Similar Datasets
Project description:WT and Ccr2-/- small intestinal macrophages
| PRJNA979195 | ENA
Project description:RNA sequencing of small intestinal ILC2s sorted from Il7rCre/+ Tph1flox/flox or Il7rCre/+ control mice at steady state
2020-04-21 | GSE145288 | GEO
Project description:Total proteome from sorted primary intestinal epithelial cells isolated from the small intestines of 4 C57Bl/6J mice
2024-10-02 | PXD055546 | Pride
Project description:Aim: We aimed to determine differences in transcriptional profiles of GPR35-positive and negative macrophages in the steady state intestine. Method: Corresponding subpopulations were sorted by FACS from intestinal lamina propria cells of unmanipulated wild-type C56BL/6 mice. RNA from 4 replicates of each group were sequenced and analyzed. Result: GPR35 positive macrophages are transcriptionally distinct from GPR35 negative macrophages overall with 2798 downregulated and 2773 upregulated genes, and regarding cytokine expression profile with higher Il1b, Tnf and Il10 mRNA expressions. Conclusion: Our study reports the first analysis on transcriptional charasteristics of intestinal macrophages depending on their GPR35 expression providing insights into the function of GPR35 in these cells.
2020-06-25 | GSE131858 | GEO
Project description:In adult mice the majority of intestinal macrophages exhibit a mature phenotype and are derived from blood monocytes. In the steady state replenishment of these cells is reduced in the absence of the chemokine receptor Ccr2. Within the intestine of mice with colitis there is marked increase in the accumulation of immature macrophages that demonstrate an inflammatory phenotype. However, whether Ccr2 is necessary for the accumulation of these immature macrophages and further for the development of colitis in susceptible mouse models is incompletely defined. Here, we ask whether Ccr2 is necessary for the development of colitis in mice lacking the receptor for IL10. We compared the development of intestinal inflammation in mice lacking IL10RA or both IL10RA and Ccr2. The absence of Ccr2 interfered with the accumulation of immature macrophages in IL10R-deficien mice, including a novel population of rounded submucosal Iba1+ cells and reduced the severity of colitis in these mice. In contrast, the absence of Ccr2 did not reduce augmented inflammatory gene expression observed in mature intestinal macrophages isolated from mice lacking IL10RA. These data suggest that both newly recruited Ccr2-dependent immature macrophages and Ccr2-independent residual mature macrophages contribute to the development of intestinal inflammation observed in IL10R-deficient mice.
2022-01-19 | GSE183960 | GEO
Project description:BACKGROUND & AIMS: Intestinal mononuclear phagocytes (MNP) are phenotypically similar, but have different functions. Macrophages contribute to the pathogenesis of inflammatory bowel disease (IBD). To understand this contribution it is necessary to distinguish macrophages from other MNPs, and identify functionally-different macrophage populations. We aimed to accurately identify intestinal macrophage populations, and to ascertain their functions in patients with inflammatory bowel disease (IBD). METHODS: We developed 12-parameter flow cytometry protocols to identify and characterise human intestinal MNPs. We then used RNA sequencing, qPCR, and flow cytometry to analyse colonic biopsies from patients with CD, UC, or non-inflamed controls, in a cross-sectional study. RESULTS: We unambiguously differentiate macrophage populations (CD45+CD64+ HLA-DR+) from dendritic cells (CD45+CD64- HLA-DR+ CD11c;). We identify two distinct subsets within the macrophage population, differentiated by their expression of the mannose receptor, CD206. Further examination of these macrophage sub-populations showed that CD206+ macrophages expressed markers consistent with a mature macrophage phenotype: high levels of CD68 and CD163, higher transcription of IL-10 and lower expression of Trem1. On the contrary, CD64+ HLA-DR- CD206- cells appear to be semi-mature intermediaries in the development of mature intestinal macrophages from their monocyte precursors. CONCLUSIONS: We identified and purified MNP and macrophage populations from human intestinal lamina propria. Thorough characterisation reveals that human colonic macrophages appear to be derived from a monocytic precursor with high CCR2 and low CD206 expression. As these cells mature they lose their proliferative properties and acquire expression of IL-10, CD206, CD63, and CD168. Targeting the newly recruited monocyte-derived cells may represent a fruitful avenue to ameliorate chronic inflammation in IBD.
