Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1183559 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:OTUD3 prevents ulcerative colitis by modulating microbiota-mediated STING activation.
| PRJNA1021199 | ENA
Project description:Ulcerative colitis (UC) develops through a complicated interaction between the host and microbiota. Intestinal fibroblasts are suggested to play crucial roles in the pathogenesis of UC. However, the influences of the host-microbiota interaction on the pathophysiology of intestinal fibroblasts remain poorly understood. Here, we reveal that OTUD3 suppresses pathologic activation of fibroblasts exposed to microbial cyclic GMP-AMP (3’3’-cGAMP) by deubiquitinating stimulator of interferon genes (STING) in the colon. Sting deficiency ameliorated dextran sodium sulfate-induced colitis in Otud3-/- mice. In addition, mice harboring an UC risk missense variant in the Otud3 gene showed pathological features of UC in the colon after transplantation of a fecal microbiome with the potential to produce excessive cGAMP from UC patients. Collectively, these results demonstrate the critical role of OTUD3 in the maintenance of intestinal homeostasis and highlight one mechanism of the interaction between the host (OTUD3 in fibroblasts) and microbiota (STING agonist) in UC development.
2025-05-12 | GSE244080 | GEO
Project description:Ulcerative colitis (UC) develops through a complicated interaction between the host and microbiota. Intestinal fibroblasts are suggested to play crucial roles in the pathogenesis of UC. However, the influences of the host-microbiota interaction on the pathophysiology of intestinal fibroblasts remain poorly understood. Here, we reveal that OTUD3 suppresses pathologic activation of fibroblasts exposed to microbial cyclic GMP-AMP (3’3’-cGAMP) by deubiquitinating stimulator of interferon genes (STING) in the colon. Sting deficiency ameliorated dextran sodium sulfate-induced colitis in Otud3-/- mice. In addition, mice harboring an UC risk missense variant in the Otud3 gene showed pathological features of UC in the colon after transplantation of a fecal microbiome with the potential to produce excessive cGAMP from UC patients. Collectively, these results demonstrate the critical role of OTUD3 in the maintenance of intestinal homeostasis and highlight one mechanism of the interaction between the host (OTUD3 in fibroblasts) and microbiota (STING agonist) in UC development.
2025-05-12 | GSE244079 | GEO
Project description:Ulcerative colitis (UC) develops through a complicated interaction between the host and microbiota. Intestinal fibroblasts are suggested to play crucial roles in the pathogenesis of UC. However, the influences of the host-microbiota interaction on the pathophysiology of intestinal fibroblasts remain poorly understood. Here, we reveal that OTUD3 suppresses pathologic activation of fibroblasts exposed to microbial cyclic GMP-AMP (3’3’-cGAMP) by deubiquitinating stimulator of interferon genes (STING) in the colon. Sting deficiency ameliorated dextran sodium sulfate-induced colitis in Otud3-/- mice. In addition, mice harboring an UC risk missense variant in the Otud3 gene showed pathological features of UC in the colon after transplantation of a fecal microbiome with the potential to produce excessive cGAMP from UC patients. Collectively, these results demonstrate the critical role of OTUD3 in the maintenance of intestinal homeostasis and highlight one mechanism of the interaction between the host (OTUD3 in fibroblasts) and microbiota (STING agonist) in UC development.
2025-05-12 | GSE244078 | GEO
Project description:Ulcerative colitis (UC) develops through a complicated interaction between the host and microbiota. Intestinal fibroblasts are suggested to play crucial roles in the pathogenesis of UC. However, the influences of the host-microbiota interaction on the pathophysiology of intestinal fibroblasts remain poorly understood. Here, we reveal that OTUD3 suppresses pathologic activation of fibroblasts exposed to microbial cyclic GMP-AMP (3’3’-cGAMP) by deubiquitinating stimulator of interferon genes (STING) in the colon. Sting deficiency ameliorated dextran sodium sulfate-induced colitis in Otud3-/- mice. In addition, mice harboring an UC risk missense variant in the Otud3 gene showed pathological features of UC in the colon after transplantation of a fecal microbiome with the potential to produce excessive cGAMP from UC patients. Collectively, these results demonstrate the critical role of OTUD3 in the maintenance of intestinal homeostasis and highlight one mechanism of the interaction between the host (OTUD3 in fibroblasts) and microbiota (STING agonist) in UC development.
