Evidence map›Paper›PMID 28018859›Full record

ArticleFrontiers in cellular and infection microbiology2016

Autophagy, TGF-β, and SMAD-2/3 Signaling Regulates Interferon-β Response in Respiratory Syncytial Virus Infected Macrophages.

Swechha M Pokharel, Niraj K Shil, Santanu Bose

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Autophagy: regulating the seesaw of bone-fat balance.Frontiers in cell and developmental biology · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Article
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  18. Transforming growth factor-β in tumour development.Frontiers in molecular biosciences · 2022
    Review
  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

3 authors at 1 institution in 1 country.

Swechha M PokharelDepartment of Veterinary Microbiology and Pathology, Washington State University Pullman, WA, USA.
Niraj K ShilDepartment of Veterinary Microbiology and Pathology, Washington State University Pullman, WA, USA.
Santanu BoseDepartment of Veterinary Microbiology and Pathology, Washington State University Pullman, WA, USA.
Washington State University · US

Funding

Molecular and cellular mechanism regulating innate immunity and inflammation during pattern recognition receptor activation and respiratory virus infectionR01AI083387 · NIAID · WASHINGTON STATE UNIVERSITY · PI BOSE, SANTANU · 2010 to 2021
$3.1M
NIAID NIH HHS R01 AI083387
6 · The paper itself

Abstract

Human respiratory syncytial virus (RSV) is a lung tropic virus causing severe airway diseases including bronchiolitis and pneumonia among infants, children, and immuno-compromised individuals. RSV triggers transforming growth factor-β (TGF-β) production from lung epithelial cells and TGF-β facilitates RSV infection of these cells. However, it is still unknown whether RSV infected myeloid cells like macrophages produce TGF-β and the role of TGF-β if any during RSV infection of these cells. Our study revealed that RSV infected macrophages produce TGF-β and as a consequence these cells activate TGF-β dependent SMAD-2/3 signaling pathway. Further mechanistic studies illustrated a role of autophagy in triggering TGF-β production from RSV infected macrophages. In an effort to elucidate the role of TGF-β and SMAD-2/3 signaling during RSV infection, we surprisingly unfolded the requirement of TGF-β-SMAD2/3 signaling in conferring optimal innate immune antiviral response during RSV infection of macrophages. Type-I interferon (e.g., interferon-β or IFN-β) is a critical host factor regulating innate immune antiviral response during RSV infection. Our study revealed that loss of TGF-β-SMAD2/3 signaling pathway in RSV infected macrophages led to diminished expression and production of IFN-β. Inhibiting autophagy in RSV infected macrophages also resulted in reduced production of IFN-β. Thus, our studies have unfolded the requirement of autophagy-TGF-β-SMAD2/3 signaling network for optimal innate immune antiviral response during RSV infection of macrophages.

Indexed as

AnimalsAntiviral AgentsAutophagyBeclin-1Disease Models, AnimalImmunity, InnateInterferon-betaInterferon Type IMacrophagesMiceMice, Inbred C57BLRAW 264.7 CellsRespiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsSignal TransductionSmad2 ProteinAntiviral AgentsBeclin-1Interferon-betaInterferon Type ISmad2 ProteinSmad2 protein, mouseSmad3 ProteinSmad3 protein, mouseTransforming Growth Factor betaautophagyinterferon-βmacrophagesrespiratory syncytial virusSMADTGF-β

Identifiers

PMID28018859
PMCPMC5149518
OpenAlexW2560320926

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.