Summary of Study ST003938

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002468. The data can be accessed directly via it's Project DOI: 10.21228/M8MR7Q This work is supported by NIH grant, U2C- DK119886.

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This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST003938
Study TitleHost sensing of microbially produced imidazole propionate is a driver and therapeutic target in atherosclerosis
Study SummaryAtherosclerosis is the main underlying cause of cardiovascular diseases (CVDs). Its prevention is based on the detection and treatment of traditional cardiovascular risk factors but often fails to identify individuals at risk for early vascular disease. Recent research has suggested new players in the pathophysiology of atherosclerosis, highlighting the need for alternative disease biomarkers and therapeutic targets to improve early diagnosis and therapy efficacy. Here, we identified that microbially produced imidazole propionate (ImP) is associated with the extent of atherosclerosis in mice and in two independent human cohorts. Furthermore, ImP administration to atherosclerosis-prone mice fed chow diet was sufficient to induce atherosclerosis without altering the lipid profile, and it was linked to activation of both systemic and local innate and adaptive immunity and inflammation. Specifically, we found that ImP caused atherosclerosis through Imidazoline-1 receptor (I1R) expressed in myeloid cells. Blocking this ImP/I1R axis inhibited the development of atherosclerosis induced by ImP as well as by high cholesterol diet in mice. Identification of the strong association of ImP with active atherosclerosis, along with the discovery of the contribution of the ImP/I1R axis to disease progression opens new avenues for improving the early diagnosis and personalized therapy of atherosclerosis.
Institute
University of Gothenburg
Last NameBeck
First NameKatharina
AddressBruna Straket 16, Gothenburg, Sweden, 41345, Sweden
Emailkatharina.beck@wlab.gu.se
Phone7803084
Submit Date2025-05-22
Raw Data AvailableYes
Raw Data File Type(s)mzML, raw(Waters)
Analysis Type DetailLC-MS
Release Date2025-06-25
Release Version1
Katharina Beck Katharina Beck
https://dx.doi.org/10.21228/M8MR7Q
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

Select appropriate tab below to view additional metadata details:

Project:

Project ID:PR002468
Project DOI:doi: 10.21228/M8MR7Q
Project Title:Host sensing of microbially produced imidazole propionate is a driver and therapeutic target in atherosclerosis
Project Summary:Atherosclerosis is the main underlying cause of cardiovascular diseases (CVDs). Its prevention is based on the detection and treatment of traditional cardiovascular risk factors but often fails to identify individuals at risk for early vascular disease. Recent research has suggested new players in the pathophysiology of atherosclerosis, highlighting the need for alternative disease biomarkers and therapeutic targets to improve early diagnosis and therapy efficacy. Here, we identified that microbially produced imidazole propionate (ImP) is associated with the extent of atherosclerosis in mice and in two independent human cohorts. Furthermore, ImP administration to atherosclerosis-prone mice fed chow diet was sufficient to induce atherosclerosis without altering the lipid profile, and it was linked to activation of both systemic and local innate and adaptive immunity and inflammation. Specifically, we found that ImP caused atherosclerosis through Imidazoline-1 receptor (I1R) expressed in myeloid cells. Blocking this ImP/I1R axis inhibited the development of atherosclerosis induced by ImP as well as by high cholesterol diet in mice. Identification of the strong association of ImP with active atherosclerosis, along with the discovery of the contribution of the ImP/I1R axis to disease progression opens new avenues for improving the early diagnosis and personalized therapy of atherosclerosis.
Institute:University of Gothenburg
Last Name:Beck
First Name:Katharina
Address:Bruna Straket 16, Gothenburg, Sweden, 41345, Sweden
Email:katharina.beck@wlab.gu.se
Phone:7803084

Subject:

Subject ID:SU004074
Subject Type:Human
Subject Species:Homo sapiens
Taxonomy ID:9606

Factors:

