Evidence map›Paper›PMID 21057089›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

A cell-impermeable cyclosporine A derivative reduces pathology in a mouse model of allergic lung inflammation.

Molly A Balsley, Miroslav Malesevic, Erik J Stemmy, Jason Gigley, Rosalyn A Jurjus, Dallen Herzog, Michael I Bukrinsky, Gunter Fischer, Stephanie L Constant

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Secreted Extracellular Cyclophilin A Is a Novel Mediator of Ventilator-induced Lung Injury.American journal of respiratory and critical care medicine · 2021
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Targeting Extracellular Cyclophilin A Reduces Neuroinflammation and Extends Survival in a Mouse Model of Amyotrophic Lateral Sclerosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  11. Extracellular cyclophilins in health and disease.Biochimica et biophysica acta · 2015
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Extracellular cyclophilin levels associate with parameters of asthma in phenotypic clusters.The Journal of asthma : official journal of the Association for the Care of Asthma · 2011
    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

9 authors at 3 institutions in 2 countries.

Molly A BalsleyDepartment of Microbiology, Immunology, and Tropical Medicine, The George Washington University Medical Center, Washington, DC 20037, USA.
Miroslav Malesevic
Erik J Stemmy
Jason Gigley
Rosalyn A Jurjus
Dallen Herzog
Michael I Bukrinsky
Gunter Fischer
Stephanie L Constant
George Washington University · USWashington University Medical Center · USMax Planck Research Unit for Enzymology of Protein Folding · DE

Funding

Contribution of cyclophilins to leukocyte recruitment in lung inflammationR01AI067254 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI BUKRINSKY, MICHAEL ILYA · 2006 to 2009
$1.3M
NIAID NIH HHS R01 AI067254NIAID NIH HHS R01-AI67254
6 · The paper itself

Abstract

Although the main regulators of leukocyte trafficking are chemokines, another family of chemotactic agents is cyclophilins. Intracellular cyclophilins function as peptidyl-prolyl cis-trans isomerases and are targets of the immunosuppressive drug cyclosporine A (CsA). Cyclophilins can also be secreted in response to stress factors, with elevated levels of extracellular cyclophilins detected in several inflammatory diseases. Extracellular cyclophilins are known to have potent chemotactic properties, suggesting that they might contribute to inflammatory responses by recruiting leukocytes into tissues. The objective of the present study was to determine the impact of blocking cyclophilin activity using a cell-impermeable derivative of CsA to specifically target extracellular pools of cyclophilins. In this study, we show that treatment with this compound in a mouse model of allergic lung inflammation demonstrates up to 80% reduction in inflammation, directly inhibits the recruitment of Ag-specific CD4(+) T cells, and works equally well when delivered at 100-fold lower doses directly to the airways. Our findings suggest that cell-impermeable analogs of CsA can effectively reduce inflammatory responses by targeting leukocyte recruitment mediated by extracellular cyclophilins. Specifically blocking the extracellular functions of cyclophilins may provide an approach for inhibiting the recruitment of one of the principal immune regulators of allergic lung inflammation, Ag-specific CD4(+) T cells, into inflamed airways and lungs.

Indexed as

AnimalsAntigensAsthmaCD4-Positive T-LymphocytesCyclophilinsCyclosporinsDisease Models, AnimalImmunosuppressive AgentsInflammationLungMiceMice, Inbred BALB CAntigensCyclophilinsCyclosporinsImmunosuppressive Agents

Identifiers

PMID21057089
PMCPMC3603141
OpenAlexW2159673528

What OpenQuestion holds

Textmetadata
LicenceTDM
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.