Evidence map›Paper›PMID 17557802›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2007

MAPK and heat shock protein 27 activation are associated with respiratory syncytial virus induction of human bronchial epithelial monolayer disruption.

Divyendu Singh, Kelly L McCann, Farhad Imani

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.2field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Programmed cell death in human respiratory syncytial virus infection.Frontiers in cellular and infection microbiology · 2025
    Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Vitamin DEuropean journal of cell biology · 2023
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Measurement of Airway Epithelial Permeability: Methods and Protocols.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  17. Review
  18. Review
  19. Review
  20. Disruption of the airway epithelial barrier in a murine model of respiratory syncytial virus infection.American journal of physiology. Lung cellular and molecular physiology · 2019
    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.

Divyendu SinghLaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Kelly L McCann
Farhad Imani
National Institutes of Health · US

Funding

Viral regulation of innate and adaptive immune responsesZ01ES101784 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI IMANI, FARHAD · 2004 to 2008
$3.0M
Intramural NIH HHS Z01 ES101784
6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) is the major cause of bronchiolitis in infants, and a common feature of RSV infections is increased lung permeability. The accumulation of fluid in the infected lungs is caused by changes in the endothelial and epithelial membrane integrity. However, the exact mechanisms of viral-induced fluid extravasation remain unclear. Here, we report that infection of human epithelial cells with RSV results in significant epithelial membrane barrier disruption as assessed by a decrease in transepithelial electrical resistance (TEpR). This decrease in TEpR, which indicates changes in paracellular permeability, was mediated by marked cellular cytoskeletal rearrangement. Importantly, the decrease in TEpR was attenuated by using p38 MAPK inhibitors (SB-203580) but was partially affected by JNK inhibitor SP-600125. Interestingly, treatment of A549 cells with MEK1/2 inhibitor (U-0126) led to a decrease in TEpR in the absence of RSV infection. The changes in TEpR were concomitant with an increase in heat shock protein 27 (Hsp27) phosphorylation and with actin microfilament rearrangement. Thus our data suggest that p38 MAPK and Hsp27 are required for RSV induction of human epithelial membrane permeability.

Indexed as

ApoptosisBronchiCapillary PermeabilityCells, CulturedCytoskeletonExtravascular Lung WaterHeat-Shock ProteinsHSP27 Heat-Shock ProteinsHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 1MAP Kinase Kinase 2MAP Kinase Signaling SystemMolecular ChaperonesNeoplasm Proteinsp38 Mitogen-Activated Protein KinasesHeat-Shock ProteinsHSP27 Heat-Shock ProteinsHSPB1 protein, humanJNK Mitogen-Activated Protein KinasesMAP2K2 protein, humanMAP Kinase Kinase 1MAP Kinase Kinase 2Molecular ChaperonesNeoplasm Proteinsp38 Mitogen-Activated Protein Kinases

Identifiers

PMID17557802
PMCPMC2231338
OpenAlexW2073172099

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.