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

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

PROVIDER: PRJNA931300 | ENA |

REPOSITORIES: ENA

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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

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

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

Project description: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

2019-05-08 | GSE116454 | GEO

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mRNAseq and proteomic data set of one week old WT (Chop wt/wt CkmmCre wt/wt Dars2 fl/fl), Chop KO (Chop ko/ko CkmmCre wt/wt Dars2 fl/fl), Dars2 KO (Chop wt/wt CkmmCre tg/wt Dars2 fl/fl) and DKO (Chop ko/ko CkmmCre tg/wt Dars2 fl/fl) mice

Project description:mRNAseq and proteomic data set of one week old WT (Chop wt/wt CkmmCre wt/wt Dars2 fl/fl), Chop KO (Chop ko/ko CkmmCre wt/wt Dars2 fl/fl), Dars2 KO (Chop wt/wt CkmmCre tg/wt Dars2 fl/fl) and DKO (Chop ko/ko CkmmCre tg/wt Dars2 fl/fl) mice

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wt&Rnase4 KO bacteria

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Differential gene expression among HEK293T WT, LRPPRC-KO, LRPPRC-KO + WT, and LRPPRC-KO + Leigh Syndrome French Canadian type LRPPRC

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