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Next Generation Sequencing of Wild Type and Nlrp6-/- T cells

ABSTRACT: Nlrp6 is expressed by T cells, but whether Nlrp6 influences the transcriptom of T cells is not known Methods: Equal numbers of Wild Type and Nlrp6-/- CD4 T cells were adoptively transfered in RAG-/- hosts, isolated from the colonic lamina propria and mRNA profiles gernerated by next generation squencing in quadruplicates using Illumina squencers. Conclusions: Our study indicates that Nlrp6 may regulate genes that are involved in apoptosis of T cells

ORGANISM(S): Mus musculus

PROVIDER: GSE116454 | GEO | 2019/05/08

REPOSITORIES: GEO

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Global genome expression analysis of lamina propria derived WT and Nlrp6-/- Ly6C-hi inflammatory monocytes

Project description:Nlrp6-/- lamina propria Ly6C-hi monocytes in response to AOM/DSS have deficient TNFÎ± production, but increased production of other pro-inflammatory cytokines as compared to WT NLRP6 is a member of the Nod-like receptor family, whose members are involved in the recognition of microbes and/or tissue injury. NLRP6 was previously demonstrated to regulate the production of IL-18 and is important for protecting mice against chemically-induced intestinal injury and colitis-associated colon cancer. However, the cellular mechanisms by which NLRP6 reduces susceptibility to colonic inflammation remain unclear. Here, we determined that NLRP6 expression is specifically upregulated in Ly6Chi inflammatory monocytes that infiltrate into the colon during dextran sulfate sodium (DSS)-induced inflammation. Adoptive transfer of WT Ly6Chi inflammatory monocytes into Nlrp6-/- mice was sufficient to protect them from mortality, significantly reducing intestinal permeability and damage. NLRP6-deficient inflammatory monocytes were specifically defective in TNFÎ± production, which was important for reducing DSS-induced mortality and dependent on autocrine IL-18 signaling by inflammatory monocytes. Our data reveal a previously unappreciated role for NLRP6 in inflammatory monocytes, which are recruited during intestinal injury to promote barrier function and limit bacteria-driven inflammation. This study also highlights the importance of early cytokine responses, particularly NLRP6-dependent and IL-18-dependent TNFÎ± production in preventing chronic dysregulated inflammation. Ly6Chi monocytes were sorted from lamina propria of WT or Nlrp6-/- mice at day 10 of AOM/2%DSS. RNA was extracted and hybridized to the mouse 2.1 ST array.

2016-03-27 | E-GEOD-79631 | biostudies-arrayexpress

Global genome expression analysis of lamina propria derived WT and Nlrp6-/- Ly6C-hi inflammatory monocytes

Project description:Nlrp6-/- lamina propria Ly6C-hi monocytes in response to AOM/DSS have deficient TNFα production, but increased production of other pro-inflammatory cytokines as compared to WT NLRP6 is a member of the Nod-like receptor family, whose members are involved in the recognition of microbes and/or tissue injury. NLRP6 was previously demonstrated to regulate the production of IL-18 and is important for protecting mice against chemically-induced intestinal injury and colitis-associated colon cancer. However, the cellular mechanisms by which NLRP6 reduces susceptibility to colonic inflammation remain unclear. Here, we determined that NLRP6 expression is specifically upregulated in Ly6Chi inflammatory monocytes that infiltrate into the colon during dextran sulfate sodium (DSS)-induced inflammation. Adoptive transfer of WT Ly6Chi inflammatory monocytes into Nlrp6-/- mice was sufficient to protect them from mortality, significantly reducing intestinal permeability and damage. NLRP6-deficient inflammatory monocytes were specifically defective in TNFα production, which was important for reducing DSS-induced mortality and dependent on autocrine IL-18 signaling by inflammatory monocytes. Our data reveal a previously unappreciated role for NLRP6 in inflammatory monocytes, which are recruited during intestinal injury to promote barrier function and limit bacteria-driven inflammation. This study also highlights the importance of early cytokine responses, particularly NLRP6-dependent and IL-18-dependent TNFα production in preventing chronic dysregulated inflammation.

2016-03-27 | GSE79631 | GEO

Estrogen Receptor β Activation Inhibits Colitis by Promoting the NLRP6-Mediated Autophagy

Project description:Estrogen receptor β (ERβ) and NOD-, LRR- and pyrin domain-containing 6 (NLRP6) are highly expressed in intestinal tissues and reduce intestinal inflammation, but their underlying mechanisms are unclear. We found that ERβ and NLRP6 levels were reduced in patients with inflammatory bowel disease (IBD), and that deletion of ERβ or NLRP6 was exacerbated colitis in mouse models. We discovered that ERβ exerted its anti-inflammatory activity by inducing NLRP6-mediated autophagy. Specifically, ERβ directly regulated NLRP6 gene expression and NLRP6 inflammasome activation through genomic and non-genomic effects. NLRP6 directly interacted with multiple autophagy-related proteins (including ULK1, BECN1, ATG5-ATG12-ATG16L1 complex, p62, and PHB2). Autophagy stimulation suppresses the inflammatory response by eliminating excess ERβ, NLRP6, ASC, Casp-1, IL-1β, TNF-α and damaged mitochondria. These findings indicate that ERβ-NLRP6-autophagy forms a negative feedback loop to maintain intestinal epithelial cell homeostasis and facilitate tissue repair.

