Evidence map›Paper›PMID 20489160›Full record

ArticleThe American journal of pathology2010

CFTR inhibition provokes an inflammatory response associated with an imbalance of the annexin A1 pathway.

Jesmond Dalli, Guglielmo Rosignoli, Richard P G Hayhoe, Aleksander Edelman, Mauro Perretti

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  7. Article
  8. Review
  9. NM23 proteins: innocent bystanders or local energy boosters for CFTR?Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  10. Article
  11. Article
  12. Synergy of cAMP and calcium signaling pathways in CFTR regulation.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  13. Article
  14. Review
  15. Article
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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 2 institutions in 2 countries.

Jesmond DalliThe William Harvey Research Institute, Barts and The London School of Medicine, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
Guglielmo Rosignoli
Richard P G Hayhoe
Aleksander Edelman
Mauro Perretti
Queen Mary University of London · GBDélégation Paris 5 · FR

Funding

Wellcome Trust 069234/Z/02/ZWellcome Trust 086867/Z/08
6 · The paper itself

Abstract

Cystic fibrosis (CF), a disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, is characterized by chronic bacterial infections and inflammation in the lung. Having previously shown that deletion of CFTR is associated with lower expression of the endogenous anti-inflammatory protein Annexin A1 (AnxA1), we investigated further this possible functional connection using a validated CFTR inhibitor. Treatment of mice with the CFTR inhibitor-172 (CFTR(172)) augmented the acute peritonitis promoted by zymosan, an effect associated with lower AnxA1 levels in peritoneal cells. Similar results were obtained with another, chemically distinct, CFTR inhibitor. The pro-inflammatory effect of CFTR(172) was lost in AnxA1(-/-), as well as CFTR(-/-) mice. Importantly, administration of hrAnxA1 and its peptido-mimetic to CFTR(-/-) animals or to animals treated with CFTR(172) corrected the exaggerated leukocyte migration seen in these animals. In vitro assays with human Polymorphonuclear leukocyte (PMN) demonstrated that CFTR(172) reduced cell-associated AnxA1 by promoting release of the protein in microparticles. We propose that the reduced impact of the counterregulatory properties of AnxA1 in CF cells contributes to the inflammatory phenotype characteristic of this disease. Thus, these findings provide an important insight into the mechanism underlying the inflammatory disease associated with CFTR inhibition while, at the same time, providing a novel pharmacological target for controlling the inflammatory phenotype of CF.

Indexed as

AnimalsAnnexin A1BenzoatesCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorHumansInflammationMiceMice, Inbred C57BLMice, KnockoutNeutrophilsPeritonitisThiazolidinesZymosan3-((3-trifluoromethyl)phenyl)-5-((3-carboxyphenyl)methylene)-2-thioxo-4-thiazolidinoneAnnexin A1BenzoatesCystic Fibrosis Transmembrane Conductance RegulatorThiazolidinesZymosan

Identifiers

PMID20489160
PMCPMC2893661
OpenAlexW2095518419

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.