We are analyzing https://link.springer.com/article/10.1186/1755-1536-5-s1-s27.

Title:
Functional role of intrahepatic monocyte subsets for the progression of liver inflammation and liver fibrosis in vivo | Fibrogenesis & Tissue Repair
Description:
Sustained inflammation upon chronic liver injury induces the development of liver fibrosis in mice and men. Experimental models of liver fibrosis highlight the importance of hepatic macrophages, so-called Kupffer cells, for perpetuating inflammation by releasing proinflammatory cytokines and chemokines as well as activating hepatic stellate cells (HSC). Recent studies in mice demonstrate that these actions are only partially conducted by liver-resident macrophages, classically termed Kupffer cells, but largely depend on recruitment of monocytes into the liver. Monocytes are circulating precursors of tissue macrophages and dendritic cells (DC), which comprise two major subsets in blood, characterized by the differential expression of chemokine receptors, adhesion molecules and distinct markers, such as Ly6C/Gr1 in mice or CD14 and CD16 in humans. Upon organ injury, chemokine receptor CCR2 and its ligand MCP-1 (CCL2) as well as CCR8 and CCL1 promote monocyte subset accumulation in the liver, namely of the inflammatory Ly6C+ (Gr1+) monocyte subset as precursors of tissue macrophages. The infiltration of proinflammatory monocytes into injured murine liver can be specifically blocked by novel anti-MCP-1 directed agents. In contrast, chemokine receptor CX3CR1 and its ligand fractalkine (CX3CL1) are important negative regulators of monocyte infiltration in hepatic inflammation by controlling their survival and differentiation into functionally diverse macrophage subsets. In patients with liver cirrhosis,
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Keywords {🔍}

liver, monocytes, pubmed, fibrosis, article, google, scholar, cas, hepatic, ccr, monocyte, cells, macrophages, cxcr, mice, central, subsets, chemokine, human, inflammation, blood, receptor, tacke, chronic, murine, differentiation, cdcd, cell, lychi, injury, inflammatory, ccl, macrophage, progression, expression, bone, marrow, lyclo, infiltration, functional, experimental, fractalkine, tissue, role, proinflammatory, stellate, hsc, intrahepatic, injured, infiltrating,

Topics {✒️}

article download pdf article number s27 increased hla-dr expression hepatic monocyte-derived macrophages cd14+cd16+ monocytes showed monocyte-related chemokine pathways classical' cd14+cd16+ subset classical' cd14+cd16+ monocytes 'classical' cd14++cd16- monocytes cx3cr1-deficient hepatic macrophages human cd14++cd16- monocytes cd14+cd16+ human monocytes reduced intrahepatic monocytes/macrophages anti-mcp-1 directed agents promote monocyte/macrophage migration exert anti-inflammatory actions chronic carbon tetrachloride repetitive carbon tetrachloride hepatic stellate cells end-stage liver cirrhosis cell-based therapeutic approaches ccr2/ccr6-deficient mice monocyte-derived cells experimental hepatological research monocyte-derived macrophages german research foundation chemokine receptor ccr8 karlmark kr ccr2-/-ccr6-/- mice resulted chemokine receptor c privacy choices/manage cookies active hepatic fibrogenesis cd14+cd16- monocytes cd14+cd16+ monocytes hepatic cell types bone marrow derived inos-producing macrophages chemokine receptor ccr2 advanced liver fibrosis swirski fk kupffer cell proliferation tumor necrosis factor murine hepatic fibrosis intrahepatic bile ducts called kupffer cells /supplements/5/s1 ziegler-heitbrock hw intrahepatic monocyte subsets chemokine receptor cx3cr1 hepatic macrophage migration

Questions {❓}

Tacke F, Kurts C: Infiltrating monocytes versus resident Kupffer cells - do alternatively activated macrophages need to be targeted alternatively?
Tacke F, Kurts C: Infiltrating monocytes versus resident Kupffer cells: do alternatively activated macrophages need to be targeted alternatively?

