potential Association Between Asthma,Frontiers in oncology · 2021
    Article
  7. Article
  8. Mechanisms of eosinophilic inflammation.Asia Pacific allergy · 2020
    Review
  9. Article
  10. Article
  11. 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

6 authors at 2 institutions in 1 country.

Yotaro TakakuAllergy Center, Saitama Medical University, Saitama, Japan.
Tomoyuki SomaAllergy Center, Saitama Medical University, Saitama, Japan.
Yoshitaka UchidaAllergy Center, Saitama Medical University, Saitama, Japan.
Takehito KobayashiAllergy Center, Saitama Medical University, Saitama, Japan.
Kazuyuki NakagomeAllergy Center, Saitama Medical University, Saitama, Japan.
Makoto NagataAllergy Center, Saitama Medical University, Saitama, Japan.
Saitama Medical University · JPSaitama Prefecture · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAsthma is a disease encompassing a variety of contributing factors. Phenotyping of asthma based on the profile of accumulated granulocytes in the airways has been performed to explore the mediators involved in allergic bronchial inflammation. The aim of this study was to clarify the characteristics of the CXC chemokine superfamily induced by IFN-γ, namely CXCR3 ligands, in the airways of patients with asthma stratified by the differential proportion of granulocytes in sputum.

methodsSputum was induced in 39 adult patients with asthma and 12 healthy subjects. Sputum samples were analyzed for total cell counts and differentials, and concentrations of IFN-γ-inducible protein 10 kDa (IP-10, CXCL10), monokine induced by IFN-γ (Mig, CXCL9), IFN-inducible T cell a chemoattractant (I-TAC, CXCL11), and IL-8 in the supernatants were assayed by ELISA.

resultsSputum concentrations of IP-10, Mig, and IL-8 were significantly higher in asthma than in healthy subjects. IP-10, Mig, and IL-8 were significantly higher in the mixed granulocyte subtype (eosinophils ≥ 2 % and neutrophils ≥ 40 % in sputum) than in healthy subjects. Additionally, IP-1 0 was significantly higher in the mixed granulocyte subtype than in eosinophil-predominant or neutrophil-predominant subtype (eosinophil percentage ≥ 2 % or neutrophil percentage ≥ 40 %). Mig and IL-8 were significantly higher in the mixed granulocyte subtype than in the paucigranulocyte subtype (eosinophils < 2 % and neutrophils < 40 % in sputum). I-TAC was not different between healthy subjects and asthmatics or granulocyte subtypes. All CXCR3 ligands were significantly associated with the composite of the eosinophil and neutrophil ratio in patients with asthma. Only Mig was significantly correlated with the total eosinophil and neutrophil ratio in patients with asthma on adjusted partial correlation analysis. Mig and IL-8 were significantly negatively correlated with forced expiratory volume in 1 s % predicted (% FEV

conclusionsCXCR3 ligands may serve as potent promoters in eosinophilic and neutrophilic airway inflammation in asthma.

Indexed as

AsthmaCXCR3 ligandsEosinophilic inflammationIP-10MigMixed granulocytic inflammationNeutrophilic inflammationSputum

Identifiers

PMID27965774
PMCPMC5142415
OpenAlexW2298214646

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.