Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1298311 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: Analyze genes involved in the negative selection of CD4CD8 double positive thymocytes from NOD-AI4 control mice, NOD-AI4-Nfkbid-/- (KO) and NOD-AI4-60A undergoing negative selection. Methods: RNA-Seq based gene expression analyses were used to identify differentially expressed genes in CD4CD8 double positive thymocytes from NOD-AI4 (control), NOD-AI4-Nfkbid-/- (KO) and NOD-AI4-60A undergoing negative selection.
2022-05-16 | GSE176566 | GEO
Project description:Gut microbiota contributes to the regulation of host immune response and homeostasis. Bile acid (BA) derivatives from gut microbiota can affect the differentiation and function of the immune cells. However, it is incompletely clear for the regulation of BA metabolites in the macrophages. We here find that BA metabolites can regulate sensitivity of macrophages to LPS and or Gram-negative bacteria. BA derivatives could induce lncRNA57RIK expression through sphingosine-1-phosphate receptor 2 (S1PR2) in the macrophages of mice and humans, which play a critical role in Gram-negative bacteria mediated IL-1β maturation and pyroptosis of macrophages. This lncRNA57RIK could bind intracellular proteases caspase-4/11 with guanylate-binding protein 1 (GBP1) in the human and mice together to cause LPS mediated activation of caspase-4/11. Murine or human lncRNA57RIK knockout (KO) macrophages did not produce response(s) to LPS or gram negative bacteria. LncRNA57RIK KO mice had also reduced inflammatory responses to LPS or Salmonella typhimurium (S.T) infection. Taken together, gut microbiota derived BA metabolites mediated lncRNA57RIK is necessary for LPS induced caspase-4/11 activation.
2024-09-21 | GSE277195 | GEO
Project description:This experiment was investigating how gut commensal bacteria and intestinal inflammation affect miRNA expression. We analyzed miRNA expression of spleen and intestine from specific pathogen free (SPF) B6 mice, germ-free (GF) B6 mice, and IL-10 knockout mice which have severe colitis by microarray. Thus we have total 6 samples: GF spleen; GF intestines; SPF spleen; SPF intestine; IL-10 KO spleen and IL-10 KO intestine. We directly isolated RNA from whole spleens or intestines without any treatments, and then did microarray analysis.
2011-11-23 | E-MEXP-3406 | biostudies-arrayexpress
Project description:In this study, we transferred gut microbiota of SS-like autoimmune dry eye disease model mice to conventional B6 mice (NOD-FMT). After the transfer, NOD-FMT mice experienced a dramatic change in the gut microbiomes and showed clinicopathological features of SS, including increased corneal fluorescein staining score, decreased tear production, elevated levels of IL-6 mRNA, decreased levels of MUC5AC mRNA encoding mucin. Additionally, we observed that NOD-FMT mice shared stereotypic B cell receptor (BCR) clonotypes with a much higher frequency compared to control group. B cell clones encoding these stereotypic BCR clonotypes developed and expanded locally in the lacrimal gland, and achieved systemic presence in certain clonotypes.
2024-06-26 | GSE263577 | GEO
Project description:Background/ Aim: Diabetes has substantive co-occurrence with disorders of gut-brain interactions (DGBIs). The pathophysiological and molecular mechanisms linking diabetes and DGBIs are unclear. miRNAs are key regulators of diabetes and gut dysmotility. We investigated whether impaired gut barrier function regulated by a key miRNA, miR-10b-5p, links diabetes and gut dysmotility. Methods: We created a new mouse line using the Mb3Cas12a/Mb3Cpf1 endonuclease to knock out mir-10b globally. Loss of function studies were conducted to characterize diabetes, gut dysmotility, and gut barrier dysfunction phenotypes in these mice. Gain of function studies were conducted by injecting these mice with a miR-10b-5p mimic. Further, we performed miRNA-sequencing analysis from colonic mucosa from mir-10b KO, WT, and miR-10b-5p mimic injected mice to confirm 1) deficiency of miR-10b-5p in KO mice, and 2) restoration of miR-10b-5p expression after the mimic injection. Results: Congenital loss of mir-10b in mice led to the development of hyperglycemia, gut dysmotility, and gut barrier dysfunction. We found increased gut permeability and reduced expression of the tight junction protein Zonula occludens-1 (ZO-1), in the colon of mir-10b KO mice. We further confirmed that patients with diabetes or IBS-C, a known DGBI that is linked to leaky gut, had significantly reduced miR-10b-5p expression. Injection of a miR-10b-5p mimic in mir-10b KO mice rescued these molecular alterations and phenotypes. Conclusion: Our study uncovered a potential pathophysiologic mechanism of gut barrier dysfunction that links both the diabetes and gut dysmotility phenotypes in mice lacking miR-10b-5p. Treatment with a miR-10b-5p mimic reversed the leaky gut, diabetic, and gut dysmotility phenotypes, highlighting the translational potential of miR-10b-5p mimic.
2023-07-13 | GSE236981 | GEO
Project description:Investigating type I interferon in prediabetic stage of DCs from NOD mice compared to C57BL/6.g7 and Rag KO mice.
2020-05-31 | GSE146452 | GEO