Evidence map›Paper›PMID 12871828›Full record

ArticleBritish journal of pharmacology2003

Substance P increases neutrophil adhesion to human umbilical vein endothelial cells.

Chiara Dianzani, Massimo Collino, Grazia Lombardi, Giovanni Garbarino, Roberto Fantozzi

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.1field-weighted citation impact, top 29% 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

23 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Neuronal regulation of bone and tendon injury repair: a focused review.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024
    Review
  4. Cutaneous innervation in impaired diabetic wound healing.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
  5. Article
  6. Evaluation of neuroprotective effects of insulin on immuno-inflammatory and systemic disorders induced by kaliotoxin, a Kv1.3 channel blocker.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Article
  7. Multiple Phenotypic Changes Define Neutrophil Priming.Frontiers in cellular and infection microbiology · 2017
    Review
  8. Article
  9. Article
  10. The role of histamine in neurogenic inflammation.British journal of pharmacology · 2013
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

5 authors at 2 institutions in 1 country.

Chiara DianzaniDepartment of Anatomy, Pharmacology and Forensic Medicine, University of Turin, 10125 Torino, Italy. chiara.dianzani@unito.it
Massimo Collino
Grazia Lombardi
Giovanni Garbarino
Roberto Fantozzi
University of Turin · ITUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Adhesion of neutrophils (PMNs) to vascular endothelial cells (EC) is a critical step in recruitment and infiltration of leukocytes into tissues during inflammation. Substance P (SP), a neuropeptide released from sensory nerves, evoked PMN adhesion to EC. The NK receptor subtype(s) and the cell type(s) involved were investigated. 2. SP was coincubated with human PMNs and EC from the human umbilical vein (HUVEC); adhesion was quantitated by computerised microimaging fluorescence analysis. 3. The proadhesive effects of SP (range 10(-18)-10(-6) M) were illustrated in a biphasic dose-response curve, with a maximum at 10(-15) M (276+/-16% adhesion vs control; P<0.01) and another one at 10(-10) M (200+/-18% adhesion vs control; P<0.01). Neurokinin A was less active and neurokinin B was inactive. The adhesion molecules LFA-1 and OKM-1, but not selectins, were involved according to results with selective mAbs. 4. The NK(1) agonist [Sar(9),Met(O(2))(11)]SP reproduced the effects of SP, whereas the NK(2) agonist [betaAla(8)]-neurokininA (4-10) acted at 10(-13)-10(-8) M only. The NK(3) agonist, senktide, was ineffective. 5. The NK(1) antagonists, CP 96,345 and L 703,606 (both 10(-6) M), abolished the effect of 10(-15) M SP and inhibited that of 10(-10) M SP by 56+/-5% (P<0.01). By comparison, the NK(2) antagonist, SR 48,968 (10(-7) M), partially antagonised the adhesion evoked by 10(-10) M SP (% inhibition: 61+/-6; P<0.05). 6. Since preincubation of PMNs and HUVEC with SP gave the same results it is clear that both cell types contributed to its proadhesive effects. 7. These results indicate that SP induced a proadhesive effect during inflammatory processes, which was mediated by NK(1) and NK(2) receptors.

Indexed as

AdultCell AdhesionCell LineEndothelial CellsFemaleHumansMaleMiddle AgedNeutrophilsSubstance PUmbilical VeinsSubstance P

Identifiers

PMID12871828
PMCPMC1573938
OpenAlexW1997106813

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.