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Microbiota derived interlukin-35 producing B cells induce regulatory immune responses and supress colitis in mice

ABSTRACT: Microbiota derived interlukin-35 producing B cells induce regulatory immune responses and supress colitis in mice

PROVIDER: PRJNA865922 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20822078.fastq.gz	Fastqsanger.gz
	SRR20822079.fastq.gz	Fastqsanger.gz
	SRR20822080.fastq.gz	Fastqsanger.gz
	SRR20822081.fastq.gz	Fastqsanger.gz
	SRR20822082.fastq.gz	Fastqsanger.gz

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Microbiota derived interlukin-35 producing B cells induce regulatory immune responses and supress colitis in mice

Project description:To investigate the immune regulatory role of microbiota derived interlukin-35 producing B cells in DSS-induced mice colitis. We then performed gene expression profiling analysis using data obtained from RNA-seq of isolated B cells from patches of colitis mice at four different time points.

2022-08-31 | GSE210506 | GEO

Gut microbiota derived metabolites 3-idoleacetic acid promotes IL-35+B cell production

Project description:Disruptions of microbiota composition by factors such as genetics have been suggested to be critical contributing factors to the growth of the worldwide epidemics of chronic illness such as metabolic diseases. IL-35-producing regulatory B and T regulatory cells are critical regulators to these illnesses. Whether microbiota-derived metabolites can regulate these IL-35+ cells maintain elusive. Here, we found gut genetic factor Reg4 associated lactobacillus could promote the generation of IL-35+ B cells through producing 3-idoleacetic acid (IAA). HuREG4IEC tg mice had markedly accumulation of IL-35+ not only in adipose tissues but also in colon tissues; whereas significantly decreased IL-35+ cells in adipose tissues and colon tissues could be detected in Reg4 KO mice. On the mechanism, IAA-mediated IL35+ B cells was through PXR), RXR and CAR in the presence of LPS. PXR KO, CAR KO and NF-B KO mice impaired the generation of IAA- IL-35+B cells. Interestingly, lower levels of IAA and IL-35 were also detected in the peripheral blood of individuals with obesity. Thus, IAA is a factor to promote the generation of IL-35+B cells to impede the development of obesity.

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Lysophosphatidylserines derived from microbiota in Crohn’s disease elicit pathological Th1 response

Project description:Microbiota alteration and IFN-γ-producing CD4+ T cell overactivation are implicated in Crohn's disease (CD) pathogenesis. However, it remains unclear how dysbiosis enhances Th1 responses, leading to intestinal inflammation. Here, we identified key metabolites that are derived from dysbiotic microbiota and induce enhanced Th1 responses and severe colitis in mouse models. Patients with CD showed elevated lysophosphatidylserine (LysoPS) concentration in their feces, accompanied with a higher relative abundance of microbiota possessing a gene encoding the phospholipid-hydrolyzing enzyme phospholipase A. LysoPS induced metabolic reprograming, thereby eliciting aberrant effector responses in both human and mouse IFN-?-producing CD4+ T cells. Administration of LysoPS into T cell-dependent mouse colitis models induced severe inflammation. LysoPS-induced aggravation of colitis was impaired in mice lacking P2ry10 and P2ry10b, and their CD4+ T cells were hypo-responsive to LysoPS. Thus, our findings elaborate on the mechanism by which metabolites elevated in patients with CD harboring dysbiotic microbiota induce intestinal pathology.

2022-05-03 | GSE169006 | GEO

Regulatory B cells suppress GVHD and prolong survival of GVHD via membrane-bound IL-35 and secretion of exosomes with membrane-bound IL-35

Project description:Interleukin 35-producing B-cells (i35-Bregs) suppress autoimmune diseases and IL-35 is immunosuppressive member of IL-12 cytokine family. It is comprised of p35 and Ebi3 subunits which are assumed to be independently secreted proteins that associate in-vivo to form non-covalently linked heterodimeric IL-35. In view of recent reports that p35 and Ebi3 are not secreted as a heterodimer but act as independent anti-inflammatory cytokines, we investigated whether i35-Bregs can suppress GVHD by secreting p35, Ebi3 or heterodimeric IL-35. Surprisingly, i35-Bregs ameliorate and prolong survival of Graft-Versus-Host-Disease (GVHD) via membrane-bound IL-35 and secrete exosomes with membrane-bound IL-35 (i35-exosomes) that upregulate checkpoint inhibitors (PD-1/LAG-3) and induce T-cell exhaustion, thereby rendering allogeneic T-cells less active, with diminished proinflammatory effects. i35-exosomes also propagate infectious tolerance mechanism by binding bystander B-lymphocytes and converting them to IL-35 producers. Adoptive transfer of i35-Bregs or i35-exosomes suppress GVHD through these mechanisms, indicating that i35-Bregs/i35-exosomes combination-immunotherapy maybe effective therapy for GVHD.

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Temporal transcriptional profiles of colonic tissue during DSS-induce colitis

Project description:Temporal transcriptional profiles of colonic tissue during DSS-induce colitis

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Project description:This study aims to investigate the protein expression profiles in a murine model of dextran sulfate sodium (DSS)-induced colitis using advanced Astral-DIA quantitative proteomics technology. A total of 12 colon tissue samples were analyzed, including 6 from healthy control mice and 6 from DSS-treated mice with induced colitis. Experimental Design Species: Mus musculus (C57BL/6 strain). Tissue Source: Colon tissues were dissected, snap-frozen in liquid nitrogen, and homogenized to extract proteins. Groups: Control Group: Healthy mice without intervention. DSS Group: Mice subjected to 2.5% DSS administration for 7 days to induce colitis, validated by histopathological assessment.

2025-09-18 | PXD063633 | Pride

Accute and repeated DSS exposure induce distinct immune responses with differential relevance to human Ulcerative Colitis

Project description:Dextran sulfate sodium (DSS)-induced colitis is a widely used model to study ulcerative colitis (UC). However, the extent to which acute versus repeated DSS exposure mimics human disease remains unclear. Using histopathology, flow cytometry, single-cell RNA sequencing (scRNA-seq) and 16S rRNA profiling we compared disease outcomes, immune infiltrate, transcriptional programs and changes in the microbiome in mice subjected to a single (acute) versus two (repeated) DSS cycles. We found that repeated cycles of DSS-induced colitis in mice result in more severe intestinal inflammation compared to a single exposure, with increased PMN and T cell infiltration, mucosal remodeling, and microbiota normalization. Single-cell transcriptomics revealed that acute vs repeated DSS exposure drives differential programs in immune cell subtypes distinctly overlapping with human UC. Overall, our findings suggest that repeated DSS exposure may more accurately models human disease, highlighting its utility for translational IBD research.

2025-10-31 | GSE306845 | GEO

Temporal transcriptional profiles of colonic tissue during DSS-induce colitis

Project description:Inflammation dramatically alters the gut microenvironment. To investigate the transcriptome changes the temporal profile of multiple signaling pathways throughout the progression of colitis, we collected the colonic tissue at a series of time points during DSS colitis for bulk RNA sequencing.

2022-09-06 | GSE210405 | GEO

35 samples

Project description:35 samples

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