Evidence map›Paper›PMID 36386581›Full record

ArticleJournal of inflammation research2022

Sympathectomy Ameliorates CFA-Induced Mechanical Allodynia via Modulating Phenotype of Macrophages in Sensory Ganglion in Mice.

Lijia Mai, Shilin Jia, Qing Liu, Yanhao Chu, Jinyue Liu, Shengyan Yang, Fang Huang, Wenguo Fan

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

3 citing papers in PubMed, 3 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

8 authors at 2 institutions in 2 countries.

Lijia Mai *Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, People's Republic of China.
Shilin Jia *Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, People's Republic of China.
Qing LiuFaculty of Dentistry, The University of Hong Kong, People's Republic of China.
Yanhao ChuInstitute of Stomatological Research, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Stomatology, Guangzhou, People's Republic of China.
Jinyue LiuInstitute of Stomatological Research, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Stomatology, Guangzhou, People's Republic of China.
Shengyan YangFaculty of Dentistry, The University of Hong Kong, People's Republic of China.
Fang HuangHospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, People's Republic of China.ORCID 0000-0003-3408-8090
Wenguo FanHospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, People's Republic of China.
Sun Yat-sen University · CNChinese University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The sympathetic nervous system (SNS) is suggested to be involved in some forms of pain, but the mechanisms of which are incompletely known. Moreover, there is a lack of information on the regulatory role of the SNS on macrophages in sensory ganglion, which plays an important role in pain development. The present study aims to investigate the effects of the SNS on orofacial inflammatory pain and examine, if any, how the SNS influences trigeminal ganglion (TG) macrophage responses. Methods: Sympathectomy was performed on male C57BL/6 mice before receiving a local injection of Complete Freund's adjuvant (CFA) to induce inflammatory pain. Effects of sympathectomy on orofacial pain were examined by Von Frey test and c-Fos expression. Polarization of TG macrophage was evaluated by immunohistochemistry and the level of norepinephrine (NE) in the TG were determined by liquid chromatography. Sympathetic signaling to TG macrophages were predicted based on single-cell analysis. Results: CFA injection induced a significant increase in mechanical allodynia, the number of c-Fos-positive neuron, and the level of NE in TG, which were largely reduced by sympathectomy. The number of M1 macrophages was markedly increased by CFA and was largely reduced by sympathectomy from 1 to 14 days post-injection. Single-cell RNA sequencing analysis and immunofluorescence staining showed that TG macrophages mainly express β2 adrenergic receptors for NE. Cell-cell communication analysis predicted sympathetic signaling that may modulate macrophage phenotypes, including Colony-stimulating factor-1, Migration inhibitory factor, Pleiotrophin and Nicotinamide phosphoribosyl transferase. Conclusion: The SNS may involve in CFA-induced mechanical allodynia via modulating macrophage phenotypes in the TG. Targeting sympathetic activation might be useful in treating some painful conditions in the orofacial region.

Indexed as

macrophages phenotypeneuroinflammationorofacial painsympathectomytrigeminal ganglion

Identifiers

PMID36386581
PMCPMC9664931
OpenAlexW4308877834

What OpenQuestion holds

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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.