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Genome-wide transcriptional profiles of Kupffer cells and alveolar macrophages from naïve and LPS-injected mice

ABSTRACT: To reveal early responses to one of septic agents, lipopolysaccharide (LPS), in tissue resident macrophages, we isolated Kupffer cells as well as alveolar macrophages from bolus LPS-injected mice at 1 and 4 hours (hr) of early time points and performed quantitative RNA sequencing

ORGANISM(S): Mus musculus

PROVIDER: GSE108553 | GEO | 2018/12/27

REPOSITORIES: GEO

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Genome-wide transcriptional profiles of Kupffer cells and alveolar macrophages from naïve and LPS-injected mice

Project description:Genome-wide transcriptional profiles of Kupffer cells and alveolar macrophages from naïve and LPS-injected mice

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The cellular and proteomic response of primary and immortalized murine Kupffer cells following immune stimulation diverges from that of monocyte-derived macrophages

Project description:Kupffer cells are the first line of defense in the liver against pathogens, yet several microbes successfully target the liver, bypass immune surveillance, and effectively develop in this tissue. Our current, albeit poor, understanding of Kupffer cell-pathogen interactions has been largely achieved through the study of primary cells, requiring isolation from a large numbers of animals. To facilitate the study of Kupffer cell biology, an immortalized rat Kupffer cell line, RKC1, was developed. We performed a comparative global proteomic analysis of RKC1 and primary rat Kupffer cells (PRKC) to characterize their respective responses to lipopolysaccharide (LPS)-mediated immune stimulation. We identified patent differences in the proteomic response profile of RKC1 and PRKC to LPS. We observed that PRKC upregulated more immune function pathways and exhibited marked changes in cellular morphology following stimulation. We consequently analyzed the cytoskeletal signaling pathways of these cells in light of the fact that macrophages are known to induce cytoskeletal changes in response to pathogens. Our findings suggest that Kupffer cells respond differently to inflammatory stimulus than do monocyte-derived macrophages, and such data may provide insight into how pathogens, such as the malaria parasite, may have evolved mechanisms of liver entry through Kupffer cells without detection.

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A human iPSC-derived multilineage liver organoid model containing Kupffer cells to study human sepsis-associated liver dysfunction [KuLOs]

Project description:To recapitulate the pathology of human septic liver, we established hiPSC-derived liver organoids containing Kupffer cells (KuLOs). We performed gene expression profiling analysis using data obtained from RNA-seq of KuLOs with/without LPS/IFNr stimulation and the KuLOs during recovery after endotoxin elimination.

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The cellular and proteomic response of primary and immortalized murine Kupffer cells following immune stimulation diverges from that of monocyte-derived macrophages

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Macrophages Solvent, AA, LPS, AA+LPS

Project description:Macrophages Solvent, AA, LPS, AA+LPS

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COMPARATIVE ANALYSIS OF THE PROTEOME OF KUPFFER CELLS AND MONOCYTES

Project description:Macrophage population in most mammalian organs consists of cells of different origin, with the exception of the central nervous system and the liver, where macrophages of monocytic origin are almost completely absent. The reasons for such distribution and the phenomenon of coexistence of the two separate macrophage lineages with different origin in mammals remain poorly understood. In present study we compared Kupffer cells and monocytes by the immunophenotype, gene expression profile, proteome and pool of mircoRNA. Observed differences do not allow to consider the resident liver macrophages as purely M2 macrophages or monocytes have purely M1 features. Two populations of macrophages of monocytic origin and resident macrophages have fundamentally different roles in maintaining homeostasis. Monocytic macrophages are involved in the regulation of inflammation, and resident macrophages are involved in the regulation of specific organ functions (nitrogen metabolism, complement system protein synthesis). However, if other indicators would be considered as markers of macrophage activity, it is worth noting that Kupffer cells possess some features of M2 macrophages. This is indicated by their expression profile of let-7b/c/d/e miRNAs, a high content of proteins associated with oxidative phosphorylation, as well as an increased level of synthesis of Arg1, IL10.

