Evidence map›Paper›PMID 26925951›Full record

ArticlePloS one2016

Nicotinic Acetylcholine Receptors Modulate Bone Marrow-Derived Pro-Inflammatory Monocyte Production and Survival.

Stéphanie St-Pierre, Wei Jiang, Patrick Roy, Camille Champigny, Éric LeBlanc, Barbara J Morley, Junwei Hao, Alain R Simard

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. 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
4.5field-weighted citation impact, top 5% 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, 69 citations in OpenAlex.

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  4. [Research progress on the role of peripheral nerves in wound healing].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
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  15. The diversity of neuroimmune circuits controlling lung inflammation.American journal of physiology. Lung cellular and molecular physiology · 2023
    Review
  16. Article
  17. Article
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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

8 authors at 3 institutions in 3 countries.

Stéphanie St-PierreDépartement de Chimie et Biochimie, Université de Moncton, Moncton, NB, Canada.
Wei JiangDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Patrick RoyDépartement de Chimie et Biochimie, Université de Moncton, Moncton, NB, Canada.
Camille ChampignyCentre de Formation Médicale du Nouveau-Brunswick, Moncton, NB, Canada.
Éric LeBlancDépartement de Chimie et Biochimie, Université de Moncton, Moncton, NB, Canada.
Barbara J MorleyBoys Town National Research Hospital, Omaha, NE, United States of America.
Junwei HaoDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Alain R SimardDépartement de Chimie et Biochimie, Université de Moncton, Moncton, NB, Canada.
Université de Moncton · CATianjin Medical University General Hospital · CNBoys Town National Research Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is increasingly clear that nicotinic acetylcholine receptors (nAChRs) are involved in immune regulation, and that their activation can protect against inflammatory diseases. Previous data have shown that nicotine diminishes the numbers of peripheral monocytes and macrophages, especially those of the pro-inflammatory phenotype. The goal of the present study was to determine if nicotine modulates the production of bone marrow -derived monocytes/macrophages. In this study, we first found that murine bone marrow cells express multiple nAChR subunits, and that the α7 and α9 nAChRs most predominant subtypes found in immune cells and their precursors. Using primary cultures of murine bone marrow cells, we then determined the effect of nicotine on monocyte colony-stimulating factor and interferon gamma (IFNγ)-induced monocyte production. We found that nicotine lowered the overall number of monocytes, and more specifically, inhibited the IFNγ-induced increase in pro-inflammatory monocytes by reducing cell proliferation and viability. These data suggested that nicotine diminishes the ratio of pro-inflammatory versus anti-inflammatory monocyte produced in the bone marrow. We thus confirmed this hypothesis by measuring cytokine expression, where we found that nicotine inhibited the production of the pro-inflammatory cytokines TNFα, IL-1β and IL-12, while stimulating the secretion of IL-10, an anti-inflammatory cytokine. Finally, nicotine also reduced the number of pro-inflammatory monocytes in the bone marrow of LPS-challenged mice. Overall, our data demonstrate that both α7 and α9 nAChRs are involved in the regulation of pro-inflammatory M1 monocyte numbers.

Indexed as

AnimalsCell CountCell DifferentiationCell ProliferationCell SurvivalColony-Stimulating FactorsGene Expression RegulationInflammationInterferon-gammaInterleukin-10MiceMice, Inbred C57BLMonocytesNicotineProtein SubunitsReceptors, NicotinicColony-Stimulating FactorsInterferon-gammaInterleukin-10NicotineProtein SubunitsReceptors, Nicotinic

Identifiers

PMID26925951
PMCPMC4771711
OpenAlexW2290662239

What OpenQuestion holds

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Registered trials

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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.