Evidence map›Paper›PMID 9312165›Full record

ArticleThe Journal of clinical investigation1997

Theophylline accelerates human granulocyte apoptosis not via phosphodiesterase inhibition.

K Yasui, B Hu, T Nakazawa, K Agematsu, A Komiyama

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Mitochondria in the center of human eosinophil apoptosis and survival.International journal of molecular sciences · 2014
    Review
  7. Review
  8. Review
  9. Article
  10. Theophylline.Pharmaceuticals (Basel, Switzerland) · 2010
    Review
  11. Article
  12. Review
  13. Article
  14. Decreased neutrophil apoptosis in tracheal fluids of preterm infants at risk of chronic lung disease.Archives of disease in childhood. Fetal and neonatal edition · 2003
    Article
  15. Article
  16. Review
  17. Review
  18. 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

5 authors at 1 institution in 1 country.

K YasuiDepartment of Pediatrics, Shinshu University School of Medicine, Matsumoto 390, Japan.
B Hu
T Nakazawa
K Agematsu
A Komiyama
Shinshu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Theophylline, in addition to its bronchodilator effect, is reported to have an antiinflammatory action that may account for its clinical effectiveness in the reduction of inflammatory cells in the airway. In bronchial asthma, such inflammatory cytokines as GM-CSF and IL-5 are upregulated and have been proposed to cause granulocyte infiltration (neutrophils and eosinophils) in the airway by inhibition of granulocyte apoptosis. We examined the abilities of theophylline to counteract the prolongation of human granulocyte survival caused by cytokines. Theophylline was shown to shorten granulocyte survival in a dose-dependent manner. Upon incubation with a therapeutical concentration of theophylline (0.1 mM; 18 microg/ml), percentages of GM-CSF (10 ng/ml)-induced delayed apoptosis increased from 18+/-2% to 38+/-3% (p < 0.02) in neutrophils and from 21+/-2% to 35+/-2% (p < 0.02; 24-h incubation) in eosinophils. The percentage of IL-5 (5 ng/ml)-induced delayed eosinophil apoptosis also increased from 22+/-4% to 33+/-2% (P < 0. 05). In contrast, cyclic AMP (cAMP)-increasing agents (3-isobutylmethylxanthine, dibutyryl cAMP, and rolipram) inhibited granulocyte apoptosis in the control and anti-Fas antibody-treated cells. In eosinophils, the expression of bcl-2 protein decreased after incubation with theophylline. These findings suggest that theophylline accelerates granulocyte apoptosis, which may play an essential role in inflammation, and controls granulocyte longevity regardless of the elevation of intracellular cAMP levels.

Indexed as

1-Methyl-3-isobutylxanthineAnti-Inflammatory Agents, Non-SteroidalApoptosisBucladesineCell SurvivalCyclic AMPDose-Response Relationship, Drugfas ReceptorGranulocyte-Macrophage Colony-Stimulating FactorGranulocytesHumansInterleukin-5Phosphodiesterase InhibitorsPhosphoric Diester HydrolasesProto-Oncogene Proteins c-bcl-2Pyrrolidinones1-Methyl-3-isobutylxanthineAnti-Inflammatory Agents, Non-SteroidalBucladesineCyclic AMPfas ReceptorGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-5Phosphodiesterase InhibitorsPhosphoric Diester HydrolasesProto-Oncogene Proteins c-bcl-2PyrrolidinonesRolipramTheophylline

Identifiers

PMID9312165
PMCPMC508350
OpenAlexW2087509980

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.