Subject type: Human; Subject species: Homo sapiens (Factor headings shown in green)

mb_sample_id local_sample_id Sample source atherosclerosis
SA4469781418blood AT
SA4469791434blood AT
SA4469801433blood AT
SA4469811432blood AT
SA4469821430blood AT
SA4469831429blood AT
SA4469841427blood AT
SA4469851426blood AT
SA4469861423blood AT
SA4469871420blood AT
SA4469881417blood AT
SA4469891439blood AT
SA4469901415blood AT
SA4469911414blood AT
SA4469921413blood AT
SA4469931412blood AT
SA4469941411blood AT
SA4469951409blood AT
SA4469961408blood AT
SA4469971406blood AT
SA4469981329blood AT
SA4469991435blood AT
SA4470001440blood AT
SA4470011327blood AT
SA4470021460blood AT
SA4470031470blood AT
SA4470041469blood AT
SA4470051468blood AT
SA4470061467blood AT
SA4470071466blood AT
SA4470081465blood AT
SA4470091463blood AT
SA4470101462blood AT
SA4470111461blood AT
SA4470121458blood AT
SA4470131441blood AT
SA4470141456blood AT
SA4470151454blood AT
SA4470161453blood AT
SA4470171452blood AT
SA4470181451blood AT
SA4470191449blood AT
SA4470201448blood AT
SA4470211444blood AT
SA4470221442blood AT
SA4470231328blood AT
SA4470241325blood AT
SA4470251472blood AT
SA4470261275blood AT
SA4470271289blood AT
SA4470281288blood AT
SA4470291287blood AT
SA4470301286blood AT
SA4470311281blood AT
SA4470321280blood AT
SA4470331279blood AT
SA4470341278blood AT
SA4470351276blood AT
SA4470361274blood AT
SA4470371291blood AT
SA4470381270blood AT
SA4470391268blood AT
SA4470401265blood AT
SA4470411263blood AT
SA4470421262blood AT
SA4470431260blood AT
SA4470441259blood AT
SA4470451256blood AT
SA4470461255blood AT
SA4470471290blood AT
SA4470481292blood AT
SA4470491324blood AT
SA4470501307blood AT
SA4470511323blood AT
SA4470521322blood AT
SA4470531321blood AT
SA4470541319blood AT
SA4470551316blood AT
SA4470561314blood AT
SA4470571313blood AT
SA4470581312blood AT
SA4470591308blood AT
SA4470601305blood AT
SA4470611293blood AT
SA4470621304blood AT
SA4470631303blood AT
SA4470641302blood AT
SA4470651300blood AT
SA4470661299blood AT
SA4470671298blood AT
SA4470681296blood AT
SA4470691295blood AT
SA4470701294blood AT
SA4470711471blood AT
SA4470721473blood AT
SA4470731253blood AT
SA4470741588blood AT
SA4470751600blood AT
SA4470761598blood AT
SA4470771596blood AT
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Collection:

Collection ID:CO004067
Collection Summary:A venous blood sample (100 mL) was collected from participants after an overnight fast. After standard processing EDTA plasma tubes, samples were stored in aliquots at -80°C.
Sample Type:Blood (plasma)

Treatment:

Treatment ID:TR004083
Treatment Summary:not applicable

Sample Preparation:

Sampleprep ID:SP004080
Sampleprep Summary:25 µL of plasma samples were extracted using 6 volumes of acetonitrile containing 100 nM of internal standards before drying the samples under a flow of nitrogen. Then, the samples were reconstituted with 5% HCl (37%) in 1-butanol, subjected to n-butyl ester derivatization and finally reconstituted in 150 µL water:acetonitrile (9:1).

Chromatography:

Chromatography ID:CH004913
Instrument Name:Waters Acquity I-Class
Column Name:Waters ACQUITY UPLC BEH C18 (50 x 2.1 mm, 1.7 µm)
Column Temperature:60°C
Flow Gradient:0-0.5 min 10%B, 0.50-2.8 min 25%B, 2.80-2.85 min 95% B, 2.85-3.8 min 95% B, 3.80-3.85 min 10% B, 3.85-5 min 10% B
Flow Rate:0.4 mL/min
Solvent A:100% Water; 0.1% Formic acid
Solvent B:100% Acetonitrile; 0.1% Formic acid
Chromatography Type:Reversed phase

Analysis:

Analysis ID:AN006467
Analysis Type:MS
Chromatography ID:CH004913
Num Factors:2
Num Metabolites:3
Units:nM for imidazole propionate and urocanate and uM for histidine
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