2025-05-12 | GSE244077 | GEO
Project description:Ulcerative colitis (UC) develops through a complicated interaction between the host and microbiota. Intestinal fibroblasts are suggested to play crucial roles in the pathogenesis of UC. However, the influences of the host-microbiota interaction on the pathophysiology of intestinal fibroblasts remain poorly understood. Here, we reveal that OTUD3 suppresses pathologic activation of fibroblasts exposed to microbial cyclic GMP-AMP (3’3’-cGAMP) by deubiquitinating stimulator of interferon genes (STING) in the colon. Sting deficiency ameliorated dextran sodium sulfate-induced colitis in Otud3-/- mice. In addition, mice harboring an UC risk missense variant in the Otud3 gene showed pathological features of UC in the colon after transplantation of a fecal microbiome with the potential to produce excessive cGAMP from UC patients. Collectively, these results demonstrate the critical role of OTUD3 in the maintenance of intestinal homeostasis and highlight one mechanism of the interaction between the host (OTUD3 in fibroblasts) and microbiota (STING agonist) in UC development.
2025-05-12 | GSE244076 | GEO
Project description:The goal of this project is to find out whether human intestinal IgA1 and IgA2 secretion, transport and reactivity towards the microbiota might be involved in dysbiosis induction during Crohn’s disease and Ulcerative colitis. Mass spectrometry was used to characterize SIgA from Crohn’s disease patient and Ulcerative colitis patient, in term of O- and N-glycosylation in order to study their reverse transcytosis capacity and their role in intestinal inflammation.
2022-06-27 | PXD024060 | Pride
Project description:Human colon biopsies (healthy and Ulcerative Colitis) LC-MS/MS
2022-01-07 | E-PROT-40 | ExpressionAtlas
Project description:Expression data from colonic biopsy samples of infliximab treated ulcerative colitis patients
2025-01-24 | E-GEOD-23597 | ExpressionAtlas
Project description:STING activation by cyclic dinucleotides in mammals induces Type I Interferon- and NFkB-related gene expression, and the lipidation of LC3B at Golgi membranes. While the mechanisms of the Interferon-related responses are well understood, the mechanism of NFkB activation mediated by STING activation, and how the multi-functional responses downstream of STING signaling are related remain unknown. We report that STING activation induces K63 and linear ubiquitin chain formation, and ubiquitin co-localizes with STING and LC3B at Golgi-derived vesicles. Loss of the LUBAC E3 ubiquitin ligase subunit, HOIP, prevents formation of the linear, but not K63-linked, ubiquitin chains. The ubiquitin and LC3B binding proteins, Optineurin and TNIP1, are co-localized with STING activation-induced, perinuclear LC3B foci via their UBAN domains, however loss of HOIP does not influence this localization, indicating they may bind the K63-linked ubiquitin chains. HOIP-mediated linear ubiquitin chains are well established to mediate NFkB downstream of TNFa and IL1beta receptor stimulation. Loss of HOIP in monocytic THP-1 cells inhibits STING-induced NFkB activation and NFkB-related gene transcription, as well as Interferon-related transcription. Further, the recently reported proton channel activity of STING that blocks LC3B lipidation at Golgi membranes is also important for both K63 and Linear ubiquitin chain formation, and NFkB signaling. Thus, STING induces HOIP and linear ubiquitin chain formation to activate NFkB.
| MSV000092940 | MassIVE