Evidence map›Paper›PMID 33080861›Full record

ArticleViruses2020

Selective Blockade of TNFR1 Improves Clinical Disease and Bronchoconstriction in Experimental RSV Infection.

Dorothea R Morris, Maria Ansar, Teodora Ivanciuc, Yue Qu, Antonella Casola, Roberto P Garofalo

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

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  10. Targeting ectromelia virus and TNF/NF-κB or STAT3 signaling for effective treatment of viral pneumonia.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

6 authors at 1 institution in 1 country.

Dorothea R MorrisDivision of Clinical and Experimental Immunology and Infectious Disease (CEIID), Department of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0003-1049-2208
Maria AnsarDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Teodora IvanciucDivision of Clinical and Experimental Immunology and Infectious Disease (CEIID), Department of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555, USA.
Yue QuDivision of Clinical and Experimental Immunology and Infectious Disease (CEIID), Department of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0003-4337-1437
Antonella CasolaDivision of Clinical and Experimental Immunology and Infectious Disease (CEIID), Department of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555, USA.
Roberto P GarofaloDivision of Clinical and Experimental Immunology and Infectious Disease (CEIID), Department of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555, USA.
The University of Texas Medical Branch at Galveston · US

Funding

UTMB Clinical and Translational Science AwardTL1TR001440 · NCATS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI HOMMEL, JONATHAN DEAN · 2015 to 2024
$3.4M
NCATS NIH HHS TL1 TR001440NIH HHS AI062885
6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis in infants and young children. Although some clinical studies have speculated that tumor necrosis factor (TNF)-α is a major contributor of RSV-mediated airway disease, experimental evidence remains unclear or conflicting. TNF-α initiates inflammation and cell death through two distinct receptors: TNF-receptor (TNFR)1 and TNFR2. Here we delineate the function of TNF-α by short-lasting blockade of either receptor in an experimental BALB/c mouse model of RSV infection. We demonstrate that antibody-mediated blockade of TNFR1, but not TNFR2, results in significantly improved clinical disease and bronchoconstriction as well as significant reductions of several inflammatory cytokines and chemokines, including IL-1α, IL-1β, IL-6, Ccl3, Ccl4, and Ccl5. Additionally, TNFR1 blockade was found to significantly reduce neutrophil number and activation status, consistent with the concomitant reduction of pro-neutrophilic chemokines Cxcl1 and Cxcl2. Similar protective activity was also observed when a single-dose of TNFR1 blockade was administered to mice following RSV inoculation, although this treatment resulted in improved alveolar macrophage survival rather than reduced neutrophil activation. Importantly, short-lasting blockade of TNFR1 did not affect RSV peak replication in the lung. This study suggests a potential therapeutic approach for RSV bronchiolitis based on selective blockade of TNFR1.

Indexed as

BronchoconstrictionAnimalsAntibodiesChemokinesCytokinesFemaleMacrophagesMiceMice, Inbred BALB CNeutrophilsReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIRespiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsTumor Necrosis Factor-alphaAntibodiesChemokinesCytokinesReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITnfrsf1a protein, mouseTnfrsf1b protein, mouseTumor Necrosis Factor-alphaBALFbronchiolitisbronchoconstrictionmacrophagesneutrophilsrespiratory syncytial virusRSVTNFTNFR1TNFR2tumor necrosis factor

Identifiers

PMID33080861
PMCPMC7588931
OpenAlexW3092772475

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.