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Butyrate-induced LncRNA lncly6c promotes Ly6Chigh to Ly6Clow/neg macrophages through lncly6c /C/EBP/Nr4A-1 axis

ABSTRACT: Gut macrophages play a critical role in maintaining the homeostasis of gut immunes. The inflammatory macrophages generally are differentiated into resident macrophages to realize their function in gut tissues. But it is unclear how these inflammatory macrophages to differentiate resident macrophages. We here found that lycLy6c, a novel ultraconserved lncRNA, may promote the differentiation of gut inflammatory macrophage into gut resident macrophages. We demonstrate gut microbiota metabolites butyrate may upregulate the expression of lncly6c. Lncly6c not only binds with transcription factor C/EBPβ but also binds with multiple components of enzyme complexes, which promote the accumulation of H3K4me3 markers on the promoter region of NrA4-1. As a result, lncly6c causes the upregulation of Nr4A-1 to promote inflammatory macrophage to differentiate the resident macrophages. These results not only offer an evidence for gut microbiota to maintaining the gut homeostasis but also suggest a potential target for the therapy for colitis-associated diseases.

ORGANISM(S): Mus musculus

PROVIDER: GSE140151 | GEO | 2019/11/09

REPOSITORIES: GEO

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Single-cell RNA seq reveals the transcriptional landscape and heterogeneity of macrophages in murine gut tissues

Project description:CD11b+ cell populations, especially macrophages are highly heterogeneous tissue resident immune cells in both mice and human. Exact subsets and their phenotype remain unknown. We here analyzed gut CD11b+ cell populations using scRNA-seq in normal, inflamed and Nlrc4 deficient mice. There existed twelve CD11b+ cell populations and subsets in SPF mice. These CD11b+ subsets were changeable dependent on inflammation and gut environment. We found consistent high expression of Ly6C, Cd62L, previously undescribed Trem1 and Ccr7 in Ly6Chigh macrophages and Cd206 and Cx3cr1 in Ly6Clow/neg cell population in different mice. However, signature genes showed that resident macrophages but not inflammatory macrophages were highly conserved in normal and inflamed mice. Gut microbiota play a role in accumulation and differentiation of gut macrophages. Both Ly6Chigh and Ly6Clow macrophages in intestine and colon tissues are similar. These uncover the transcriptional landscape and phenotypic heterogeneity of CD11b+ cells, especially macrophages in gut tissues.

2019-10-16 | GSE138902 | GEO

Macrophage-restricted Interleukin-10 receptor-, but not IL-10 deficiency causes severe spontaneous colitis

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Triggering of NOD2 receptor converts inflammatory Ly6Chigh into Ly6Clow monocytes with patrolling properties.

Project description:In the present study, we demonstrate that NOD2 receptor triggering by muramyl dipeptide converts blood inflammatory Ly6Chigh monocytes into patrolling Ly6Clow monocytes. Muramyl dipeptide administration to Nr4a1-/- mice, which lack Ly6Clow monocytes, and to Ly6Clow-depleted mice leads to the emergence of blood patrolling monocytes expressing phenotypic profile of typical Ly6Clow monocytes, including high expression of CX3CR1 and LFA1. Furthermore using intravital microscopy in live animal models of inflammatory diseases, we observed that converted Ly6Chigh monocytes are capable of patrolling the endothelium of blood vessels and their presence contributes to reduce the inflammatory response following muramyl dipeptide injection.

2019-01-14 | GSE101496 | GEO

The commensal bacterium Lactiplantibacillus plantarum imprints innate memory-like responses in mononuclear phagocytes

Project description:Gut microbiota is a constant source of antigens and stimuli to which the resident immune system has developed tolerance. However, the mechanisms by which mononuclear phagocytes, specifically monocytes/macrophages, cope with these usually pro-inflammatory signals is poorly understood. Here, we show that innate immune memory promotes anti-inflammatory homeostasis using as a model strains of the commensal bacterium, Lactiplantibacillus plantarum. Priming of monocytes/macrophages with bacteria, especially in its live form, enhances bacterial intracellular survival and decreases the release of pro-inflammatory signals to the environment, with lower production of TNF and higher levels of IL-10. Analysis of the transcriptomic landscape of these cells shows downregulation of pathways associated with the production of reactive oxygen species (ROS) and the release of cytokines, chemokines and antimicrobial peptides. Indeed, the induction of ROS prevents memory-induced bacterial survival. In addition, there is a dysregulation in gene expression of several metabolic pathways leading to decreased glycolytic and respiratory rates in memory cells. These data support commensal microbe-specific metabolic changes in innate immune memory cells that might contribute to homeostasis in the gut.

2021-07-06 | GSE159496 | GEO

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Project description:Advanced age is associated with chronic low-grade inflammation, which is usually referred to as inflammaging. Elderly are also known to have an altered gut microbiota composition. However, whether inflammaging is a cause or consequence of an altered gut microbiota composition is not clear. In this study gut microbiota from young or old conventional mice was transferred to young germ-free mice. Four weeks after gut microbiota transfer immune cell populations in spleen, Peyer’s patches, and mesenteric lymph nodes from conventionalized germ-free mice were analyzed by flow cytometry. In addition, whole-genome gene expression in the ileum was analyzed by microarray. Gut microbiota composition of donor and recipient mice was analyzed with 16S rDNA sequencing. Here we show by transferring aged microbiota to young germ-free mice that certain bacterial species within the aged microbiota promote inflammaging. This effect was associated with lower levels of Akkermansia and higher levels of TM7 bacteria and Proteobacteria in the aged microbiota after transfer. The aged microbiota promoted inflammation in the small intestine in the germ-free mice and enhanced leakage of inflammatory bacterial components into the circulation was observed. Moreover, the aged microbiota promoted increased T cell activation in the systemic compartment. In conclusion, these data indicate that the gut microbiota from old mice contributes to inflammaging after transfer to young germ-free mice.

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2019-05-29 | E-MTAB-6518 | biostudies-arrayexpress

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2020-02-27 | E-MTAB-8798 | biostudies-arrayexpress

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2018-05-15 | GSE114434 | GEO

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