Evidence map›Paper›PMID 2156895›Full record

ArticleThe Journal of clinical investigation1990

The adenosine/neutrophil paradox resolved: human neutrophils possess both A1 and A2 receptors that promote chemotaxis and inhibit O2 generation, respectively.

B N Cronstein, L Daguma, D Nichols, A J Hutchison, M Williams

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
12.1field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 377 citations in OpenAlex.

  1. Trial
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  8. Article
  9. The role of adenosine AInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Adenosine: a partially discovered medicinal agent.Future journal of pharmaceutical sciences · 2021
    Review
  18. Article
  19. Review
  20. Late Protective Effect of Netrin-1 in the Murine Acetaminophen Hepatotoxicity Model.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article

65 more citing papers are in PubMed but not listed here.

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 1 country.

B N CronsteinDepartment of Medicine, New York University Medical Center, New York 10016.
L Daguma
D Nichols
A J Hutchison
M Williams
Columbia University Irving Medical Center · USNew York University · US

Funding

INHIBITION OF NEUTROPHIL MEDIATED TISSUE INJURYK08AR001490 · NIAMS · NEW YORK UNIVERSITY · PI CRONSTEIN, BRUCE NEIL · 1986 to 1989
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THE EFFECT OF AGING ON THE IMMUNE RESPONSEP01AG004860 · NIA · NEW YORK UNIVERSITY · PI GOTTESMAN, SUSAN R S · 1985 to 1994
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NIAMS NIH HHS AR-01490NIA NIH HHS AG-04860
6 · The paper itself

Abstract

Occupancy of specific receptors on neutrophils by adenosine or its analogues diminishes the stimulated release of toxic oxygen metabolites from neutrophils, while paradoxically promoting chemotaxis. We now report evidence that two distinct adenosine receptors are found on neutrophils (presumably the A1 and A2 receptors of other cell types). These adenosine receptors modulate chemotaxis and O2- generation, respectively. N6-Cyclopentyladenosine (CPA), a selective A1 agonist, promoted neutrophil chemotaxis to the chemoattractant FMLP as well as or better than 5'N-ethylcarboxamidoadenosine (NECA). In contrast, CPA did not inhibit O2- generation stimulated by FMLP. Pertussis toxin completely abolished promotion of chemotaxis by CPA but enhanced inhibition by NECA of O2- generation. Disruption of microtubules by colchicine or vinblastine also abrogated the enhancement by NECA of chemotaxis whereas these agents did not markedly interfere with inhibition by NECA of O2- generation. FMLP receptors, once they have bound ligand, shift to a high affinity state and become associated with the cytoskeleton. NECA significantly increased association of [3H]FMLP with cytoskeletal preparations as it inhibited O2-. Disruption of microtubules did not prevent NECA from increasing association of [3H]FMLP with cytoskeletal preparations. Additionally, CPA (A1 agonist) did not increase binding of [3H]FMLP to the cytoskeleton as well as NECA (A2 agonist). These studies indicate that occupancy of one class of adenosine receptors (A1) promotes chemotaxis by a mechanism requiring intact microtubules and G proteins whereas engagement of a second class of receptors (A2) inhibits O2- generation. Signalling via A2 receptors is independent of microtubules, insensitive to pertussis toxin and is associated with binding of [3H]FMLP to cytoskeletal preparations.

Indexed as

Chemotaxis, LeukocyteAdenosineAdenosine-5'-(N-ethylcarboxamide)Cells, CulturedColchicineHumansNeutrophilsN-Formylmethionine Leucyl-PhenylalanineReceptors, PurinergicSuperoxidesAdenosineAdenosine-5'-(N-ethylcarboxamide)ColchicineN(6)-cyclopentyladenosineN-Formylmethionine Leucyl-PhenylalanineReceptors, PurinergicSuperoxides

Identifiers

PMID2156895
PMCPMC296546
OpenAlexW2087167599

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.