ArticleFrontiers in immunology2021
TREM1 Regulates Neuroinflammatory Injury by Modulate Proinflammatory Subtype Transition of Microglia and Formation of Neutrophil Extracellular Traps
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 47 citations in OpenAlex.
- Evolution of neutrophil extracellular traps in the pathology of stroke.Neural regeneration research · 2026Article
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- The role of DAP12 in immune-related inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- CD204 regulates microglial/macrophage M1/M2 polarization and alleviates neuroinflammation following intracerebral hemorrhage.Scientific reports · 2026Article
- HIV gp120 induces TREM1 expression through TLR-PGE₂ signalling in human monocyte-derived microglia.Journal of neuroinflammation · 2026Article
- Cell type-specific gene regulatory atlas prioritizes drug targets and repurposable medicines in Alzheimer's disease.Genome research · 2026Article
- Study on the Function and Mechanism of Neutrophil Extracellular Traps in Regulating Necroptosis Following Traumatic Brain Injury.Brain and behavior · 2026Article
- Targeting the interactions between neutrophils and microglia: a novel strategy for anti-inflammatory treatment of stroke.Acta pharmacologica Sinica · 2026Review
- Article
- The role of neutrophils in vasospasm and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage: Is it time for a SAH clinical trial targeting neutrophils?Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Review
- The TREM1-AQP4 axis mediates neuroinflammatory injury and brain edema after experimental subarachnoid hemorrhage.European journal of medical research · 2025Article
- Triggering Receptor Expressed on Myeloid Cells-1 (TREM-1) in Inflammation and Disease: Mechanisms, Therapeutic Potential, and Future Directions.International journal of molecular sciences · 2025Review
- hUMSC-Exosomes suppress TREM1-p38 MAPK signaling via HMGB1-dependent mechanisms to reprogram microglial function and promote neuroprotection in ischemic stroke.Journal of nanobiotechnology · 2025Article
- Gut-derived macrophages link intestinal damage to brain injury after cardiac arrest through TREM1 signaling.Cellular & molecular immunology · 2025Article
- Role of triggering receptor expressed on myeloid cells 1/2 in secondary injury after cerebral hemorrhage.World journal of clinical cases · 2025Review
- The properties of TREM1 and its emerging role in pain-related diseases.Molecular brain · 2025Review
- Bronchoalveolar lavage single-cell transcriptomics reveals immune dysregulations driving COVID-19 severity.PloS one · 2025Article
- Pilot Screening of TREM1 Inhibitors in Cell-Based Reporter Assays Reflecting TREM1/DAP12 Receptor Assembly and Functionality.ACS chemical neuroscience · 2025Article
- Role of TREM1 in the sevoflurane-induced inflammatory activation of microglia in vitro.Ibrain · 2025Article
- Integrated bioinformatics analysis of the effects of chronic pain on patients with spinal cord injury.Frontiers in cellular neuroscience · 2025Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation is a key process in the pathogenesis of subarachnoid hemorrhage (SAH) and contributes to poor outcome in patients. The purpose of this study is to explore the effect of triggering receptor expressed on myeloid cells 1 (TREM1) in the SAH, as well as its potential mechanism. In our study, plasma levels of soluble TREM1 was increased significantly after SAH and correlated to SAH severity and serum C-reactiveprotein. TREM1 inhibitory peptide LP17 alleviated the neurological deficits, attenuated brain water content, and reduced neuronal damage after SAH. Meanwhile, TREM1 inhibitory peptide decreased neuroinflammation (evidenced by the decreased levels of markers including IL-6, IL-1β, TNF-α) by attenuating proinflammatory subtype transition of microglia (evidenced by the decreased levels of markers including CD68, CD16, CD86) and decreasing the formation of neutrophil extracellular traps (evidenced by the decreased levels of markers including CitH3, MPO, and NE). Further mechanistic study identified that TREM1 can activate downstream proinflammatory pathways through interacting with spleen tyrosine kinase (SYK). In conclusion, inhibition of TREM1 alleviates neuroinflammation by attenuating proinflammatory subtype transition of microglia and decreasing the formation of neutrophil extracellular traps through interacting with SYK after SAH. TREM1 may be a a promising therapeutic target for SAH.
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