Evidence map›Paper›PMID 15778738›Full record

ArticleBritish journal of pharmacology2005

Expression of functional NK1 receptors in human alveolar macrophages: superoxide anion production, cytokine release and involvement of NF-kappaB pathway.

Claudio Bardelli, Gabriele Gunella, Federica Varsaldi, Pietro Balbo, Elisa Del Boca, Ilaria Seren Bernardone, Angela Amoruso, Sandra Brunelleschi

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Role of neuron and non-neuronal cell communication in persistent orofacial pain.Journal of dental anesthesia and pain medicine · 2019
    Review
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  13. Neural control of airway inflammation.Current allergy and asthma reports · 2009
    Review
  14. Article
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  18. Article
  19. Metalloelastase in lungs and alveolar macrophages is modulated by extracellular substance P in mice.American journal of physiology. Lung cellular and molecular physiology · 2008
    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

8 authors at 1 institution in 1 country.

Claudio BardelliDepartment of Medical Sciences, School of Medicine, University of Piemonte Orientale A. Avogadro, Via Solaroli, 17, 28100 Novara, Italy.
Gabriele Gunella
Federica Varsaldi
Pietro Balbo
Elisa Del Boca
Ilaria Seren Bernardone
Angela Amoruso
Sandra Brunelleschi
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1 Substance P (SP) is deeply involved in lung pathophysiology and plays a key role in the modulation of inflammatory-immune processes. We previously demonstrated that SP activates guinea-pig alveolar macrophages (AMs) and human monocytes, but a careful examination of its effects on human AMs is still scarce. 2 This study was undertaken to establish the role of SP in human AM isolated from healthy smokers and non-smokers, by evaluating the presence of tachykinin NK(1) receptors (NK-1R) and SP's ability to induce superoxide anion (O(2)(-)) production and cytokine release, as well as activation of the nuclear factor-kappaB (NF-kappaB) pathway. 3 By Western blot analysis and immunofluorescence, we demonstrate that authentic NK-1R are present on human AMs, a three-fold enhanced expression being observed in healthy smokers. These NK-1R are functional, as SP and NK(1) agonists dose-dependently induce O(2)(-) production and cytokine release. In AMs from healthy smokers, SP evokes an enhanced respiratory burst and a significantly increased release of tumor necrosis factor-alpha as compared to healthy non-smokers, but has inconsistent effects on IL-10 release. The NK(1) selective antagonist CP 96,345 ((2S,3S)-cis-2-diphenylmethyl-N[(2-methoxyphenyl)-methyl]-1-azabicyclo-octan-3-amine)) competitively antagonized SP-induced effects. 4 SP activates the transcription factor NF-kappaB, a three-fold increased nuclear translocation being observed in AMs from healthy smokers. This effect is receptor-mediated, as it is reproduced by the NK(1) selective agonist [Sar(9)Met(O(2))(11)]SP and reverted by CP 96,345. 5 These results clearly indicate that human AMs possess functional NK-1R on their surface, which are upregulated in healthy smokers, providing new insights on the mechanisms involved in tobacco smoke toxicity.

Indexed as

AdultAgedCytokinesDose-Response Relationship, DrugFemaleGene Expression RegulationHumansMacrophages, AlveolarMaleMiddle AgedNF-kappa BReceptors, Neurokinin-1Signal TransductionSmokingSubstance PSuperoxidesCytokinesNF-kappa BReceptors, Neurokinin-1Substance PSuperoxides

Identifiers

PMID15778738
PMCPMC1576149
OpenAlexW2072811915

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.