Evidence map›Paper›PMID 33209301›Full record

ArticleClinical & translational immunology2020

Fibrocyte localisation to the ASM bundle in asthma: bidirectional effects on cell phenotype and behaviour.

Ruth Saunders, Davinder Kaur, Dhananjay Desai, Rachid Berair, Latifa Chachi, Richard D Thompson, Salman H Siddiqui, Christopher E Brightling

Open access · goldAbstract read
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Article in Clinical & translational immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 29 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Ruth SaundersDepartment of Respiratory Sciences Institute for Lung Health University of Leicester Leicester UK.
Davinder KaurDepartment of Respiratory Sciences Institute for Lung Health University of Leicester Leicester UK.
Dhananjay DesaiDepartment of Respiratory Sciences Institute for Lung Health University of Leicester Leicester UK.
Rachid BerairDepartment of Respiratory Sciences Institute for Lung Health University of Leicester Leicester UK.
Latifa ChachiDepartment of Respiratory Sciences Institute for Lung Health University of Leicester Leicester UK.
Richard D ThompsonUniversity Hospitals Birmingham NHS Foundation Trust Birmingham UK.
Salman H SiddiquiDepartment of Respiratory Sciences Institute for Lung Health University of Leicester Leicester UK.
Christopher E BrightlingDepartment of Respiratory Sciences Institute for Lung Health University of Leicester Leicester UK.
University of Leicester · GBNIHR Leicester Biomedical Research Centre · GBUniversity Hospitals Birmingham NHS Foundation Trust · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

objectivesAirway hyper-responsiveness and persistent airflow obstruction contribute to asthma pathogenesis and symptoms, due in part to airway smooth muscle (ASM) hypercontractility and increased ASM mass. Fibrocytes have been shown to localise to the ASM in asthma however it is not known whether fibrocytes localise to the ASM in nonasthmatic eosinophilic bronchitis (NAEB) and chronic obstructive pulmonary disease (COPD). In addition, the potential consequences of fibrocyte localisation to ASM as regards asthma pathophysiology has not been widely studied.

methodsFibrocytes and proliferating cells were enumerated in ASM in bronchial tissue using immunohistochemistry. The effects of primary ASM and fibrocytes upon each other in terms of phenotype and behaviour following co-culture were investigated by assessing cell number, size, apoptotic status, phenotype and contractility in

resultsIncreased fibrocyte number in the ASM was observed in asthma versus NAEB, but not NAEB and COPD versus controls, and confirmed in asthma versus controls. ASM proliferation was not detectably different in asthmatics versus healthy controls

conclusionFurther understanding of mechanisms of fibrocyte recruitment to and/or differentiation within the ASM may identify novel therapeutic targets to modulate ASM dysfunction in asthma.

Indexed as

airway hyper‐responsivenessairway remodellingairway smooth muscleasthmafibrocytes

Identifiers

PMID33209301
PMCPMC7662089
OpenAlexW3104627686

What OpenQuestion holds

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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.