Evidence map›Paper›PMID 27840928›Full record

ArticleMolecular medicine reports2016

Activation of the cholinergic anti-inflammatory system by nicotine attenuates arthritis via suppression of macrophage migration.

Sha Li, Bin Zhou, Ben Liu, Yaou Zhou, Huali Zhang, Tong Li, Xiaoxia Zuo

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Sha LiDepartment of Rheumatology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Bin ZhouDepartment of Rheumatology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Ben LiuDepartment of Emergency, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Yaou ZhouDepartment of Rheumatology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Huali ZhangDepartment of Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, Hunan 410008, P.R. China.
Tong LiDepartment of Rheumatology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Xiaoxia ZuoDepartment of Rheumatology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Central South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of the cholinergic anti-inflammatory pathway (CAP), which relies on the alpha-7 nicotinic acetylcholine receptor, has been reported to reduce proinflammatory cytokine levels in experimental arthritis. To gain more insight regarding the role of the CAP in the pathogenesis of arthritis, the present study focused on the modulation of macrophage infiltration. In a mouse model of collagen‑induced arthritis (CIA), nicotine and vagotomy were used to stimulate and inhibit the CAP, respectively. Subsequently, arthritic scores were measured and histopathological assessment of joint sections was conducted. Cluster of differentiation (CD)11b‑positive macrophages in the synovium were studied by immunofluorescence histochemistry. The serum levels of chemokines, including macrophage inflammatory protein (MIP)‑1α, monocyte chemoattractant protein (MCP)‑1 and MIP‑2 were evaluated by ELISA. Furthermore, the expression levels of C‑C chemokine receptor (CCR)2 and intercellular adhesion molecule (ICAM)‑1 in the synovium were evaluated by immunohistochemical staining. The results indicated that treatment with nicotine significantly attenuated the clinical and histopathological changes associated with arthritis, reduced CD11b‑positive macrophages in the synovium, and downregulated the serum expression levels of MIP‑1α and MCP‑1. Conversely, vagotomy aggravated arthritis and upregulated the expression levels of MCP‑1. However, MIP‑2 expression did not differ among the control, CIA, vagotomy and nicotine groups. In addition, the expression levels of CCR2 were reduced in the nicotine group; however, they were increased in the vagotomy group compared with in the untreated CIA group. The expression levels of ICAM‑1 in the synovium were also influenced by activation of the CAP. Taken together, the present results indicated that nicotine‑induced activation of the CAP in mice with CIA may reduce the number of macrophages in the synovium, which may serve a role in alleviating arthritis in mice.

Indexed as

AnimalsAnti-Inflammatory AgentsArthritis, ExperimentalBiopsyCell MembraneCell MovementChemokine CCL2ChemokinesDisease Models, AnimalEndothelial CellsImmunophenotypingIntercellular Adhesion Molecule-1MacrophagesMaleMiceNicotineAnti-Inflammatory AgentsChemokine CCL2ChemokinesIntercellular Adhesion Molecule-1Nicotine

Identifiers

PMID27840928
PMCPMC5355730
OpenAlexW2545545742

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.