Evidence map›Paper›PMID 18412948›Full record

ArticleBMC cell biology2008

The influence of nicotine on granulocytic differentiation - inhibition of the oxidative burst and bacterial killing and increased matrix metalloproteinase-9 release.

Minqi Xu, James E Scott, Kan-Zhi Liu, Hannah R Bishop, Diane E Renaud, Richard M Palmer, Abdel Soussi-Gounni, David A Scott

Open access · goldAbstract read
In one paragraph

Article in BMC cell biology, 2008. 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
2.2field-weighted citation impact, top 13% 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, 52 citations in OpenAlex.

  1. Review
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  6. Review
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  8. Review
  9. Review
  10. Article
  11. Nicotine induces neutrophil extracellular traps.Journal of leukocyte biology · 2016
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Neutrophils in periodontal inflammation.Frontiers of oral biology · 2012
    Review
  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

8 authors at 3 institutions in 3 countries.

Minqi XuDepartment of Oral Biology, University of Manitoba, Winnipeg, Canada. xmq075@hotmail.com
James E Scott
Kan-Zhi Liu
Hannah R Bishop
Diane E Renaud
Richard M Palmer
Abdel Soussi-Gounni
David A Scott
University of Manitoba · CAUniversity of Louisville · USKing's College London · GB

Funding

PHS HHS H75/CCH424215-01
6 · The paper itself

Abstract

backgroundNeutrophils leave the bone marrow as terminally differentiated cells, yet little is known of the influence of nicotine or other tobacco smoke components on neutrophil differentiation. Therefore, promyelocytic HL-60 cells were differentiated into neutrophils using dimethylsulfoxide in the presence and absence of nicotine (3-(1-methyl-2-pyrrolidinyl) pyridine). Differentiation was evaluated over 5 days by monitoring terminal differentiation markers (CD11b expression and formazan deposition); cell viability, growth phase, kinetics, and apoptosis; assessing cellular morphology and ultrastructure; and conformational changes to major cellular components. Key neutrophil effector functions (oxidative burst, bacterial killing, matrix metalloproteinase release) were also examined.

resultsNicotine increased the percentage of cells in late differentiation phases (metamyelocytes, banded neutrophils and segmented neutrophils) compared to DMSO alone (p < 0.05), but did not affect any other marker of neutrophil differentiation examined. However, nicotine exposure during differentiation suppressed the oxidative burst in HL-60 cells (p < 0.001); inhibited bacterial killing (p < 0.01); and increased the LPS-induced release of MMP-9, but not MMP-2 (p < 0.05). These phenomena may be alpha-7-acetylcholine nicotinic receptor-dependent. Furthermore, smokers exhibited an increased MMP-9 burden compared to non-smokers in vivo (p < 0.05).

conclusionThese findings may partially explain the known increase in susceptibility to bacterial infection and neutrophil-associated destructive inflammatory diseases in individuals chronically exposed to nicotine.

Indexed as

Porphyromonas gingivalisalpha7 Nicotinic Acetylcholine ReceptorBacteriolysisBungarotoxinsCell CycleCell DifferentiationCell LineHumansImmunophenotypingMatrix Metalloproteinase 9NeutrophilsNicotineReceptors, NicotinicRespiratory BurstSmokingalpha7 Nicotinic Acetylcholine ReceptorBungarotoxinsChrna7 protein, humanMatrix Metalloproteinase 9NicotineReceptors, Nicotinic

Identifiers

PMID18412948
PMCPMC2375863
OpenAlexW2081583714

What OpenQuestion holds

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LicenceCC BY
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.