Evidence map›Paper›PMID 18519743›Full record

ArticleJournal of leukocyte biology2008

Pulmonary eosinophilia requires interleukin-5, eotaxin-1, and CD4+ T cells in mice immunized with respiratory syncytial virus G glycoprotein.

Teresa R Johnson, Marc E Rothenberg, Barney S Graham

Open access · greenAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Regulation of eotaxin expression in skin allergic diseases.Postepy dermatologii i alergologii · 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

3 authors at 2 institutions in 1 country.

Teresa R JohnsonVaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892-3017, USA. teresaj@nih.gov
Marc E Rothenberg
Barney S Graham
National Institute of Allergy and Infectious Diseases · USCincinnati Children's Hospital Medical Center · US

Funding

Factors Contributing To Immune-Enhanced Disease In The Pathogenesis of RSVZIAAI005029 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI GRAHAM, BARNEY · 2009 to 2017
$6.2M
Immune-enhanced Disease In the Pathogenesis of RSVZ01AI005029 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI GRAHAM, BARNEY SCOTT · 2002 to 2008
$1.4M
6 · The paper itself

Abstract

Severe illness, type 2 cytokine production, and pulmonary eosinophilia are adverse immune responses resulting from respiratory syncytial virus (RSV) challenge of vvGs-immunized mice. We have shown IL-4 and IL-13 activity must be simultaneously inhibited to reduce disease severity. We now address the contributions of IL-5, eotaxin-1, and CD4+ and CD8+ T cells to the induction of disease-enhancing immune responses. Depletion of CD4+ T cells during immunization prevented IL-4, IL-13, and eotaxin-1 production, diminished eosinophilia, and reduced weight loss. Conversely, CD8+ T cell depletion did not decrease eosinophilia, weight loss, or type 2 cytokines but did dramatically reduce mucus production and increase eotaxin production. Anti-IL-5 administration at immunization or challenge significantly decreased pulmonary eosinophilia. Strikingly, there were not concomitant decreases in weight loss. Following RSV challenge eotaxin-1-deficient mice immunized with vvGs exhibited significantly less eosinophilia without decreased weight loss or type 2 cytokine production. We conclude CD4+ T cell production of IL-5 and induction of eotaxin-1 are required for vvGs-induced eosinophilia following RSV challenge, while CD8+ T cells appear to down-regulate eotaxin-1 and mucus production. In summary, we demonstrate that pulmonary eosinophilia 1) is a by-product of memory CD4+ T cell activation, 2) does not necessarily correlate with mucus production, and, most importantly, 3) is not required for the RSV G-induced illness in mice. These findings have important implications for the evaluation of candidate RSV vaccines.

Indexed as

AnimalsBronchoalveolar LavageCD4-Positive T-LymphocytesChemokine CCL11Enzyme-Linked Immunosorbent AssayImmunizationInterleukin-13Interleukin-4Interleukin-5LungMiceMice, Inbred BALB CMice, KnockoutPulmonary EosinophiliaRespiratory Syncytial VirusesRespiratory Syncytial Virus InfectionsCcl11 protein, mouseChemokine CCL11G glycoprotein, Respiratory syncytial virusInterleukin-13Interleukin-4Interleukin-5Respiratory Syncytial Virus VaccinesViral Fusion Proteins

Identifiers

PMID18519743
PMCPMC2516895
OpenAlexW2141538789

What OpenQuestion holds

Textmetadata
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.