2018-12-26 | GSE124350 | GEO
Project description:Self-maintaining gMacs are present in the submucosal and myenteric plexus of the intestine where they maintain enteric neurons and submucosal vasculature YFP-positive and YFP-negative CD11b+, CD64+ macrophages were sorted from lamina propria and muscularis externa of Cx3cr1CreERT2.Rosa26-LSL-YFP animals, 35 weeks after tamoxifen administration. Four biological replicates each. YFP-positive and YFP-negative were compared within lamina propria and muscularis externa
2018-07-30 | E-MTAB-6977 | biostudies-arrayexpress
Project description:Cryptopatches (CP) and isolated lymphoid follicles (ILF) are evolutionary ancient lymphoid structures found in the intestines of all vertebrates. These structures are demarcated by a poorly characterised subset of mononuclear phagocytes (MPh), called CP/ILF-associated (CIA)-MPh. CIA-MPh expressed very high levels of lysozyme M (LysM), but they did not express Ly6G or CD64, normally associated with LysM-expressing neutrophils or macrophages, respectively. In order to understand the ontogeny and function of these newly identified MPh subset, we performed genome-wide transcriptional profiling of CIA-MPh and other cell types expressing LysM (i.e., neutrophils and macrophages) in the small intestine as well as of CD11b+ CD103- cDC2. Using Lyz2-GFP reporter mice, we developed a sorting strategy allowing us to highly purify neutrophils, macrophages, CD11b+ CD103- cDC2 and CIA-MPh. The RNA of each sample was extracted using the ImmGen protocol with phase lock tubes. The libraries were prepared using the SMARTer Ultra Low Input RNA kit (Clontech) according to the manufacturer’s instructions. The material was enriched for poly-A sequences and single-end Next Generation Sequencing was performed on a HiSeq 2500 machine (Illumina).
2020-11-24 | E-MTAB-9505 | biostudies-arrayexpress
Project description:Human noroviruses (HuNoVs) are a major cause of diarrheal disease, yet critical aspects of their biology, including cellular tropism, remain unclear. While research traditionally focused on the intestinal epithelium, the hypothesis that HuNoV infects macrophages has been recurrently discussed and is investigated here by a zebrafish larval model. Our study reveals that HuNoV capsid proteins and double-stranded RNA colocalize within intestinal macrophages of infected zebrafish larvae, while the negative-strand RNA intermediate was detected within FACS-sorted macrophages. Flow cytometry confirms viral replication within these macrophages, constituting ~9% of HuNoV?s host cells. Single-cell RNA-sequencing reaffirms their role in viral replication, as all three open reading frames were mapped to individual macrophages. Yet, macrophages were not required for productive infection given the limited changes in viral loads upon their absence. Identifying macrophages as host cells prompts a reevaluation of their role in HuNoV pathogenesis, offering new directions for understanding and controlling this infection.
2024-08-07 | GSE261163 | GEO
Project description:Communications between immune cells are essential to ensure appropriate coordination of their activities. Here, we observed the infiltration of activated macrophages into the joint-footpads of chikungunya virus (CHIKV)-infected animals. Large numbers of CD64+MHCII+ and CD64+MHCII- macrophages were present in the joint-footpad, preceded by the recruitment of their CD11b+Ly6C+ inflammatory monocyte precursors. Regulation of these myeloid subsets was highly dependent on IFNγ and GM-CSF secreted by CHIKV-specific CD4+ T cells. Transcriptomic and gene ontology analyses of CD64+MHCII+ and CD64+MHCII- macrophages revealed 89 differentially expressed genes, including genes involved in T cell proliferation and differentiation pathways. Depletion of CD64+MHCII+ macrophages from CHIKV-infected mice reduced disease pathology, demonstrating that these cells play a pro-inflammatory role in CHIKV infection. Together, these results highlight the synergistic dynamics of immune cell crosstalk in driving CHIKV immunopathogenesis. This study provides new insights in the disease mechanism and offers opportunities for development of novel anti-CHIKV therapeutics.
2024-01-12 | GSE208540 | GEO