Evidence map›Paper›PMID 26477783›Full record

ArticleRespirology (Carlton, Vic.)2016

Differential neutrophil activation in viral infections: Enhanced TLR-7/8-mediated CXCL8 release in asthma.

Francesca S M Tang, David Van Ly, Kirsten Spann, Patrick C Reading, Janette K Burgess, Dominik Hartl, Katherine J Baines, Brian G Oliver

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Respirology (Carlton, Vic.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  10. Neutrophil extracellular traps in chronic lung disease: implications for pathogenesis and therapy.European respiratory review : an official journal of the European Respiratory Society · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 7 institutions in 2 countries.

Francesca S M TangWoolcock Institute of Medical Research, The University of Sydney, Sydney, New South Wales, Australia.
David Van LyWoolcock Institute of Medical Research, The University of Sydney, Sydney, New South Wales, Australia.
Kirsten SpannSchool of Biomedical Science, Faculty of Health, Queensland University of Technology, Brisbane, Queensland, Australia.
Patrick C ReadingWHO Collaborating Centre for Reference and Research on Influenza, Peter Doherty Institute for Infection and Immunity, Melbourne, Victoria, Australia.
Janette K BurgessWoolcock Institute of Medical Research, The University of Sydney, Sydney, New South Wales, Australia.
Dominik HartlDepartment of Pediatrics I, University of Tübingen, Tübingen, Germany.
Katherine J BainesPriority Research Centre for Asthma and Respiratory Disease, The University of Newcastle, Newcastle, New South Wales, Australia.
Brian G OliverWoolcock Institute of Medical Research, The University of Sydney, Sydney, New South Wales, Australia.
Woolcock Institute of Medical Research · AUChildren's Medical Research Institute · AUPeter Doherty Institute · AUQueensland University of Technology · AUUniversity of Newcastle Australia · AUUniversity of Sydney · AUUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectiveRespiratory viral infections are a major cause of asthma exacerbations. Neutrophils accumulate in the airways and the mechanisms that link neutrophilic inflammation, viral infections and exacerbations are unclear. This study aims to investigate anti-viral responses in neutrophils from patients with and without asthma and to investigate if neutrophils can be directly activated by respiratory viruses.

methodsNeutrophils from peripheral blood from asthmatic and non-asthmatic individuals were isolated and stimulated with lipopolysaccharide (LPS) (1 μg/mL), f-met-leu-phe (fMLP) (100 nM), imiquimod (3 μg/mL), R848 (1.5 μg/mL), poly I:C (10 μg/mL), RV16 (multiplicity of infection (MOI)1), respiratory syncytial virus (RSV) (MOI1) or influenza virus (MOI1). Cell-free supernatants were collected after 1 h of neutrophil elastase (NE) and matrix metalloproteinase (MMP)-9 release, or after 24 h for CXCL8 release.

resultsLPS, fMLP, imiquimod and R848 stimulated the release of CXCL8, NE and MMP-9 whereas poly I:C selectively induced CXCL8 release only. R848-induced CXCL8 release was enhanced in neutrophils from asthmatics compared with non-asthmatic cells (P < 0.01). RSV triggered the release of CXCL8 and NE from neutrophils, whereas RV16 or influenza had no effect.

conclusionNeutrophils release CXCL8, NE and MMP-9 in response to viral surrogates with R848-induced CXCL8 release being specifically enhanced in asthmatic neutrophils. Toll-like receptor (TLR7/8) dysregulation may play a role in neutrophilic inflammation in viral-induced exacerbations.

Indexed as

AsthmaVirus DiseasesAdultFemaleHumansInflammationInterleukin-8Leukocyte ElastaseLipopolysaccharidesMaleMatrix Metalloproteinase 9Neutrophil ActivationNeutrophilsN-Formylmethionine Leucyl-PhenylalanineOrthomyxoviridaeRespiratory Syncytial VirusesCXCL8 protein, humanInterleukin-8Leukocyte ElastaseLipopolysaccharidesMatrix Metalloproteinase 9N-Formylmethionine Leucyl-PhenylalanineToll-Like Receptorsasthmainnate immune responsesneutrophilsrespiratory virusesrhinovirus

Identifiers

PMID26477783
PMCPMC5324549
OpenAlexW2167105314

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.