---
title: "Ursodeoxycholic Acid (UDCA) Reduces Sepsis-Associated Platelet Dysfunction via TREM2 Signaling"
id: "pubmed-42250286"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42250286"
content_type: "clinical_feed_article"
specialty: "Critical Care"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42250286/"
doi: "10.1016/j.intimp.2026.116978"
published_at: "2026-09-15T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Ursodeoxycholic Acid (UDCA) Reduces Sepsis-Associated Platelet Dysfunction via TREM2 Signaling
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42250286
- **Specialty:** [Critical Care](https://medichelpline.com/clinical-feed/critical-care.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42250286/)
- **DOI:** [10.1016/j.intimp.2026.116978](https://doi.org/10.1016%2Fj.intimp.2026.116978)
- **Published At:** 2026-09-15T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Sepsis causes immune dysregulation and coagulopathy; the study evaluated whether **ursodeoxycholic acid (UDCA)** modulates platelet function through **TREM2** signaling. - An integrated approach combined a retrospective MIMIC‑IV cohort (n = 6,476), causal mediation analysis, mechanistic experiments in LPS-induced septic mice and TREM2-knockout mice, computational docking, and a prospective pilot in 8 septic patients. - Retrospective analysis found UDCA use was associated with reduced hospital mortality (total effect -0.2287, P < 0.001); mediation analysis indicated 69.8% of this association was mediated by increased **platelet** counts (natural indirect effect -0.1597, P < 0.001). - In LPS-treated mice, platelet TREM2 expression was downregulated and Syk–PI3K–Akt phosphorylation increased, coinciding with platelet hyperactivation; UDCA reversed these changes. - Effects of UDCA on TREM2 expression and downstream signaling were reduced or absent in **TREM2-knockout** mice, supporting a TREM2-linked mechanism. - Computational docking suggested a potential interaction between UDCA and TREM2 (details provided in full text but not reported in the abstract). - In the prospective pilot (n = 8), UDCA increased platelet counts (from 161.6 ± 106.2 to 211.4 ± 100.1 ×10^9/L, P = 0.001) and selectively inhibited ADP-induced aggregation (from 49.23 ± 20.45% to 31.63 ± 26.28%, P = 0.001) without significant changes in global coagulation parameters. - Authors conclude UDCA may improve sepsis outcomes by modulating platelet homeostasis in a **TREM2-associated** manner and propose TREM2 as a potential target for sepsis-associated coagulopathy. - Conflict of interest: authors declared no competing interests.
## Clinical Analysis & Structured Key Points
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Epub 2026 Jun 6. # Ursodeoxycholic acid attenuates sepsis-associated platelet dysfunction through TREM2-linked signaling [Li Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+L&cauthor_id=42250286)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#full-view-affiliation-1 "Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China; Department of Critical Care Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China."), [Qingyuan Yang](https://pubmed.ncbi.nlm.nih.gov/?term=Yang+Q&cauthor_id=42250286)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#full-view-affiliation-2 "Department of Biopharmaceuticals, School of Pharmacy, Tianjin Medical University, Tianjin, China."), [Hang Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+H&cauthor_id=42250286)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#full-view-affiliation-3 "Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China."), [Ying Qi](https://pubmed.ncbi.nlm.nih.gov/?term=Qi+Y&cauthor_id=42250286)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#full-view-affiliation-3 "Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China."), [Yuhan Xie](https://pubmed.ncbi.nlm.nih.gov/?term=Xie+Y&cauthor_id=42250286)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#full-view-affiliation-3 "Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China."), [Zhongren