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Gut-derived indole propionic acid alleviates liver fibrosis by modulating pro-fibrogenic macrophage phenotype and biological function

ABSTRACT: Gut-derived indole propionic acid alleviates liver fibrosis by modulating pro-fibrogenic macrophage phenotype and biological function

PROVIDER: PRJNA1160868 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30660914_1.fastq.gz	Fastqsanger.gz
	SRR30660914_2.fastq.gz	Fastqsanger.gz
	SRR30660915_1.fastq.gz	Fastqsanger.gz
	SRR30660915_2.fastq.gz	Fastqsanger.gz

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Gut-derived indole propionic acid alleviates liver fibrosis by modulating pro-fibrogenic macrophage phenotype and biological function

Project description:Recently, gut metabolites have been recognized to play significant roles in liver diseases via the gut-liver axis. In this study, we investigate the regulatory effects of the tryptophan metabolite, indole-3-propionic acid (IPA), on immune cells during liver fibrogenesis using single-cell RNA sequencing (scRNA-seq).

2024-09-20 | GSE277148 | GEO

RNA sequencing of L4-L6 mouse Dorsal Root Ganglia 3 days post sciatic nerve crush and naive following 10 days of Indole-3-propionic acid treatment

Project description:Purpose: compare the response of DRG neurons to indole-3-propionic acid treatment before and after sciatic nerve injury Results: we found that IPA induced transcription changes before and after injury inside the DRG tissue. In particular expression of immune system related genes

2022-01-01 | GSE161342 | GEO

Maternal Helminths Rewire the Microbiota to Promote Offspring Antiviral Immunity via Indole-3-Propionic Acid

Project description:Maternal environmental exposures are critical in shaping offspring immunity. Yet, the role of helminths, mammals’ symbiotic evolutionary partners that have been eliminated from modern societies, remains poorly understood. Here, we show that maternal helminth infection enhances type I interferon (IFN-I) signaling in the offspring’s lung epithelium, conferring broad and lasting protection against respiratory viruses. Using cross-fostering, antibiotics, and gnotobiotic systems, we demonstrate that this antiviral immunity is mediated by helminth-altered maternal microbiota. Mechanistically, we identify the microbial tryptophan metabolite indole-3-propionic acid (IPA) as a key driver of IFN-I responses in lung epithelium. Furthermore, the tryptophan metabolic pathway is enriched in the microbiome of helminth-infected human populations, and IPA alone is sufficient to enhance IFN-I signaling in human bronchial epithelial cells. We uncover a conserved trans-kingdom mechanism by which maternal helminths imprint offspring antiviral immunity and propose that microbial metabolites could be harnessed to restore early-life antiviral defenses in helminth-depleted societies.

2026-07-01 | GSE299495 | GEO

Maternal Helminths Rewire the Microbiota to Promote Offspring Antiviral Immunity via Indole-3-Propionic Acid

Project description:Maternal Helminths Rewire the Microbiota to Promote Offspring Antiviral Immunity via Indole-3-Propionic Acid

| PRJNA1274826 | ENA

Microbial metabolite Indole-3-propionic acid drives mitochondrial respiration in CD4+ T cells to confer protection against intestinal inflammation

Project description:The gut microbiota and its metabolites critically regulate immune cell phenotype, function, and energy metabolism. We screened a collection of gut microbiota-related metabolites to identify modulators of mitochondrial metabolism in T cells. Here, we show that indole-3-propionic acid (IPA) stimulates mitochondrial respiration of CD4+ T cells by increasing the oxidation of fatty acids and amino acids (FAO and AAO), while inhibiting glycolytic capacity. IPA also impacts CD4+ T cell behavior by inhibiting their differentiation to TH1 and TH17 phenotypes. Mechanistically, the metabolic and immune effects of IPA are mediated by Peroxisome Proliferator-Activated Receptor-beta/delta. The administration of IPA rescues mitochondria respiration in mice with gut bacteria depletion or colitis by enhancing FAO and AAO in colonic CD4+ T cells. Adoptive transfer experiments show that IPA acts on CD4+T cells to exert its protective effect against inflammation. Collectively, our study reveals that the anti-inflammatory effects of IPA are mediated by metabolic reprogramming of CD4+ T cells toward the enhancement of mitochondrial respiration.

2025-08-28 | PXD057537 | Pride

Enhanced growth and productivity of useful metabolites by indole-3-propionic acid treatment in Lemna aequinoctialis culture

Project description:Enhanced growth and productivity of useful metabolites by indole-3-propionic acid treatment in Lemna aequinoctialis culture

| PRJNA1222289 | ENA

Microbiota-indole-3-propionic acid-heart axis mediates the protection of leflunomide against αPD1-induced cardiotoxicity in mice

Project description:Microbiota-indole-3-propionic acid-heart axis mediates the protection of leflunomide against αPD1-induced cardiotoxicity in mice

| PRJNA1208476 | ENA

Kentucky assay: Indole

Project description:Kentucky assay: Indole

| PRJNA610533 | ENA

Chemotherapy-driven intestinal dysbiosis and microbial indole-3-propionic acid rewire bone marrow myelopoiesis to promote anti-metastatic immunity

Project description:Chemotherapy-driven intestinal dysbiosis and microbial indole-3-propionic acid rewire bone marrow myelopoiesis to promote anti-metastatic immunity

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Effect of topical application of propionic acid on gene expression in the skin lesions of AD mice

Project description:Secondary metabolites such as short chain fatty acids (SCFAs) are primarily responsible for skin microbiota to modulate skin homeostasis. We here report propionic acid can relieve AD in mice. To further explore the mechanism underlying the modulation of skin microbiota-derived propionic acid on AD, we performed RNA-seq analysis on the skin lesions of ctrl or propionic acid-treated MC903 induced AD mice.

2026-06-30 | GSE270153 | GEO

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