Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1283927 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: Gut microbiota-derived metabolites play a pivotal role in the maintenance of local gut homeostasis and can even induce systemic effects via accumulation in the bloodstream. Here, we demonstrate that mono-colonization of germ-free (GF) mice with Clostridium sporogenes protects mice from inflamation and death induced by DSS colitis. Method: 8-12-week-old male mice (GF, SPF and GF colonized with C. sporogenes (CS)) were treated with 2.5% DSS in drinking water for 5 days and colon tissue was isolated on day 7. RNA was isolated from the colon tissue and RNA sequenzing was performed. Results: Mono-colonization of GF mice with Clostridium sporogenes protected the mice from DSS colitis induced death, while producing high amounts of indole-3-propionic acid (IPA), branched chain (BCFA) and short-chain (SCFA) fatty acids. In comparison to CS mice, SPF mice showed much higher levels of inflammatory related genes and a worse histological score. Conclusion: Histological stainings and the RNAseq both showed high levels of protection of C. sporogenes colonized mice in colitis, compared to SPF and GF animals. The data provide evidence for a therapeutic potential of C. sporogenes for IBD patients.
2024-10-15 | GSE264024 | GEO
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
Project description:Hepatocellular carcinoma is one of the most prevalent malignancies worldwide, and the role of stress in hepatocellular carcinoma progression remains incompletely understood. In this study, we integrated clinical and preclinical models to investigate how stress-associated gut microbiota remodeling contributes to hepatocellular carcinoma progression. Stress profoundly altered the gut microbiota, with Phocaeicola vulgatus significantly reduced. Restoration of Phocaeicola vulgatus or administration of its tryptophan-derived metabolite indole-3-propionic acid attenuated hepatocellular carcinoma progression in vivo. Single-cell RNA sequencing was performed to characterize changes in the hepatocellular carcinoma tumor microenvironment. Indole-3-propionic acid treatment reduced endothelial JAM2 expression and was associated with reduced JAM2-F11R-mediated endothelial-macrophage crosstalk. These findings support a role for the stress-gut microbiota-metabolite-tumor microenvironment axis in hepatocellular carcinoma progression and suggest potential translational targets for microbiome-based therapeutic strategies.
2026-05-13 | GSE330363 | GEO
Project description:Quantification of indolelactic acid (ILA), indoxyl sulfate, indole-3-propionic acid, cortisol, tryptophan, thyroxine (T4), kynurenine and serotonin
2025-05-20 | MSV000097925 | MassIVE
Project description:Genomic DNA of 61 strains of proteolytic Clostridium botulinum or Clostridium sporogenes was subjected to analysis by DNA microarray.
2008-12-31 | E-MEXP-1637 | biostudies-arrayexpress
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
Project description:Acne vulgaris is a chronic inflammatory dermatosis where conventional therapies of-ten face limitations in efficacy and safety, necessitating the development of microbi-ome-targeted interventions. This study investigated the immunomodulatory potential of microbiome-derived tryptophan metabolites as a novel therapeutic strategy for Cutibacterium acnes-induced inflammation, focusing on the aryl hydrocarbon receptor (AHR) pathway. We evaluated indole-3-lactic acid (ILA), indole-3-acrylic acid (IAA), and indole-3-propionic acid (IPA) in comparison to tapinarof, utilizing C. ac-nes-stimulated human epidermal keratinocytes and a C. acnes-induced acne mouse model. In vitro, ILA and IPA significantly suppressed C. acnes-driven inflammatory mediators, including TNF-α, IL-1β, and COX2, whereas IAA demonstrated limited ef-ficacy. In vivo, ILA treatment exhibited superior therapeutic activity, markedly reduc-ing inflammatory cell infiltration, epidermal hyperplasia, and IL-1β expression. Tran-scriptomic analysis confirmed that ILA attenuates inflammatory signaling (e.g., IL-17 and TNF pathways) while upregulating AHR-responsive genes such as CYP1A1 and CYP1B1. Collectively, these findings establish ILA as a potent postbiotic that mitigates cutaneous inflammation through selective activation of the AHR. Future studies should prioritize the clinical translation of ILA-based topical fomulations, with rigorous evaluation of their efficacy and safety in well-designed human trials, to support their development as a non-antibiotic therapeutic alternative for acne management.
2026-01-05 | GSE315350 | GEO
Project description:Indole-3-pyruvate (I3P), an endogenous metabolite derived from tryptophan by gut microbiota and IL4I1 enzyme in humans can potentially activate the transcriptional activity of the Aryl Hydrocarbon receptor. Here we test this by stimulating AHR proficient U-87MG cells with I3P alone or in combination with the AHR antagonist SR1.
2020-08-19 | GSE143240 | GEO
Project description:Altered tryptophan catabolism has been identified in inflammatory diseases like rheumatoid arthritis (RA) and spondyloarthritis (SpA), but the causal mechanisms linking tryptophan metabolites to disease are unknown. Using the collagen-induced arthritis (CIA) model we identify alterations in tryptophan metabolism, and specifically indole, that correlate with disease. We demonstrate that both bacteria and dietary tryptophan are required for disease, and indole supplementation is sufficient to induce disease in their absence. When mice with CIA on a low-tryptophan diet were supplemented with indole, we observed significant increases in serum IL-6, TNF, and IL-1β; splenic RORγt+CD4+ T cells and ex vivo collagen-stimulated IL-17 production; and a pattern of anti-collagen antibody isotype switching and glycosylation that corresponded with increased complement fixation. IL-23 neutralization reduced disease severity in indole-induced CIA. Finally, exposure of human colon lymphocytes to indole increased expression of genes involved in IL-17 signaling and plasma cell activation. Altogether, we propose a mechanism by which intestinal dysbiosis during inflammatory arthritis results in altered tryptophan catabolism, leading to indole stimulation of arthritis development. Blockade of indole generation may present a novel therapeutic pathway for RA and SpA.
2023-11-13 | GSE241655 | GEO