Evidence map›Paper›PMID 1699953›Full record

ArticleThe Journal of cell biology1990

Tumor necrosis factor and CD11/CD18 (beta 2) integrins act synergistically to lower cAMP in human neutrophils.

C Nathan, E Sanchez

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of cell biology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 147 citations in OpenAlex.

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  18. Evaluation of the effects of defensins on neutrophil functions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 1996
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  19. Endogenously opsonized particles divert prostanoid action from lethal to protective in models of experimental endotoxemia.Proceedings of the National Academy of Sciences of the United States of America · 1995
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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

2 authors at 1 institution in 1 country.

C NathanBeatrice and Samuel A. Seaver Laboratory, Department of Medicine, Cornell University Medical Center, New York 10021.
E Sanchez
NewYork–Presbyterian Hospital · US

Funding

OXIDATIVE INJURY BY HUMAN NEUTROPHILSR01CA045218 · NCI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI NATHAN, CARL F · 1987 to 1996
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NCI NIH HHS CA45218
6 · The paper itself

Abstract

The ability of neutrophils (PMN) to undergo a prolonged respiratory burst in response to cytokines such as tumor necrosis factor-alpha (TNF) depends on expression of CD11/CD18 (beta 2) integrins and interaction with matrix protein-coated surfaces (Nathan, C., S. Srimal, C. Farber, E. Sanchez, L. Kabbash, A. Asch, J. Gailit, and S. D. Wright. 1989. J. Cell Biol. 109:1341-1349). We tested the hypothesis that changes in cAMP mediate the joint action of cytokines and integrins. When plated on FBS- or fibrinogen-coated surfaces, PMN responded to TNF with a sustained fall in intracellular cAMP. This did not occur without TNF; in suspended PMN; in PMN treated with anti-CD18 mAb; or in PMN genetically deficient in beta 2 integrins. A preceding fall in cAMP appeared essential for TNF to induce a respiratory burst, because drugs that elevate cAMP blocked the burst if added any time before, but not after, its onset. Adenosine analogues and cytochalasins also block the TNF-induced respiratory burst if added before, but not after, its onset. Both also blocked the TNF-induced fall in cAMP. The effect of cytochalasins led us to examine the relationship between cAMP and actin reorganization. The same conditions that led to a sustained fall in cAMP led at the same time to cell spreading and the assembly of actin filaments. As with the respiratory burst, cAMP-elevating agents inhibited TNF-induced cell spreading and actin filament assembly if added before, but not after, spreading began. Thus, occupation of TNF receptors and engagement of CD18 integrins interact synergistically in PMN to promote a fall in cAMP. The fall in cAMP is closely related to cell spreading and actin reorganization. These changes are necessary for TNF to induce a prolonged respiratory burst. We conclude that integrins can act jointly with cytokines to affect cell shape and function through alterations in the level of a second messenger, cAMP.

Indexed as

1-Methyl-3-isobutylxanthine2-ChloroadenosineActin CytoskeletonActinsAntigens, DifferentiationBlood ProteinsBucladesineCD11 AntigensCD18 AntigensCell AdhesionCell MovementColforsinCyclic AMPHumansHydrogen PeroxideIntegrins1-Methyl-3-isobutylxanthine2-ChloroadenosineActinsAntigens, DifferentiationBlood ProteinsBucladesineCD11 AntigensCD18 AntigensColforsinCyclic AMPHydrogen PeroxideIntegrinsOxygenPlasticsReceptors, Leukocyte-AdhesionTumor Necrosis Factor-alpha

Identifiers

PMID1699953
PMCPMC2116341
OpenAlexW2137356321

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.