Evidence map›Paper›PMID 27795621›Full record

ArticleMediators of inflammation2016

CCR9 Is a Key Regulator of Early Phases of Allergic Airway Inflammation.

C López-Pacheco, G Soldevila, G Du Pont, R Hernández-Pando, E A García-Zepeda

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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    Review
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  13. Inflammation- and Gut-Homing Macrophages, Engineered toInternational journal of molecular sciences · 2021
    Article
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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

5 authors at 2 institutions in 1 country.

C López-PachecoCBRL, Ciudad de México, Mexico; Departamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, 04510 Ciudad de México, Mexico.
G SoldevilaDepartamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, 04510 Ciudad de México, Mexico.
G Du PontCBRL, Ciudad de México, Mexico; Departamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, 04510 Ciudad de México, Mexico.
R Hernández-PandoDepartamento de Patología Experimental, Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán", Tlalpan, 14080 Ciudad de México, Mexico.
E A García-ZepedaCBRL, Ciudad de México, Mexico; Departamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, 04510 Ciudad de México, Mexico.ORCID 0000-0002-0352-5115
Universidad Nacional Autónoma de México · MXInstituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Airway inflammation is the most common hallmark of allergic asthma. Chemokine receptors involved in leukocyte recruitment are closely related to the pathology in asthma. CCR9 has been described as a homeostatic and inflammatory chemokine receptor, but its role and that of its ligand CCL25 during lung inflammation remain unknown. To investigate the role of CCR9 as a modulator of airway inflammation, we established an OVA-induced allergic inflammation model in CCR9-deficient mice. Here, we report the expression of CCR9 and CCL25 as early as 6 hours post-OVA challenge in eosinophils and T-lymphocytes. Moreover, in challenged CCR9-deficient mice, cell recruitment was impaired at peribronchial and perivenular levels. OVA-administration in CCR9-deficient mice leads to a less inflammatory cell recruitment, which modifies the expression of IL-10, CCL11, and CCL25 at 24 hours after OVA challenge. In contrast, the secretion of IL-4 and IL-5 was not affected in CCR9-deficient mice compared to WT mice. These results demonstrate for the first time that CCR9 and CCL25 expressions are induced in the early stages of airway inflammation and they have an important role modulating eosinophils and lymphocytes recruitment at the first stages of inflammatory process, suggesting that they might be a potential target to regulate inflammation in asthma.

Indexed as

Gene Expression RegulationAnimalsBronchoalveolar Lavage FluidCell SeparationChemokines, CCCytokinesEnzyme-Linked Immunosorbent AssayEosinophilsFemaleFlow CytometryHypersensitivityImmunoglobulin EInflammationLeukocytesLungLymphocytesCC chemokine receptor 9Ccl25 protein, mouseChemokines, CCCytokinesImmunoglobulin EReceptors, CCR

Identifiers

PMID27795621
PMCPMC5067335
OpenAlexW2529233317

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.