Evidence map›Paper›PMID 31798831›Full record

ArticleClinical and translational allergy2019

Reduced expression of miR-146a in human bronchial epithelial cells alters neutrophil migration.

Anet Kivihall, Alar Aab, Jerzy Soja, Krzysztof Sładek, Marek Sanak, Alan Altraja, Bogdan Jakiela, Grazyna Bochenek, Ana Rebane

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational allergy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.8field-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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
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  4. Potential roles of microRNAs in chronic rhinosinusitis: from mechanistic insights to clinical studies.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026
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  11. MiRNA-146a-A Key Player in Immunity and Diseases.International journal of molecular sciences · 2023
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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

9 authors at 3 institutions in 2 countries.

Anet Kivihall1Institute of Biomedicine and Translational Medicine, University of Tartu, Ravila 14B, 50414 Tartu, Estonia.ORCID 0000-0002-3648-1139
Alar Aab1Institute of Biomedicine and Translational Medicine, University of Tartu, Ravila 14B, 50414 Tartu, Estonia.
Jerzy Soja2Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.
Krzysztof Sładek2Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.
Marek Sanak2Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.
Alan Altraja3Department of Pulmonary Medicine, University of Tartu, Tartu, Estonia.
Bogdan Jakiela2Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.
Grazyna Bochenek2Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.
Ana Rebane1Institute of Biomedicine and Translational Medicine, University of Tartu, Ravila 14B, 50414 Tartu, Estonia.
Jagiellonian University · PLUniversity of Tartu · EETartu University Hospital · EE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe role of miRNAs in the pathogenesis and determining the phenotypes of asthma is not fully elucidated. miR-146a has been previously shown to suppress inflammatory responses in different cells. In this study, we investigated the functions of miR-146a in human bronchial epithelial cells (HBECs) in association with neutrophilic, eosinophilic, and paucigranulocytic phenotypes of asthma.

methodsBronchial brushing specimens and brochial mucosal biopsy samples were collected from adult patients with asthma and from age- and gender-matched non-asthmatic individuals. The expression of miR-146a in bronchial brushing specimens, bronchial biopsy tissue sections or cultured primary bronchial epithelial cells was analyzed by RT-qPCR or by in situ hybridization. The expression of direct and indirect miR-146a target genes was determined by RT-qPCR or ELISA. The migration of neutrophils was studied by neutrophil chemotaxis assay and flow cytometry. For statistical analysis, unpaired two-way Student's

resultsReduced expression of miR-146a was found in bronchial brushing specimens from asthma patients as compared to non-asthmatics and irrespective of the phenotype of asthma. In the same samples, the neutrophil attracting chemokines IL-8 and CXCL1 showed increased expression in patients with neutrophilic asthma and increased IL-33 expression was found in patients with eosinophilic asthma. Linear regression analysis revealed a significant negative association between the expression of miR-146a in bronchial brushings and neutrophil cell counts in bronchoalveolar lavage fluid of patients with asthma. In bronchial biopsy specimens, the level of miR-146a was highest in the epithelium as determined with in situ hybridization. In primary conventional HBEC culture, the expression of miR-146a was induced in response to the stimulation with IL-17A, TNF-α, and IL-4. The mRNA expression and secretion of IL-8 and CXCL1 was inhibited in both stimulated and unstimulated HBECs transfected with miR-146a mimics. Supernatants from HBECs transfected with miR-146a had reduced capability of supporting neutrophil migration in neutrophil chemotaxis assay.

conclusionOur results suggest that decreased level of miR-146a in HBECs from patients with asthma may contribute to the development of neutrophilic phenotype of asthma.

Indexed as

Airway epitheliumEndotypeHBECmicroRNAmiR-146a

Identifiers

PMID31798831
PMCPMC6880603
OpenAlexW2990985235

What OpenQuestion holds

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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.