Evidence map›Paper›PMID 21411730›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Phospholipase C-β3 is a key modulator of IL-8 expression in cystic fibrosis bronchial epithelial cells.

Valentino Bezzerri, Pio d'Adamo, Alessandro Rimessi, Carmen Lanzara, Sergio Crovella, Elena Nicolis, Anna Tamanini, Emmanouil Athanasakis, Maela Tebon, Giulia Bisoffi and 6 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00037765 (Gene Modifiers of Cystic Fibrosis Lung Disease), which is not on this map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 15% 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.

NCT00037765 active not recruitingnot on this map

Gene Modifiers of Cystic Fibrosis Lung Disease

TypeobservationalSponsorUniversity of North Carolina, Chapel HillRan2001 to 2027Enrolled600ConditionsCystic Fibrosis, Lung Diseases
3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. International journal of molecular sciences · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Update in Cystic Fibrosis 2018.American journal of respiratory and critical care medicine · 2019
    Review
  15. Article
  16. Article
  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

16 authors at 5 institutions in 2 countries.

Valentino BezzerriLaboratory of Molecular Pathology, University Hospital of Verona, 37126 Verona, Italy.
Pio d'Adamo
Alessandro Rimessi
Carmen Lanzara
Sergio Crovella
Elena Nicolis
Anna Tamanini
Emmanouil Athanasakis
Maela Tebon
Giulia Bisoffi
Mitchell L Drumm
Michael R Knowles
Paolo Pinton
Paolo Gasparini
Giorgio Berton
Giulio Cabrini
University of Verona · ITUniversity of Trieste · ITUniversity of Ferrara · ITCase Western Reserve University · USUniversity of North Carolina at Chapel Hill · US

Funding

Translational Research in Cystic FibrosisP30DK027651 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI DRUMM, MITCHELL L · 1986 to 2014
$15.6M
Gene Modifiers in CF Lung DiseaseR01HL068890 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KNOWLES, MICHAEL R · 2001 to 2014
$9.5M
NHLBI NIH HHS HL68890NHLBI NIH HHS R01 HL068890NIDDK NIH HHS DK27651NIDDK NIH HHS P30 DK027651Telethon GGP09128
6 · The paper itself

Abstract

Respiratory insufficiency is the major cause of morbidity and mortality in patients affected by cystic fibrosis (CF). An excessive neutrophilic inflammation, mainly orchestrated by the release of IL-8 from bronchial epithelial cells and amplified by chronic bacterial infection with Pseudomonas aeruginosa, leads to progressive tissue destruction. The anti-inflammatory drugs presently used in CF patients have several limitations, indicating the need for identifying novel molecular targets. To address this issue, we preliminarily studied the association of 721 single nucleotide polymorphisms from 135 genes potentially involved in signal transduction implicated in neutrophil recruitment in a cohort of F508del homozygous CF patients with either severe or mild progression of lung disease. The top ranking association was found for a nonsynonymous polymorphism of the phospholipase C-β3 (PLCB3) gene. Studies in bronchial epithelial cells exposed to P. aeruginosa revealed that PLCB3 is implicated in extracellular nucleotide-dependent intracellular calcium signaling, leading to activation of the protein kinase Cα and Cβ and of the nuclear transcription factor NF-κB p65. The proinflammatory pathway regulated by PLCB3 acts by potentiating the Toll-like Receptors' signaling cascade and represents an interesting molecular target to attenuate the excessive recruitment of neutrophils without completely abolishing the inflammatory response.

Indexed as

Adenosine TriphosphateCalciumCell Line, TransformedCystic FibrosisEnzyme ActivationEpithelial CellsGene ExpressionGene FrequencyGenotypeGreen Fluorescent ProteinsHost-Pathogen InteractionsHumansInterleukin-8IsoenzymesLung DiseasesMicroscopy, FluorescenceAdenosine TriphosphateCalciumGreen Fluorescent ProteinsInterleukin-8IsoenzymesPhospholipase C betaPLCB3 protein, humanProtein Kinase CProtein Kinase C betaToll-Like ReceptorsTranscription Factor RelA

Identifiers

PMID21411730
PMCPMC4166552
OpenAlexW2098645242

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.