Evidence map›Paper›PMID 8971006›Full record

ArticleJournal of virology1996

Transcriptional activation of the interleukin-8 gene by respiratory syncytial virus infection in alveolar epithelial cells: nuclear translocation of the RelA transcription factor as a mechanism producing airway mucosal inflammation.

R Garofalo, M Sabry, M Jamaluddin, R K Yu, A Casola, P L Ogra, A R Brasier

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

102 citing papers in PubMed, 215 citations in OpenAlex.

  1. Article
  2. Frontiers in cellular and infection microbiology · 2025
    Article
  3. Regulatory role of microRNAs in virus-mediated inflammation.Journal of inflammation (London, England) · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Respiratory syncytial virus infection induces the release of transglutaminase 2 from human airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

42 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

R GarofaloDepartment of Medicine, University of Texas Medical Branch, Galveston 77555-1060, USA.
M Sabry
M Jamaluddin
R K Yu
A Casola
P L Ogra
A R Brasier
The University of Texas Medical Branch at Galveston · US

Funding

CORE--LABORATORYP30HD027841 · NICHD · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI GOLDBLUM, RANDALL M · 1990 to 2002
$793k
MUCOSAL IMMUNE RESPONSE TO RESPIRATORY SYNCYTIAL VIRUSR01AI015939 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI GAROFALO, ROBERTO P · 1985 to 1998
–
NIAID NIH HHS AI/HL 15939-14A1NICHD NIH HHS R30HD 27841
6 · The paper itself

Abstract

The most common cause of epidemic pediatric respiratory disease, respiratory syncytial virus (RSV), stimulates interleukin-8 (IL-8) synthesis upon infecting airway epithelium, an event necessary for the development of mucosal inflammation. We investigated the mechanism for enhanced IL-8 production in human A549 type II pulmonary epithelial cells. Infection with sucrose-purified RSV (pRSV) produced a time-dependent increase in the transcriptional initiation rate of the IL-8 gene. Transient transfection of the human IL-8 promoter mutated in the binding site for nuclear factor-kappaB (NF-kappaB) demonstrated that this sequence was essential for pRSV-activated transcription. Gel mobility shift assays demonstrated pRSV induction of sequence-specific binding complexes; these complexes were supershifted only by antibodies directed to the potent NF-kappaB transactivating subunit RelA. Both Western immunoblot and indirect immunofluorescence assays showed that cytoplasmic RelA in uninfected cells became localized to the nucleus after pRSV infection. RelA activation requires replicating RSV, because neither conditioned medium nor UV-inactivated pRSV was able to stimulate its translocation. We conclude that RelA undergoes changes in subcellular distribution in airway epithelial cells upon pRSV infection. The ability of replicating RSV to activate RelA translocation may play an important role in activating IL-8 and other inflammatory gene products necessary for airway mucosal inflammation seen in RSV disease.

Indexed as

Transcriptional ActivationCell NucleusDNA-Binding ProteinsEpithelial CellsEpitheliumHumansInflammationInterleukin-8LungNF-kappa BRespiratory Syncytial VirusesTranscription Factor RelATranscription FactorsTumor Cells, CulturedDNA-Binding ProteinsInterleukin-8NF-kappa BTranscription Factor RelATranscription Factors

Identifiers

PMID8971006
PMCPMC190974
OpenAlexW2106491281

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.