Evidence map›Paper›PMID 35768823›Full record

ArticleJournal of neuroinflammation2022

Transient post-operative overexpression of CXCR2 on monocytes of traumatic brain injury patients drives monocyte chemotaxis toward cerebrospinal fluid and enhances monocyte-mediated immunogenic cell death of neurons in vitro.

Huayang Wang, Qibing Huang, Zhijie Zhang, Jian Ji, Tao Sun, Donghai Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 14 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

6 authors at 2 institutions in 1 country.

Huayang Wang *Department of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
Qibing Huang *Department of Neurosurgical Intensive Care Unit, Qilu Hospital of Shandong University, Jinan, China.
Zhijie ZhangDepartment of Ultrasound, Shandong Maternal and Child Health Hospital, Jinan, China.
Jian JiDepartment of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, China.
Tao SunDepartment of Neurosurgery, Qilu Hospital of Shandong University, # 107 Wenhuaxi Road, Jinan, Shandong, China.
Donghai WangDepartment of Neurosurgery, Qilu Hospital of Shandong University, # 107 Wenhuaxi Road, Jinan, Shandong, China. drwangdonghai@163.com.
Qilu Hospital of Shandong University · CNShandong Maternal and Child Health Hospital · CN

Funding

Clinical Practical New Technology Development Foundation of Qilu Hospital 2019-7Key Technology Research and Development Program of Shandong 2019GSF108064Key Technology Research and Development Program of Shandong 2019GSF108247National Natural Science Foundation of China 81702815Natural Science Foundation of Shandong Province ZR2020LZL015
6 · The paper itself

Abstract

backgroundAfter traumatic brain injury (TBI), peripheral monocytes infiltrate into the central nervous system due to disruption of the blood-brain barrier, and play an important role in neuroinflammation. However, the mechanisms regulating the movement and function of peripheral monocytes after TBI have not been fully investigated.

methodsTBI patients who underwent surgery at our hospital were recruited. CXCR2 expression in CD14

resultsTransient CXCR2 upregulation in monocytes from the peripheral blood and CSF of TBI patients was detected soon after surgery and was associated with unfavorable outcomes. TBI serum and CSF promoted CXCR2 expression in monocytes, and dexamethasone reversed this effect. Peripheral monocytes from TBI patients showed enhanced chemotaxis toward the CSF and increased inflammatory cytokine secretion. The CXCR2 antagonist SB225002 decreased monocyte chemotaxis toward TBI CSF, and lowered pro-inflammatory cytokine secretion in monocytes treated with TBI serum. SB225002 also relieved ICD in nerve cells co-cultured with TBI serum-treated monocytes.

conclusionsCXCR2 is transiently overexpressed in the peripheral monocytes of TBI patients post-surgery, and drives peripheral monocyte chemotaxis toward CSF and monocyte-mediated ICD of nerve cells. Therefore, CXCR2 may be a target for monocyte-based therapies for TBI.

Indexed as

Brain Injuries, TraumaticMonocytesNeuronsReceptors, Interleukin-8BCell DeathChemotaxisCytokinesHumansImmunogenic Cell DeathCXCR2 protein, humanCytokinesReceptors, Interleukin-8BChemotaxisCXCR2Immunogenic cell deathMonocytesTraumatic brain injury

Identifiers

PMID35768823
PMCPMC9245242
OpenAlexW4283697066

What OpenQuestion holds

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LicenceCC BY
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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.