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Ornithine decarboxylase supports ILC3 responses in infectious and autoimmune colitis through positive regulation of IL-22 transcription

ABSTRACT: Ornithine decarboxylase supports ILC3 responses in infectious and autoimmune colitis through positive regulation of IL-22 transcription

PROVIDER: PRJNA884137 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21706546_1.fastq.gz	Fastqsanger.gz
	SRR21706546_2.fastq.gz	Fastqsanger.gz
	SRR21706547_1.fastq.gz	Fastqsanger.gz
	SRR21706547_2.fastq.gz	Fastqsanger.gz
	SRR21706548_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Ornithine decarboxylase supports ILC3 responses in infectious and autoimmune colitis through positive regulation of IL-22 transcription

Project description:Group 3 innate lymphoid cells (ILC3s) are RORγT+ lymphocytes that are predominately enriched in mucosal tissues and produce IL-22 and IL-17A. They are the innate counterparts of Th17. While Th17 lymphocytes utilize unique metabolic pathways in their differentiation program, it is unknown whether ILC3s make similar metabolic adaptations. We employed single-cell RNA sequencing and metabolomic profiling of intestinal ILC subsets to identify an enrichment of polyamine biosynthesis in ILC3s, converging on the rate-limiting enzyme ornithine decarboxylase (ODC1). In vitro and in vivo studies demonstrated that exogenous supplementation with the polyamine putrescine or its biosynthetic substrate, ornithine, enhanced ILC3 production of IL-22. Conditional deletion of ODC1 in ILC3s impaired mouse antibacterial defense against C. rodentium infection, which was associated with a decrease in anti-microbial peptide production by the intestinal epithelium. Furthermore, in a model of anti-CD40 colitis, deficiency of ODC1 in ILC3s markedly reduced the production of IL-22 and severity of inflammatory colitis. We conclude that cell-intrinsic polyamine biosynthesis facilitates efficient defense against enteric pathogens as well as augments autoimmune colitis, thus representing an attractive target to modulate ILC3 function in intestinal disease.

2022-10-06 | GSE214152 | GEO

Ornithine aminotransferase supports polyamine synthesis in pancreatic cancer

Project description:Pancreatic ductal adenocarcinoma (PDA) cells have a distinct dependence on de novo ornithine synthesis from glutamine via ornithine aminotransferase (OAT), which supports polyamine synthesis and is required for tumor growth. This directional OAT activity is normally largely restricted to infancy and contrasts with the reliance of most adult normal tissues and other cancer types on arginase (ARG) to generate arginine-derived ornithine, the substrate for polyamine synthesis. This dependence associates with arginine depletion in PDA tumor microenvironment, and is driven by mutant KRAS, which induces the expression of OAT and polyamine synthesis enzymes, including the rate-limiting enzyme ornithine decarboxylase-1 (ODC1). Loss of OAT, but not ARG2, largely mimics loss of ODC1, altering the transcriptional profiles in PDA cells, which in turn correlate with alterations in open chromatin states.

2023-01-01 | GSE193411 | GEO

Ornithine decarboxylase is sufficient for prostate tumorigenesis via androgen receptor signaling

Project description:Ornithine decarboxylase is sufficient for prostate tumorigenesis via androgen receptor signaling

2016-06-03 | GSE82179 | GEO

Ornithine decarboxylase supports ILC3 responses in infectious and autoimmune colitis through positive regulation of IL-22 transcription.

Project description:Group 3 innate lymphoid cells (ILC3s) are RORγT+ lymphocytes that are predominately enriched in mucosal tissues and produce IL-22 and IL-17A. They are the innate counterparts of Th17 cells. While Th17 lymphocytes utilize unique metabolic pathways in their differentiation program, it is unknown whether ILC3s make similar metabolic adaptations. We employed single-cell RNA sequencing and metabolomic profiling of intestinal ILC subsets to identify an enrichment of polyamine biosynthesis in ILC3s, converging on the rate-limiting enzyme ornithine decarboxylase (ODC1). In vitro and in vivo studies demonstrated that exogenous supplementation with the polyamine putrescine or its biosynthetic substrate, ornithine, enhanced ILC3 production of IL-22. Conditional deletion of ODC1 in ILC3s impaired mouse antibacterial defense against Citrobacter rodentium infection, which was associated with a decrease in anti-microbial peptide production by the intestinal epithelium. Furthermore, in a model of anti-CD40 colitis, deficiency of ODC1 in ILC3s markedly reduced the production of IL-22 and severity of inflammatory colitis. We conclude that ILC3-intrinsic polyamine biosynthesis facilitates efficient defense against enteric pathogens as well as exacerbates autoimmune colitis, thus representing an attractive target to modulate ILC3 function in intestinal disease.

