Evidence map›Paper›PMID 24205331›Full record

ArticlePloS one2013

Critical role of TLR4 in human metapneumovirus mediated innate immune responses and disease pathogenesis.

Thangam Sudha Velayutham, Deepthi Kolli, Teodora Ivanciuc, Roberto P Garofalo, Antonella Casola

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Receptors and host factors: key players in human metapneumovirus infection.Frontiers in cellular and infection microbiology · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
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 1 institution in 1 country.

Thangam Sudha VelayuthamDepartment of Pediatrics, University of Texas Medical Branch, Galveston, Texas, United States of America.
Deepthi Kolli
Teodora Ivanciuc
Roberto P Garofalo
Antonella Casola
The University of Texas Medical Branch at Galveston · US

Funding

Virus, Tissue Culture and ImmunoassayP01AI062885 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI BRASIER, ALLAN R. · 2005 to 2022
$23.9M
Synthetic Organic Chemistry CoreP30ES006676 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI ELFERINK, CORNELIS JOHAN · 1995 to 2017
$21.7M
Innate Immune Response to Human Metapneumovirus InfectionR01AI079246 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI CASOLA, ANTONELLA · 2010 to 2014
$1.9M
NIAID NIH HHS P01 AI062885NIAID NIH HHS R01 AI079246NIEHS NIH HHS P30 ES006676
6 · The paper itself

Abstract

Human metapneumovirus (hMPV) is one of the main causes of acute respiratory tract infections in children, elderly and immunocompromised patients. The mammalian Toll-like receptors (TLR) were identified as critical regulators of innate immunity to a variety of microbes, including viruses. We have recently shown that hMPV-induced cytokine, chemokine and type I interferon secretion in dendritic cells occurs via TLR4, however, its role in hMPV-induced disease is unknown. In this study, wild-type(WT) and TLR4-deficient mice (TLR4⁻/⁻) were infected with hMPV and examined for clinical disease parameters, such as body weight loss and airway obstruction, viral clearance, lung inflammation, dendritic cell maturation, T-cell proliferation and antibody production. Our results demonstrate that absence of TLR4 in hMPV-infected mice significantly reduced the inflammatory response as well as disease severity, shown by reduced body weight loss and airway obstruction and hyperresponsiveness (AHR), compared to WT mice. Levels of cytokines and chemokines were also significantly lower in the TLR4⁻/⁻ mice. Accordingly, recruitment of inflammatory cells in the BAL, lungs, as well as in lymph nodes, was significantly reduced in the TLR4⁻/⁻ mice, however, viral replication and clearance, as well as T-cell proliferation and neutralizing antibody production, were not affected. Our findings indicate that TLR4 is important for the activation of the innate immune response to hMPV, however it does play a role in disease pathogenesis, as lack of TLR4 expression is associated with reduced clinical manifestations of hMPV disease, without affecting viral protection.

Indexed as

Immunity, InnateAirway ObstructionAnimalsAntibodies, NeutralizingBody WeightBronchoalveolar LavageCell ProliferationDendritic CellsFemaleMetapneumovirusMiceT-LymphocytesToll-Like Receptor 4Virus ReplicationAntibodies, NeutralizingToll-Like Receptor 4

Identifiers

PMID24205331
PMCPMC3812158
OpenAlexW2048545336

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.