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The microbial metabolite imidazole propionate modulates hypothalamic activity and stress-induced behaviors

ABSTRACT: The microbial metabolite imidazole propionate modulates hypothalamic activity and stress-induced behaviors

PROVIDER: PRJNA1282701 | ENA |

REPOSITORIES: ENA

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	SRR34230807_1.fastq.gz	Fastqsanger.gz
	SRR34230807_2.fastq.gz	Fastqsanger.gz

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The microbial metabolite imidazole propionate modulates hypothalamic activity and stress-induced behaviors

Project description:Neural circuits driving mammalian behaviors are highly plastic and modulated by internal and external factors, including the gut microbiome. We identify imidazole propionate (ImP), a microbial metabolite linked to metabolic disorders, as a key modulator of brain activity and behavior. Bacterially derived ImP enters the systemic circulation and brain, where it alters neuronal gene expression and activity in the hypothalamus without inducing overt neuroinflammation. Elevating systemic ImP promotes stress-related pathways and disrupts GABAergic/glutamatergic signaling in the hypothalamus before peripheral glucose dysregulation occurs. Similarly, colonization with the ImP-producing bacterium Eggerthella lenta elevates behavioral and molecular features of stress. In a mouse model of type 2 diabetes, the gut microbiome exhibits an enhanced ability to produce ImP, leading to elevated systemic levels that are associated with heightened stress responses. In humans, higher ImP associates with reduced hypothalamic reactivity to food cues, impaired stress-coping, and increased emotional eating, mirroring the causal links between ImP, hypothalamic activity, and stress-related behaviors in mice. Overall, these findings establish ImP as a notable microbial metabolite that links gut dysbiosis to altered hypothalamic function and stress in metabolic disease.

2025-06-26 | GSE300937 | GEO

Imidazole propionate (ImP): effect on human aortic endothelial cells

Project description:Imidazole propionate (ImP): effect on human aortic endothelial cells

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Imidazole propionate is a driver and therapeutic target in atherosclerosis [scRNA-seq]

Project description:Atherosclerosis is the main underlying cause of cardiovascular diseases (CVDs). Its prevention is based on traditional cardiovascular risk factor-based scores but often fails to identify individuals at early stages of the disease. Here, we identified microbially produced imidazole propionate (ImP) as an early biomarker of atherosclerosis in mice and in two independent human cohorts. Furthermore, ImP administration induced atherosclerosis without altering lipid metabolism and it was associated with activation of both systemic and local innate and adaptive immunity and inflammation. Here, we used single-cell RNA-seq to characterize the local changes of aorta-derived cells in mice under treatment with ImP for 4 and 8 weeks. Notably, ImP caused atherosclerosis through the Imidazoline-1 receptor (I1R), and the blockade of the ImP/I1R axis inhibited the development of atherosclerosis induced by ImP as well as by high cholesterol diet in mice. Identification of ImP as an early biomarker for atherosclerosis and uncovering the contribution of the ImP/I1R axis in disease progression open new avenues to improve atherosclerosis early diagnosis and therapy.

2025-07-16 | GSE298392 | GEO

Imidazole propionate is a driver and therapeutic target in atherosclerosis [scRNA-seq]

Project description:Imidazole propionate is a driver and therapeutic target in atherosclerosis [scRNA-seq]

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A Hypothalamic Circuit that Modulates Feeding and Parenting Behaviors

Project description:A Hypothalamic Circuit that Modulates Feeding and Parenting Behaviors

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Imidazole propionate is an early biomarker and therapeutic target for atherosclerosis [bulk RNA-seq]

Project description:Atherosclerosis is the main underlying cause of cardiovascular diseases (CVDs). Its prevention is based on traditional cardiovascular risk factor-based scores but often fails to identify individuals at early stages of the disease. Here, we identified microbially produced imidazole propionate (ImP) as an early biomarker of atherosclerosis in mice and in two independent human cohorts. Furthermore, ImP administration induced atherosclerosis without altering lipid metabolism and it was associated with activation of both systemic and local innate and adaptive immunity and inflammation. Notably, ImP caused atherosclerosis through the Imidazoline-1 receptor (I1R), and the blockade of the ImP/I1R axis inhibited the development of atherosclerosis induced by ImP as well as by high cholesterol diet in mice. Here, we profiled three cell lines which represent cell types typically found in aortas (bone marrow-derived macrophages, mouse embryonic fibroblasts and mouse aortic endothelial cells) upon in vitro stimulation with ImP at different time points to better understand the transcriptional regulation of the ImP/I1R axis and its role in the development of the disease. Identification of ImP as an early biomarker for atherosclerosis and uncovering the contribution of the ImP/I1R axis in disease progression open new avenues to improve atherosclerosis early diagnosis and therapy.

2025-07-16 | GSE297831 | GEO

Host sensing of microbially produced imidazole propionate is a driver and therapeutic 1 target in atherosclerosis

Project description:Atherosclerosis is the main underlying cause of cardiovascular diseases (CVDs). Its prevention is based on the detection and treatment of traditional cardiovascular risk factors1 but often fails to identify individuals at risk for early vascular disease2. Recent research has suggested new players in the pathophysiology of atherosclerosis3, 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.

2025-09-15 | PXD063955 | Pride

Gut bacterial metabolite imidazole propionate potentiates Alzheimer's disease pathology.

Project description: Not available

| S-EPMC12157550 | biostudies-literature

Imidazole propionate is an early biomarker and therapeutic target for atherosclerosis [bulk RNA-seq]

Project description:Imidazole propionate is an early biomarker and therapeutic target for atherosclerosis [bulk RNA-seq]

| PRJNA1266247 | ENA

A genomic atlas of mouse hypothalamic development

Project description:The hypothalamus is a central regulator of many behaviors essential for survival such as temperature regulation, food intake and circadian rhythms. However, the molecular pathways that mediate hypothalamic development are largely unknown. To identify genes expressed in developing mouse hypothalamus, microarray analysis at 12 different developmental time points was performed. Developmental in situ hybridization was conducted for 1,045 genes dynamically expressed by microarray analysis. In this way, we identified markers that stably labeled each major hypothalamic nucleus over the entire course of neurogenesis, and thus constructed a detailed molecular atlas of the developing hypothalamus. As proof of concept for the utility of this data, we used these markers to analyze the phenotype of mice where Sonic Hedgehog (Shh) was selectively deleted from hypothalamic neuroepithelium, demonstrating an essential role for Shh in anterior hypothalamic patterning. Our results serve as a resource for functional investigations of hypothalamic development, connectivity, physiology, and dysfunction. Affymetrix MOE430 microarrays were used to analyze the expression patterns of mouse hypothalamic and preoptic area tissues. The results were compared across the variables of Strain, Sex and Age.

2010-05-27 | E-GEOD-21278 | biostudies-arrayexpress

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