Evidence map›Paper›PMID 36698311›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2023

Gut microbial metabolite hyodeoxycholic acid targets the TLR4/MD2 complex to attenuate inflammation and protect against sepsis.

Jiaxin Li, Yuqi Chen, Rui Li, Xianglong Zhang, Tao Chen, Fengyi Mei, Ruofan Liu, Meiling Chen, Yue Ge, Hongbin Hu and 17 more

Open access · greenAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
10.5field-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

48 citing papers in PubMed, 68 citations in OpenAlex.

  1. Indole-3-carboxaldehyde fromGut microbes · 2026
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  4. Higher abundance ofmSystems · 2026
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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

27 authors at 5 institutions in 2 countries.

Jiaxin LiDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China; Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Yuqi ChenDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Rui LiDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Xianglong ZhangDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Tao ChenDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Fengyi MeiDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Ruofan LiuDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Meiling ChenDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Yue GeDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Hongbin HuDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Rongjuan WeiDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Zhenfeng ChenDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Hongying FanDepartment of Microbiology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou 510515, China.
Zhenhua ZengDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Yongqiang DengDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Haihua LuoDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Shuiwang HuDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Shumin CaiDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Feng WuDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Nengxian ShiDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Zhang WangInstitute of Ecological Sciences, School of Life Sciences, South China Normal University, Guangzhou 510515, China.
Yunong ZengDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Ming XieDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Yong JiangDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Zhongqing ChenDepartment of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. Electronic address: zhongqingchen2008@163.com.
Wei JiaCenter for Translational Medicine and Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, China; School of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong 999077, China. Electronic address: weijia1@hkbu.edu.hk.
Peng ChenDepartment of Pathophysiology, Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China; Microbiome Medicine Center, Zhujiang Hospital, Southern Medical University, Guangzhou 510515, China. Electronic address: perchen@smu.edu.cn.
Southern Medical University · CNNanfang Hospital · CNHong Kong Baptist University · HKSouth China Normal University · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis, a critical condition resulting from the systemic inflammatory response to a severe microbial infection, represents a global public health challenge. However, effective treatment or intervention to prevent and combat sepsis is still lacking. Here, we report that hyodeoxycholic acid (HDCA) has excellent anti-inflammatory properties in sepsis. We discovered that the plasma concentration of HDCA was remarkably lower in patients with sepsis and negatively correlated with the severity of the disease. Similar changes in HDCA levels in plasma and cecal content samples were observed in a mouse model of sepsis, and these changes were associated with a reduced abundance of HDCA-producing strains. Interestingly, HDCA administration significantly decreased systemic inflammatory responses, prevented organ injury, and prolonged the survival of septic mice. We demonstrated that HDCA suppressed excessive activation of inflammatory macrophages by competitively blocking lipopolysaccharide binding to the Toll-like receptor 4 (TLR4) and myeloid differentiation factor 2 receptor complex, a unique mechanism that characterizes HDCA as an endogenous inhibitor of inflammatory signaling. Additionally, we verified these findings in TLR4 knockout mice. Our study highlights the potential value of HDCA as a therapeutic molecule for sepsis.

Indexed as

Gastrointestinal MicrobiomeSepsisAnimalsDeoxycholic AcidInflammationLipopolysaccharidesLymphocyte Antigen 96MiceMice, Inbred C57BLToll-Like Receptor 4Deoxycholic Acidhyodeoxycholic acidLipopolysaccharidesLy96 protein, mouseLymphocyte Antigen 96Tlr4 protein, mouseToll-Like Receptor 4gut microbiotahyodeoxycholic acidsepsisToll-like receptor 4

Identifiers

PMID36698311
PMCPMC10124078
OpenAlexW4318165720

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.