Evidence map›Paper›PMID 32862402›Full record

ArticleTranslational stroke research2021

TREM-1 Exacerbates Neuroinflammatory Injury via NLRP3 Inflammasome-Mediated Pyroptosis in Experimental Subarachnoid Hemorrhage.

Pengfei Xu, Ye Hong, Yi Xie, Kang Yuan, Juanji Li, Rui Sun, Xiaohao Zhang, Xiaolei Shi, Rongrong Li, Jiaonan Wu and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Translational stroke research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 1 pooled it
11.1field-weighted citation impact, top 1% 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

123 citing papers in PubMed, 1 synthesis or guideline pooled it, 247 citations in OpenAlex.

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63 more citing papers are in PubMed but not listed here.

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

13 authors at 6 institutions in 1 country.

Pengfei Xu *Stroke Center & Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230036, Anhui, China.
Ye Hong *Department of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, 210002, Jiangsu, China.
Yi Xie *Department of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, 210002, Jiangsu, China.
Kang YuanDepartment of Neurology, Jinling Hospital, Nanjing Medical University, Nanjing, 210002, Jiangsu, China.
Juanji LiDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, 210002, Jiangsu, China.
Rui SunDepartment of Neurology, Changhai Hospital, Second Military Medical University/Naval Medical University, Shanghai, 200433, China.
Xiaohao ZhangDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, 210002, Jiangsu, China.
Xiaolei ShiDepartment of Neurology, Yijishan Hospital, The First Affiliated Hospital of Wannan Medical College, Wuhu, 241001, Anhui, China.
Rongrong LiDepartment of Neurology, Jinling Hospital, Medical School of Nanjing University, Nanjing, 210002, Jiangsu, China.
Jiaonan WuStroke Center & Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230036, Anhui, China.
Xinfeng LiuStroke Center & Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230036, Anhui, China.
Wei HuStroke Center & Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230036, Anhui, China. andinghu@ustc.edu.cn.
Wen SunStroke Center & Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230036, Anhui, China. sunwen_medneuro@163.com.
University of Science and Technology of China · CNNanjing General Hospital of Nanjing Military Command · CNNanjing Medical University · CNFirst Affiliated Hospital of Wannan Medical College · CNNanjing University · CNSecond Military Medical University · CN

Funding

Joint Foundation of New Medicine of University of Science and Technology of China WK9110000084National Natural Science Foundation of China 81501193National Natural Science Foundation of China 81701180Natural Science Foundation of Anhui Province No. 200805Q
6 · The paper itself

Abstract

Neuroinflammation contributes to the pathogenesis of early brain injury induced by subarachnoid hemorrhage (SAH). Previous reports have demonstrated that triggering receptor expressed on myeloid cells 1 (TREM-1) regulates inflammatory response caused by ischemic stroke or myocardial infarction. However, whether TREM-1 could modulate neuroinflammation after SAH remains largely unknown. Here, using a mouse model of SAH, we found that the expression of TREM-1 was mainly located in microglia cells and increased to peak at 24 h following SAH. Then, TREM-1 antagonist or mimic was intranasally administrated to investigate its effect on SAH. TREM-1 inhibition with LP17 improved neurological deficits, mitigated brain water content, and preserved brain-blood barrier integrity 24 h after SAH, whereas recombinant TREM-1, a mimic of TREM-1, deteriorated these outcomes. In addition, LP17 administration restored long-term sensorimotor coordination and cognitive deficits. Pharmacological blockade of TREM-1 reduced TUNEL-positive and FJC-positive neurons, and CD68-stained microglia in ipsilateral cerebral cortex. Neutrophil invasion was inhibited as protein level of myeloperoxidase (MPO), and MPO-positive cells were both decreased. Moreover, we found that LP17 treatment ameliorated microglial pyroptosis by diminishing levels of N-terminal fragment of GSDMD (GSDMD-N) and IL-1β production. Mechanistically, both in vivo and in vitro, we depicted that TREM-1 can trigger microglial pyroptosis via activating NLRP3 inflammasome. In conclusion, our results revealed the critical role of TREM-1 in neuroinflammation following SAH, suggesting that TREM-1 inhibition might be a potential therapeutic approach for SAH.

Indexed as

Subarachnoid HemorrhageHumansInflammasomesNeuroinflammatory DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinPyroptosisTriggering Receptor Expressed on Myeloid Cells-1InflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinTREM1 protein, humanTriggering Receptor Expressed on Myeloid Cells-1MicrogliaNLRP3 inflammasomePyroptosisSubarachnoid hemorrhageTREM-1

Identifiers

PMID32862402
OpenAlexW3082314084

What OpenQuestion holds

Textmetadata
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.