Evidence map›Paper›PMID 32326200›Full record

ReviewBiomolecules2020

Possible Mechanisms of Eosinophil Accumulation in Eosinophilic Pneumonia.

Kazuyuki Nakagome, Makoto Nagata

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  6. Review
  7. Article
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  16. Article
  17. Article
  18. Review
  19. CCL4 Regulates Eosinophil Activation in Eosinophilic Airway Inflammation.International journal of molecular sciences · 2022
    Article
  20. 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

2 authors at 1 institution in 1 country.

Kazuyuki NakagomeDepartment of Respiratory Medicine, Saitama Medical University, Saitama 350-0495, Japan.ORCID 0000-0003-3138-1451
Makoto NagataDepartment of Respiratory Medicine, Saitama Medical University, Saitama 350-0495, Japan.
Saitama Medical University · JP

Funding

Ministry of Education, Culture, Sports, Science and Technology 15K09228
6 · The paper itself

Abstract

Eosinophilic pneumonia (EP), including acute EP and chronic EP, is characterized by the massive pulmonary infiltration of eosinophils into the lung. However, the mechanisms underlying the selective accumulation of eosinophils in EP have not yet been fully elucidated. We reported that bronchoalveolar lavage fluid (BALF) from EP patients induced the transmigration of eosinophils across endothelial cells in vitro. The concentrations of eotaxin-2 (CCL24) and monocyte chemotactic protein (MCP)-4 (CCL13), which are CC chemokine receptor (CCR) 3 ligands, were elevated in the BALF of EP patients, and anti-CCR3 monoclonal antibody inhibited the eosinophil transmigration induced by the BALF of EP patients. The concentration of macrophage inflammatory protein 1β (CCL4), a CCR5 ligand that induces eosinophil migration, was increased in the BALF of EP patients. Furthermore, the concentration of interleukin (IL) 5 was increased in the BALF of EP patients, and it has been reported that anti-IL-5 antibody treatment resulted in remission and the reduction of glucocorticoid use in some cases of chronic EP. The concentrations of lipid mediators, such as leukotriene (LT) B

Indexed as

AnimalsEosinophilsExtracellular Matrix ProteinsHumansLipidsLungPulmonary EosinophiliaReceptors, CCR3Extracellular Matrix ProteinsLipidsReceptors, CCR3chemokinescytokineseosinophilic pneumoniaeosinophilspneumonia

Identifiers

PMID32326200
PMCPMC7226607
OpenAlexW3017776224

What OpenQuestion holds

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LicenceCC BY
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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.