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Bone marrow-derived monocytes give rise to self-renewing and fully differentiated Kupffer cells

Project description:Self-renewing tissue-resident macrophages are thought to be exclusively derived from embryonic progenitors. However, whether circulating monocytes can also give rise to such macrophages has not been formally investigated. Here we use a new model of diphtheria toxin-mediated depletion of liver-resident Kupffer cells to generate niche availability and show that circulating monocytes engrafted in the liver, gradually adopt the transcriptional profile of their depleted counterparts and become long-lived self-renewing cells. Underlining the physiological relevance of our findings, circulating monocytes also contribute to the expanding pool of macrophages in the liver shortly after birth, when macrophage niches become available during normal organ growth. Thus, like embryonic precursors, monocytes can and do give rise to self-renewing tissue-resident macrophages if the niche is available to them. Clec4F+ Kupffer cells were isolated and sorted from livers from adult WT mice or KC-DTR or KC-DTR littermate control mice +/- 50ng DT at indicated timepoints. 19 samples (arrays) in total. RNA was isolated, amplified with Nugene pico kit, converted to cDNA and then hybridised on Affymetrix GeneChip Mouse Gene 1.0 ST Arrays.

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Project description:The innate immune system functions as the first line of defense against cancer cells, particularly the detection and clearance of cancer cells by phagocytosis. The liver resident macrophages, known as Kupffer cells, have the largest population of body’s tissue resident macrophages and constitute the first line of defense against cancer cells invading the liver. However, the molecule mechanisms underlying the detection and phagocytosis of cancer cells by Kupffer cells are still unclear. Here, using in vivo genome-wide CRISPR-Cas9 knockout screening, we found that Ermap expressed on cancer cells delivered the pro-phagocytosis ‘eat me’ signal to promote Kupffer cells phagocytosis and control over liver metastasis of various cancer cells. Ermap ligated Galectin-9 expressed on Kupffer cells surface in a glycosylation dependent manner. Galectin-9 further formed a bridging complex with Ermap and transmembrane receptor Dectin-2 expressed on Kupffer cells to promote the detection and phagocytosis of cancer cells by Kupffer cells. Patients with tumors expressing low ERMAP had more liver metastases. Thus, our study identifies the Ermap–Galectin-9–Dectin-2 axis as an ‘eat me’ signal for Kupffer cells to engulf cancer cells and control liver metastasis.

2023-08-03 | GSE232126 | GEO

CircRNA, lncRNA and mRNA expression profiles in normal and LPS-induced septic cardiomyopathy mice

Project description:To further explore the expression of circRNA, lncRNA and mRNA in mice with septic cardiomyopathy, we have employed microarray analysis as a discovery platform to identify circRNAs and lncRNAs with the potential to play role in the pathophysiology process of LPS-induced septic cardiomyopathy in mice. Six hours after intraperitoneal injection of LPS(10mg/kg) or saline solution, eight mice (LPS group, n=4; Cont group, n=4) were anesthetized and the heart were collected. And then total RNA was extracted and used for microarray detection.

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Liver-derived signals sequentially reprogram myeloid enhancers to initiate and maintain Kupffer cell identity (ATAC-Seq)

Project description:Tissue environment plays a powerful role in establishing and maintaining the distinct phenotypes of resident macrophages, but the underlying molecular mechanisms remain poorly understood. Here, we characterized transcriptomic and epigenetic changes in repopulating liver macrophages following acute Kupffer cell depletion as a means to infer signaling pathways and transcription factors that promote Kupffer cell differentiation. We obtain evidence that combinatorial interactions of the Notch ligand DLL4 and transforming growth factor-b (TGF-β) family ligands produced by sinusoidal endothelial cells and endogenous LXR ligands were required for the induction and maintenance of Kupffer cell identity. DLL4 regulation of the Notch transcriptional effector RBPJ activated poised enhancers to rapidly induce LXRα and other Kupffer cell lineage-determining factors. These factors in turn reprogrammed the repopulating liver macrophage enhancer landscape to converge on that of the original resident Kupffer cells. Collectively, these findings provide a framework for understanding how macrophage progenitor cells acquire tissue-specific phenotypes.

2019-10-08 | GSE128659 | GEO

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