Schema {🗺️}

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         headline:Functional role of intrahepatic monocyte subsets for the progression of liver inflammation and liver fibrosis in vivo
         description:Sustained inflammation upon chronic liver injury induces the development of liver fibrosis in mice and men. Experimental models of liver fibrosis highlight the importance of hepatic macrophages, so-called Kupffer cells, for perpetuating inflammation by releasing proinflammatory cytokines and chemokines as well as activating hepatic stellate cells (HSC). Recent studies in mice demonstrate that these actions are only partially conducted by liver-resident macrophages, classically termed Kupffer cells, but largely depend on recruitment of monocytes into the liver. Monocytes are circulating precursors of tissue macrophages and dendritic cells (DC), which comprise two major subsets in blood, characterized by the differential expression of chemokine receptors, adhesion molecules and distinct markers, such as Ly6C/Gr1 in mice or CD14 and CD16 in humans. Upon organ injury, chemokine receptor CCR2 and its ligand MCP-1 (CCL2) as well as CCR8 and CCL1 promote monocyte subset accumulation in the liver, namely of the inflammatory Ly6C+ (Gr1+) monocyte subset as precursors of tissue macrophages. The infiltration of proinflammatory monocytes into injured murine liver can be specifically blocked by novel anti-MCP-1 directed agents. In contrast, chemokine receptor CX3CR1 and its ligand fractalkine (CX3CL1) are important negative regulators of monocyte infiltration in hepatic inflammation by controlling their survival and differentiation into functionally diverse macrophage subsets. In patients with liver cirrhosis, 'non-classical' CD14+CD16+ monocytes are found activated in blood as well as liver and promote pro-inflammatory along with pro-fibrogenic actions by the release of distinct cytokines and direct interactions with HSC, indicating that the findings from murine models can be translated into pathogenesis of human liver fibrosis. Moreover, experimental animal models indicate that monocytes/macrophages and DCs are not only critical for fibrosis progression, but also for fibrosis regression, because macrophages can also degrade extracellular matrix proteins and exert anti-inflammatory actions. The recently identified cellular and molecular pathways for monocyte subset recruitment, macrophage differentiation and interactions with other hepatic cell types in injured liver may therefore represent interesting novel targets for future therapeutic approaches in liver fibrosis.
         datePublished:2012-06-06T00:00:00Z
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            Liver Fibrosis
            Hepatic Fibrosis
            Hepatic Stellate Cell
            Chemokine Receptor CCR2
            Fibrosis Progression
            Internal Medicine
            Cell Biology
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      headline:Functional role of intrahepatic monocyte subsets for the progression of liver inflammation and liver fibrosis in vivo
      description:Sustained inflammation upon chronic liver injury induces the development of liver fibrosis in mice and men. Experimental models of liver fibrosis highlight the importance of hepatic macrophages, so-called Kupffer cells, for perpetuating inflammation by releasing proinflammatory cytokines and chemokines as well as activating hepatic stellate cells (HSC). Recent studies in mice demonstrate that these actions are only partially conducted by liver-resident macrophages, classically termed Kupffer cells, but largely depend on recruitment of monocytes into the liver. Monocytes are circulating precursors of tissue macrophages and dendritic cells (DC), which comprise two major subsets in blood, characterized by the differential expression of chemokine receptors, adhesion molecules and distinct markers, such as Ly6C/Gr1 in mice or CD14 and CD16 in humans. Upon organ injury, chemokine receptor CCR2 and its ligand MCP-1 (CCL2) as well as CCR8 and CCL1 promote monocyte subset accumulation in the liver, namely of the inflammatory Ly6C+ (Gr1+) monocyte subset as precursors of tissue macrophages. The infiltration of proinflammatory monocytes into injured murine liver can be specifically blocked by novel anti-MCP-1 directed agents. In contrast, chemokine receptor CX3CR1 and its ligand fractalkine (CX3CL1) are important negative regulators of monocyte infiltration in hepatic inflammation by controlling their survival and differentiation into functionally diverse macrophage subsets. In patients with liver cirrhosis, 'non-classical' CD14+CD16+ monocytes are found activated in blood as well as liver and promote pro-inflammatory along with pro-fibrogenic actions by the release of distinct cytokines and direct interactions with HSC, indicating that the findings from murine models can be translated into pathogenesis of human liver fibrosis. Moreover, experimental animal models indicate that monocytes/macrophages and DCs are not only critical for fibrosis progression, but also for fibrosis regression, because macrophages can also degrade extracellular matrix proteins and exert anti-inflammatory actions. The recently identified cellular and molecular pathways for monocyte subset recruitment, macrophage differentiation and interactions with other hepatic cell types in injured liver may therefore represent interesting novel targets for future therapeutic approaches in liver fibrosis.
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         Liver Fibrosis
         Hepatic Fibrosis
         Hepatic Stellate Cell
         Chemokine Receptor CCR2
         Fibrosis Progression
         Internal Medicine
         Cell Biology
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         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1755-1536-5-S1-S27/MediaObjects/13069_2012_Article_99_Fig1_HTML.jpg
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