ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
TREM-1-accentuated lung injury via miR-155 is inhibited by LP17 nanomedicine.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.
- Expression of MicroRNAs in Sepsis-Related Organ Dysfunction: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Effects of AntagomiRs on Different Lung Diseases in Human, Cellular, and Animal Models.International journal of molecular sciences · 2019Pooled it
- AI-Designed TREM1-Targeted LYTAC Nanoparticles Reprogram the Neuroimmune Microenvironment in Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies.Signal transduction and targeted therapy · 2025Review
- TREM-1 inhibitor specificity and timing of treatment initiation can impact its therapeutic efficacy in cancer and inflammatory disease.Frontiers in oncology · 2025Article
- Screening of Phytocompounds Against the NF-kB Pathway Genes and Lung Elevated Proteins Associated with Acute Respiratory Distress Syndrome.Recent advances in inflammation & allergy drug discovery · 2025Article
- Small molecules as ligands in the tuning of immune regulatory receptors.Frontiers in immunology · 2025Review
- TREM-1 and TREM-2 as therapeutic targets: clinical challenges and perspectives.Frontiers in immunology · 2024Article
- Regulation of alveolar macrophage death in pulmonary fibrosis: a review.Apoptosis : an international journal on programmed cell death · 2023Review
- A diagnostic model for sepsis-induced acute lung injury using a consensus machine learning approach and its therapeutic implications.Journal of translational medicine · 2023Article
- Long Noncoding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Promotes HIV-1 Replication through Modulating microRNAs in Macrophages.Journal of virology · 2023Article
- Article
- Melatonin Alters the miRNA Transcriptome of Inflammasome Activation in Murine Microglial Cells.Neurochemical research · 2022Article
- miR-155-3p: processing by-product or rising star in immunity and cancer?Open biology · 2022Review
- Novel Combined Preparation and Investigation of Bergenin-Loaded Albumin Nanoparticles for the Treatment of Acute Lung Injury: In Vitro and In Vivo Evaluations.Inflammation · 2022Article
- TREM-1 Modulates Dendritic Cells Maturation and Dendritic Cell-Mediated T-Cell Activation Induced by ox-LDL.Oxidative medicine and cellular longevity · 2022Article
- Article
- Biocompatible N-acetyl-nanoconstruct alleviates lipopolysaccharide-induced acute lung injury in vivo.Scientific reports · 2021Article
- MicroRNA-155 Modulates Macrophages' Response to Non-Tuberculous Mycobacteria through COX-2/PGE2 Signaling.Pathogens (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Triggering receptors expressed on myeloid cell-1 (TREM-1) is a superimmunoglobulin receptor expressed on myeloid cells. Synergy between TREM-1 and Toll-like receptor amplifies the inflammatory response; however, the mechanisms by which TREM-1 accentuates inflammation are not fully understood. In this study, we investigated the role of TREM-1 in a model of LPS-induced lung injury and neutrophilic inflammation. We show that TREM-1 is induced in lungs of mice with LPS-induced acute neutrophilic inflammation. TREM-1 knockout mice showed an improved survival after lethal doses of LPS with an attenuated inflammatory response in the lungs. Deletion of TREM-1 gene resulted in significantly reduced neutrophils and proinflammatory cytokines and chemokines, particularly IL-1β, TNF-α, and IL-6. Physiologically deletion of TREM-1 conferred an immunometabolic advantage with low oxygen consumption rate (OCR) sparing the respiratory capacity of macrophages challenged with LPS. Furthermore, we show that TREM-1 deletion results in significant attenuation of expression of miR-155 in macrophages and lungs of mice treated with LPS. Experiments with antagomir-155 confirmed that TREM-1-mediated changes were indeed dependent on miR-155 and are mediated by downregulation of suppressor of cytokine signaling-1 (SOCS-1) a key miR-155 target. These data for the first time show that TREM-1 accentuates inflammatory response by inducing the expression of miR-155 in macrophages and suggest a novel mechanism by which TREM-1 signaling contributes to lung injury. Inhibition of TREM-1 using a nanomicellar approach resulted in ablation of neutrophilic inflammation suggesting that TREM-1 inhibition is a potential therapeutic target for neutrophilic lung inflammation and acute respiratory distress syndrome (ARDS).
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Registered trials
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.