Ding](https://pubmed.ncbi.nlm.nih.gov/?term=Ding+Z&cauthor_id=42250286)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#full-view-affiliation-4 "Department of Biopharmaceuticals, School of Pharmacy, Tianjin Medical University, Tianjin, China. Electronic address: dingzr@tmu.edu.cn."), [Bing Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+B&cauthor_id=42250286)[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#full-view-affiliation-5 "Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China. Electronic address: drchenb@163.com.") Affiliations Expand ### Affiliations * 1 Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China; Department of Critical Care Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. * 2 Department of Biopharmaceuticals, School of Pharmacy, Tianjin Medical University, Tianjin, China. * 3 Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China. * 4 Department of Biopharmaceuticals, School of Pharmacy, Tianjin Medical University, Tianjin, China. Electronic address: dingzr@tmu.edu.cn. * 5 Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China. Electronic address: drchenb@163.com. * PMID: **42250286** * DOI: [ 10.1016/j.intimp.2026.116978 ](https://doi.org/10.1016/j.intimp.2026.116978) Item in Clipboard # Ursodeoxycholic acid attenuates sepsis-associated platelet dysfunction through TREM2-linked signaling Li Li et al. Int Immunopharmacol. 2026. Show details Display options Display options Format Abstract PubMed PMID Int Immunopharmacol Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Int+Immunopharmacol%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Int+Immunopharmacol%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42250286/) . 2026 Sep 15:185:116978. doi: 10.1016/j.intimp.2026.116978. Epub 2026 Jun 6. ### Authors [Li Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+L&cauthor_id=42250286)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#short-view-affiliation-1 "Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China; Department of Critical Care Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China."), [Qingyuan Yang](https://pubmed.ncbi.nlm.nih.gov/?term=Yang+Q&cauthor_id=42250286)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#short-view-affiliation-2 "Department of Biopharmaceuticals, School of Pharmacy, Tianjin Medical University, Tianjin, China."), [Hang Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+H&cauthor_id=42250286)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#short-view-affiliation-3 "Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China."), [Ying Qi](https://pubmed.ncbi.nlm.nih.gov/?term=Qi+Y&cauthor_id=42250286)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#short-view-affiliation-3 "Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China."), [Yuhan Xie](https://pubmed.ncbi.nlm.nih.gov/?term=Xie+Y&cauthor_id=42250286)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#short-view-affiliation-3 "Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China."), [Zhongren Ding](https://pubmed.ncbi.nlm.nih.gov/?term=Ding+Z&cauthor_id=42250286)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#short-view-affiliation-4 "Department of Biopharmaceuticals, School of Pharmacy, Tianjin Medical University, Tianjin, China. Electronic address: dingzr@tmu.edu.cn."), [Bing Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+B&cauthor_id=42250286)[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42250286/#short-view-affiliation-5 "Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China. Electronic address: drchenb@163.com.") ### Affiliations * 1 Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China; Department of Critical Care Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. * 2 Department of Biopharmaceuticals, School of Pharmacy, Tianjin Medical University, Tianjin, China. * 3 Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China. * 4 Department of Biopharmaceuticals, School of Pharmacy, Tianjin Medical University, Tianjin, China. Electronic address: dingzr@tmu.edu.cn. * 5 Department of Critical Care Medicine, The Second Hospital of Tianjin Medical University, Tianjin, China. Electronic address: drchenb@163.com. * PMID: **42250286** * DOI: [ 10.1016/j.intimp.2026.116978 ](https://doi.org/10.1016/j.intimp.2026.116978) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract Sepsis remains a major clinical challenge characterized by immune dysregulation and coagulopathy. Ursodeoxycholic acid (UDCA) has been suggested to confer benefit in sepsis, but its mechanism remains unclear. This study explored whether UDCA modulates platelet function during sepsis via triggering receptor expressed on myeloid cells 2 (TREM2), an immunoreceptor with an emerging role in platelet biology. We employed an integrated strategy combining a retrospective cohort of 6476 sepsis patients (MIMIC-IV) with exploratory causal mediation analysis, mechanistic studies in LPS-induced septic and TREM2-knockout mice, computational docking suggesting a potential interaction between UDCA and TREM2, and a prospective pilot study in 8 septic patients receiving UDCA. Retrospective analysis showed that UDCA was associated with reduced hospital mortality (total effect -0.2287, P < 0.001), with 69.8% of this association mediated by increased platelet counts (natural indirect effect -0.1597, P < 0.001). Mechanistically, LPS downregulated platelet TREM2 and increased Syk-PI3K-Akt phosphorylation, accompanied by platelet hyperactivation. UDCA was associated with increased TREM2 expression and attenuated downstream signaling, and these effects were attenuated or not observed in TREM2-knockout mice. In the pilot clinical study, UDCA increased platelet counts (from 161.6 ± 106.2 to 211.4 ± 100.1 × 109/L, P = 0.001) and selectively inhibited ADP-induced aggregation (from 49.23 ± 20.45% to 31.63 ± 26.28%, P = 0.001) without significantly altering global coagulation parameters. In conclusion, these findings suggest that UDCA may be associated with improved sepsis outcomes by modulating platelet homeostasis in a TREM2-associated manner, providing preliminary translational support for TREM2 as a potential target in sepsis-associated coagulopathy. **Keywords:** Coagulopathy; Immunopharmacology; Platelets; Sepsis; TREM2; Ursodeoxycholic acid. Copyright © 2026 Elsevier B.V. All rights reserved. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. ## Similar articles * [ TREM2 improves coagulopathy and lung inflammation in sepsis through the AKT-mTOR pathway. ](https://pubmed.ncbi.nlm.nih.gov/39970715/) Zhou C, Liang C, Zhang R, Wang Y, Luo S, Pan J.Zhou C, et al.Int Immunopharmacol. 2025 Mar 26;150:114330. doi: 10.1016/j.intimp.2025.114330. Epub 2025 Feb 18.Int Immunopharmacol. 2025.PMID: 39970715 * [ Endoplasmic Reticulum Stress-Induced triggering Receptor Expressed on Myeloid Cells 2 (TREM2) Downregulation Exacerbates Platelet Activation and Myocardial Infarction in Patients With Coronary Artery Disease. ](https://pubmed.ncbi.nlm.nih.gov/40551335/) Wu X, Pan G, Chang L, Liu Q, Liu Y, Zhang W, Guo Y, Zhang G, Zhong H, Qi Z, Zhang J, Xue R, Chen S, Hu H, Dong J, Zhang S, Ding Z.Wu X, et al.J Am Heart Assoc. 2025 Jul;14(13):e041220. doi: 10.1161/JAHA.124.041220. Epub 2025 Jun 23.J Am Heart Assoc. 2025.PMID: 40551335Free PMC article. * [ Ursodeoxycholic acid protects against sepsis-induced acute kidney injury by activating Nrf2/HO-1 and inhibiting NF-κB pathway. ](https://pubmed.ncbi.nlm.nih.gov/39885380/) Lou Y, Shi H, Sha N, Li F, Gu X, Lin H.Lou Y, et al.BMC Nephrol. 2025 Jan 30;26(1):45. doi: 10.1186/s12882-025-03977-9.BMC Nephrol. 2025.PMID: 39885380Free PMC article. * [ TREM2 alleviates sepsis-induced acute lung injury by attenuating ferroptosis via the SHP1/STAT3 pathway. ](https://pubmed.ncbi.nlm.nih.gov/39814108/) Wu S, He Y, Li J, Zhuang H, Wang P, He X, Guo Y, Li Z, Shen H, Ye L, Lin F.Wu S, et al.Free Radic Biol Med. 2025 Mar 1;229:111-126. doi: 10.1016/j.freeradbiomed.2025.01.022. Epub 2025 Jan 13.Free Radic Biol Med. 2025.PMID: 39814108 * [ Tyrphostin AG538 inhibits platelet activation and thrombosis via TREM2 agonism. ](https://pubmed.ncbi.nlm.nih.gov/41046073/) Liu Q, Yang Q, Wang Y, Liu C, Jin M, Chen D, Ding Z.Liu Q, et al.Biochem Pharmacol. 2025 Dec;242(Pt 3):117379. doi: 10.1016/j.bcp.2025.117379. 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