Evidence map›Paper›PMID 33673645›Full record

ArticleCells2021

Eosinophil Responses at the Airway Epithelial Barrier during the Early Phase of Influenza A Virus Infection in C57BL/6 Mice.

Meenakshi Tiwary, Robert J Rooney, Swantje Liedmann, Kim S LeMessurier, Amali E Samarasinghe

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  8. Eosinophil-Epithelial Cell Interactions in Asthma.International archives of allergy and immunology · 2024
    Review
  9. Multicompartmental analysis of the murine pulmonary immune response by spectral flow cytometry.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
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  13. Review
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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.

Meenakshi TiwaryDivision of Pulmonology, Allergy-Immunology and Sleep, Department of Pediatrics, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.ORCID 0000-0003-2468-8076
Robert J RooneyDivision of Pulmonology, Allergy-Immunology and Sleep, Department of Pediatrics, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Swantje LiedmannDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Kim S LeMessurierDivision of Pulmonology, Allergy-Immunology and Sleep, Department of Pediatrics, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Amali E SamarasingheDivision of Pulmonology, Allergy-Immunology and Sleep, Department of Pediatrics, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
University of Tennessee Health Science Center · USSt. Jude Children's Research Hospital · US

Funding

Eosinophils as Regulators of Host Immunity against Influenza InfectionsR01AI125481 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SAMARASINGHE, AMALI · 2017 to 2021
$1.9M
NIAID NIH HHS R01 AI125481
6 · The paper itself

Abstract

Eosinophils, previously considered terminally differentiated effector cells, have multifaceted functions in tissues. We previously found that allergic mice with eosinophil-rich inflammation were protected from severe influenza and discovered specialized antiviral effector functions for eosinophils including promoting cellular immunity during influenza. In this study, we hypothesized that eosinophil responses during the early phase of influenza contribute to host protection. Using in vitro and in vivo models, we found that eosinophils were rapidly and dynamically regulated upon influenza A virus (IAV) exposure to gain migratory capabilities to traffic to lymphoid organs after pulmonary infection. Eosinophils were capable of neutralizing virus upon contact and combinations of eosinophil granule proteins reduced virus infectivity through hemagglutinin inactivation. Bi-directional crosstalk between IAV-exposed epithelial cells and eosinophils occurred after IAV infection and cross-regulation promoted barrier responses to improve antiviral defenses in airway epithelial cells. Direct interactions between eosinophils and airway epithelial cells after IAV infection prevented virus-induced cytopathology in airway epithelial cells in vitro, and eosinophil recipient IAV-infected mice also maintained normal airway epithelial cell morphology. Our data suggest that eosinophils are important in the early phase of IAV infection providing immediate protection to the epithelial barrier until adaptive immune responses are deployed during influenza.

Indexed as

AnimalsCell Adhesion MoleculesDisease Models, AnimalEosinophilsEpithelial CellsGene Expression ProfilingHumansInfluenza A virusMiceCell Adhesion Moleculesactivationadhesion moleculescell damagemigration

Identifiers

PMID33673645
PMCPMC7997358
OpenAlexW3135095003

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.