ArticleCell and tissue research2018
The triggering receptor expressed by myeloid cells-1 activates TLR4-MyD88-NF-κB-dependent signaling to aggravate ventilation-induced lung inflammation and injury in mice.
Article in Cell and tissue research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- The properties of TREM1 and its emerging role in pain-related diseases.Molecular brain · 2025Review
- The role of triggering receptor expressed on myeloid cells-1 (TREM-1) in central nervous system diseases.Molecular brain · 2022Review
- Knockdown of triggering receptor expressed on myeloid cells 1 (TREM1) inhibits endoplasmic reticulum stress and reduces extracellular matrix degradation and the apoptosis of human nucleus pulposus cells.Experimental and therapeutic medicine · 2022Article
- Ventilator-induced lung injury results in oxidative stress response and mitochondrial swelling in a mouse model.Laboratory animal research · 2022Article
- Ventilator-induced lung-injury in mouse models: Is there a trap?Laboratory animal research · 2021Review
- TREM-1 promoted apoptosis and inhibited autophagy in LPS-treated HK-2 cells through the NF-κB pathway.International journal of medical sciences · 2021Article
- Short-Term Lincomycin Exposure Depletion of Murine Microbiota Affects Short-Chain Fatty Acids and Intestinal Morphology and Immunity.Antibiotics (Basel, Switzerland) · 2020Article
- Effects of simvastatin on iNOS and caspase‑3 levels and oxidative stress following smoke inhalation injury.Molecular medicine reports · 2020Article
- MicroRNA‑25/ATXN3 interaction regulates human colon cancer cell growth and migration.Molecular medicine reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The triggering receptor expressed by myeloid cells-1 (TREM-1) plays an important role in infectious and autoimmune diseases but how it contributes to ventilation-induced lung injury (VILI) and inflammation is unclear. Here, we examine the possibility that TREM-1 activates signaling dependent on Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (Myd88) and nuclear factor (NF)-κB, which leads in turn to VILI. In a mouse model of VILI, which we validated based on lung edema and histopathology as well as cytokine levels, we examine mRNA and protein levels of TREM-1, TLR4, MyD88, NF-κB and its inhibitory protein I-κB in animals subjected to ventilation at normal or high tidal volume. The extent of lung edema, injury and inflammation were higher in the high tidal volume animals, as were the expression levels of all proteins examined. Treatment with TREM-1 agonist aggravated these effects, whereas treatment with TREM-1 antagonist attenuated them. Our results suggest that aggravation of VILI by TREM-1 in mice may be associated with TLR4-MyD88-NF-κB-dependent signaling.
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