Evidence map›Paper›PMID 19641187›Full record

ArticleBlood2009

Eosinophil viability is increased by acidic pH in a cAMP- and GPR65-dependent manner.

Leah C Kottyan, Ann R Collier, Khanh H Cao, Kathryn A Niese, Megan Hedgebeth, Caius G Radu, Owen N Witte, Gurjit K Khurana Hershey, Marc E Rothenberg, Nives Zimmermann

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06357104 (Detoxification From the Lipid Tract by Cocktail Design), which is not on this map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.2field-weighted citation impact, top 9% 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.

NCT06357104 phase4completednot on this mapstarted 2024, after this paper: background citation

Detoxification From the Lipid Tract by Cocktail Design

TypeinterventionalSponsorPachankis, Yang I., M.D.Ran2024 to 2024Enrolled1ConditionsCOVID-19 Vaccine Adverse ReactionArmselectroencephalogram biofeedback, electrical brain stimulation, ultra-low frequency transcranial magnetic stimulation, Sertraline Hydrochloride, Clonazepam
3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Activation of the proton-sensing GPCR, GPR65 on fibroblast-like synoviocytes contributes to inflammatory joint pain.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Airway acidification impaired host defense againstEmerging microbes & infections · 2022
    Article
  13. Review
  14. Physiological relevance of proton-activated GPCRs.Pflugers Archiv : European journal of physiology · 2022
    Review
  15. Article
  16. Review
  17. pH and Proton Sensor GPR65 Determine Susceptibility to Atopic Dermatitis.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  18. Review
  19. Review
  20. Review
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

10 authors at 3 institutions in 2 countries.

Leah C KottyanCincinnati Children's Hospital Medical Center, OH, USA.
Ann R Collier
Khanh H Cao
Kathryn A Niese
Megan Hedgebeth
Caius G Radu
Owen N Witte
Gurjit K Khurana Hershey
Marc E Rothenberg
Nives Zimmermann
Cincinnati Children's Hospital Medical Center · USHoward Hughes Medical Institute · USUniversity of Cincinnati Medical Center · US

Funding

Howard Hughes Medical InstitutePHS HHS R21A1079251
6 · The paper itself

Abstract

The microenvironment of the lung in asthma is acidic, yet the effect of acidity on inflammatory cells has not been well established. We now demonstrate that acidity inhibits eosinophil apoptosis and increases cellular viability in a dose-dependent manner between pH 7.5 and 6.0. Notably, acidity induced eosinophil cyclic adenosine 5'-monophosphate (cAMP) production and enhanced cellular viability in an adenylate cyclase-dependent manner. Furthermore, we identify G protein-coupled receptor 65 (GPR65) as the chief acid-sensing receptor expressed by eosinophils, as GPR65-deficient eosinophils were resistant to acid-induced eosinophil cAMP production and enhanced viability. Notably, GPR65(-/-) mice had attenuated airway eosinophilia and increased apoptosis in 2 distinct models of allergic airway disease. We conclude that eosinophil viability is increased in acidic microenvironments in a cAMP- and GPR65-dependent manner.

Indexed as

AcidsAnimalsApoptosisAsthmaCells, CulturedCell SurvivalCyclic AMPDisease Models, AnimalEosinophilsFemaleHydrogen-Ion ConcentrationMaleMiceMice, Inbred BALB CMice, TransgenicPneumoniaAcidsCyclic AMPGPR65 protein, mouseProtonsReceptors, G-Protein-Coupled

Identifiers

PMID19641187
PMCPMC2756132
OpenAlexW1999837154

What OpenQuestion holds

Textmetadata
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.