2023-06-05 | GSE151864 | GEO

WT and NLRP6 KO CD103+ and CD103- B cell expression

Project description:CD103+ and CD103- B cells from Wildtype Non-obese diabetic mice and NLRP6-deficient (ko) NOD mice were investigated for their gene expression All B cells were isolated from the spleen of female non-diabetic mice aged 12-16 weeks and gated on Live, single TCRbeta-CD11c-CD11b-CD19+

2023-02-08 | GSE224472 | GEO

NLRP6 controls PTEN stability by promoting autophagic degradation of p85α to drive tumorigenesis

Project description:To identify NLRP6-associated proteins in living cells, we applied an APEX2-based labelling method combined with mass spectrometry. In brief, APEX2 was genetically fused to NLRP6. In the presence of hydrogen peroxide, APEX2 catalysed biotin-phenol to become a biotin-phenol radical that covalently bound to NLRP6 neighbouring proteins (<20 nm). The biotinylated proteins were enriched and collected by streptavidin beads. One-dimensional SDS–PAGE followed by liquid chromatography-tandem mass spectrometry (GeLC–MS/MS) was performed to identify the proteins. To detect ubiquitinated p85α, a Flag-tagged p85α plasmid was transfected into cells. The cell lysates were immunoprecipitated with anti-Flag and separated on a 6% SDS–PAGE gel. After in-gel digestion, the resulting peptides were extracted for GeLC–MS/MS analysis.

2023-07-02 | PXD037436 | Pride

NLRP6 controls PTEN stability by promoting autophagic degradation of p85α to drive tumorigenesis

2023-07-02 | PXD037460 | Pride

Effect of deficiency of NLRP6 on hepatic lipids accumulation during non-alcoholic fatty liver disease in mice.

Project description:Nonalcoholic fatty liver disease (NAFLD) is one of the main causes of liver diseases in the world. At present, the pathogenesis of NAFLD is not completely clear, and the regulatory role of inflammatory corpuscles in NAFLD-related metabolic diseases is increasingly prominent. NLRP6 is a member of the NLRs family of pattern recognition receptors and is related to the occurrence and development of NAFLD, but the specific mechanism is still unclear. We report here that NLRP6 is an important regulator of liver lipid metabolism, and its absence will affect the formation and accumulation of lipid droplets in the liver. In the HFD-induced NAFLD model group, NLRP6 deletion increased the mouse lipid content and aggravated hepatocyte steatosis by up-regulating the expressions of ADRP and CIDEC and down-regulating the expression of ApoB100.On the contrary, overexpression of NLRP6 in hepatocytes can significantly reduce intracellular lipid content and lipid droplets, and reduce the expression of ADRP and CIDEC. Indicated that NLRP6 can inhibit the accumulation of lipid droplets in hepatocytes by regulating the expression of ADRP, CIDEC and ApoB100, and thus alleviating the symptoms of NAFLD.

2024-01-31 | GSE239747 | GEO

Next Generation Sequencing of Wild Type and Nlrp6-/- T cells

Project description:Next Generation Sequencing of Wild Type and Nlrp6-/- T cells

| PRJNA478531 | ENA

NLRP6 does not impact mouse microbiota

Project description:The NLR protein NLRP6 does not impact gut microbiota composition

| PRJEB22561 | ENA

Comparison of gene expression profile in RAG2+ B lineage cells from the small intestinal lamina propria and RAG2+ B lineage cells from the bone marrow

Project description:We used a RAG2-GFP reporter mouse to show that RAG+ B lineage cells can be found in the small intestinal lamina proria in normally-housed mice at weaning age. We used microarry expression analysis to compare the RAG2+ population in the gut to the RAG2+ B lineage population in the bone marrow. Microarray was used to compare RAG2+ lamina propria B cells to RAG2+ bone marrow B cells. For each experiment, RAG2-GFP+ cells from 8-12 post-natal day 17-25 RAG2-GFP reporter mice were sorted from small intestinal lamina propria lymphocyte preparations and bone marrow. RNA extracted from trizol was used for the analysis. 3 independent replicates were performed.

2013-07-12 | E-GEOD-48805 | biostudies-arrayexpress

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