| S-EPMC9659397 | biostudies-literature

Ornithine aminotransferase supports polyamine synthesis in pancreatic cancer

Project description:Ornithine aminotransferase supports polyamine synthesis in pancreatic cancer

| PRJNA796043 | ENA

EPLIN-Beta is a novel substrate of ornithine decarboxylase antizyme 1, mediating cellular migration

Project description:Polyamines promote cellular proliferation, and their levels are controlled by ornithine decarboxylase antizyme 1 (Az1), through the proteasome-mediated, ubiquitin-independent degradation of ornithine decarboxylase (ODC), the rate-limiting enzyme of polyamine biosynthesis. Az1-mediated degradation of other substrates such as cyclin D1, DNp73 and Mps1 also regulate cell growth and centrosome amplification. Collectively, the currently known six Az1-substrates are all linked with tumorigenesis. To understand if Az1-mediated protein degradation might play a key role in regulating cellular process associated with tumorigenesis, we employed quantitative proteomics to identify novel Az1 substrates. Here, we describe the identification of LIM domain and Actin-binding protein 1 (LIMA1), also known as epithelial protein lost in neoplasm (EPLIN), as a new target of Az1. Interestingly, between the two isoforms of EPLIN-Alpha and -Beta, only EPLIN-Beta is the substrate of Az1, degraded in an ubiquitination-independent manner. Absence of Az1 led to elevated EPLIN-Beta levels, which caused enhanced cellular migration of Az1-/- cells. Consistently, higher levels of LIMA1 correlated with poorer overall survival of colorectal cancer patients. Taken together, this study identifies EPLIN-Beta as a novel Az1 substrate regulating cellular migration.

2023-06-08 | PXD039865 | Pride

Ornithine Decarboxylase Activity in Gastric Epithelial Cells Contributes to the Pathogenesis of Helicobacter pylori

Project description:Ornithine Decarboxylase Activity in Gastric Epithelial Cells Contributes to the Pathogenesis of Helicobacter pylori

| PRJNA753859 | ENA

Trained ILC3 Responses Promote Intestinal Defense

Project description:Group 3 innate lymphoid cells (ILC3) are innate immune effectors that contribute to host defense. Whether ILC3 functions are stably modified following pathogen encounter is unknown. Here we assess the impact of a time-restricted enterobacterial challenge to long-term ILC3 activation. We found that intestinal ILC3 persist for months in an activated state following exposure to Citrobacter rodentium. Upon rechallenge, these “trained” ILC3 proliferate, display enhanced interleukin (IL)-22 responses, and have a superior cell-intrinsic capacity to control infection compared to naïve ILC3. Metabolic changes occur in C. rodentium-exposed ILC3 but only trained ILC3 have enhanced proliferative capacity that contributes to elevated IL-22 production. Accordingly, a limited encounter with a pathogen can promote durable phenotypic and functional changes in intestinal ILC3 that contribute to long-term mucosal defense.

2022-01-31 | GSE191167 | GEO

Ornithine Decarboxylase in Gastric Epithelial Cells Promotes the Immunopathogenesis of Helicobacter pylori Infection

Project description:Colonization by H. pylori is associated with a wide range of gastric diseases, ranging from superficial gastritis to more severe pathologies, including intestinal metaplasia and adenocarcinoma. The interplay of the host response and the pathogen affect the outcome of disease. One major component of the mucosal response to H. pylori is the activation of a strong, but inefficient immune response that fails to control the infection and frequently causes tissue damage. We have shown that polyamines can regulate H. pylori-induced inflammation. Chemical inhibition of ornithine decarboxylase (ODC), which generates putrescine from L-ornithine, reduces gastritis in mice and adenocarcinoma incidence in gerbils infected with H. pylori. However, we have also demonstrated that Odc deletion in myeloid cells enhances M1 macrophage activation and gastritis. Here we used a genetic approach to assess the specific role of gastric epithelial ODC during H. pylori infection. Deletion of Odc in gastric epithelial cells reduces gastritis, attenuates epithelial proliferaton, alters the metabolome, and dowregulates the expression of immune mediators induced by H. pylori. Inhibition of ODC activity in gastric epithelial cells reduces H. pylori-induced NF-B activation and CXCL8 mRNA expression. Chronic inflammation is a major risk factor for the progression to more severe pathologies associated with H. pylori infection and we now show that epithelial ODC plays an important role in mediating this inflammatory response.

2022-06-15 | MTBLS3235 | MetaboLights

Genes modulated by DNA demethylation in UM1 cells

Project description:Ornithine decarboxylase antizyme 1 mediates DNA demethylation. Using a human oral cancer cell line, UM1, genes induiced by DNA demethylation were screened. To verify the methylation status of those induced genes, the gene expression profile was compared with that of 5-Aza-2’-deoxycytidine treated sample. Keywords: DNA demthylation, ornithine decarboxylase antizyme 1, 5-Aza-2’-deoxycytidine

2005-09-16 | GSE3168 | GEO

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