Neutrophils

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John G. Brain - One of the best experts on this subject based on the ideXlab platform.

  • a tlr2 s100a9 cxcl 2 signaling network is necessary for neutrophil recruitment in acute and chronic liver injury in the mouse
    Journal of Hepatology, 2014
    Co-Authors: Anna Moles, Lindsay B. Murphy, Caroline L. Wilson, Jayashree Bagchi Chakraborty, Chris Fox, Eek Joong Park, Jelena Mann, Fiona Oakley, Rachel Howarth, John G. Brain
    Abstract:

    Background & Aims Neutrophils are important immune effectors required for sterile and non-sterile inflammatory responses. However, Neutrophils are associated with pathology in drug-induced liver injury, acute alcoholic liver disease, and ischemia-reperfusion injury. An understanding of the complex mechanisms that control neutrophil recruitment to the injured liver is desirable for developing strategies aimed at limiting neutrophil-mediated cellular damage. Methods Wt, tlr2 −/− , tlr4 −/− , and s100a9 −/− mice were administered CCl 4 either acutely (8, 24, 48, or 72h) or chronically (8weeks) and livers investigated by histological (IHC for Neutrophils, fibrogenesis, proliferation, and chemotactic proteins) or molecular approaches (qRT-PCR for neutrophil chemoattractant chemokines and cytokines as well as pro-fibrogenic genes). Results Mice lacking TLR2 or S100A9 failed to recruit Neutrophils to the injured liver and had a defective hepatic induction of the neutrophil chemokine CXCL-2. Hierarchy between TLR2 and S100A9 proved to be complex. While induction of S100A9 was dependent on TLR2 in isolated Neutrophils, there was a more complicated two-way signalling cross-talk between TLR2 and S100A9 in whole liver. However, wound-healing and regenerative responses of the liver were unaffected in these genetic backgrounds as well as in wild type mice, in which Neutrophils were depleted by infusion of Ly-6G antibody. Conclusions We have identified TLR2 and S100A8/S100A9 as key regulators of hepatic CXCL-2 expression and neutrophil recruitment. This novel TLR2-S100A9-CXCL-2 pathway may be of use in development of new strategies for selectively manipulating Neutrophils in liver disease without impairing normal wound healing and regenerative responses.

  • A TLR2/S100A9/CXCL-2 signaling network is necessary for neutrophil recruitment in acute and chronic liver injury in the mouse
    Journal of Hepatology, 2013
    Co-Authors: Anna Moles, Lindsay B. Murphy, Caroline L. Wilson, Jayashree Bagchi Chakraborty, Chris Fox, Eek Joong Park, Jelena Mann, Fiona Oakley, Rachel Howarth, John G. Brain
    Abstract:

    Background & Aims Neutrophils are important immune effectors required for sterile and non-sterile inflammatory responses. However, Neutrophils are associated with pathology in drug-induced liver injury, acute alcoholic liver disease, and ischemia-reperfusion injury. An understanding of the complex mechanisms that control neutrophil recruitment to the injured liver is desirable for developing strategies aimed at limiting neutrophil-mediated cellular damage. Methods Wt, tlr2 −/− , tlr4 −/− , and s100a9 −/− mice were administered CCl 4 either acutely (8, 24, 48, or 72h) or chronically (8weeks) and livers investigated by histological (IHC for Neutrophils, fibrogenesis, proliferation, and chemotactic proteins) or molecular approaches (qRT-PCR for neutrophil chemoattractant chemokines and cytokines as well as pro-fibrogenic genes). Results Mice lacking TLR2 or S100A9 failed to recruit Neutrophils to the injured liver and had a defective hepatic induction of the neutrophil chemokine CXCL-2. Hierarchy between TLR2 and S100A9 proved to be complex. While induction of S100A9 was dependent on TLR2 in isolated Neutrophils, there was a more complicated two-way signalling cross-talk between TLR2 and S100A9 in whole liver. However, wound-healing and regenerative responses of the liver were unaffected in these genetic backgrounds as well as in wild type mice, in which Neutrophils were depleted by infusion of Ly-6G antibody. Conclusions We have identified TLR2 and S100A8/S100A9 as key regulators of hepatic CXCL-2 expression and neutrophil recruitment. This novel TLR2-S100A9-CXCL-2 pathway may be of use in development of new strategies for selectively manipulating Neutrophils in liver disease without impairing normal wound healing and regenerative responses.

Anna Moles - One of the best experts on this subject based on the ideXlab platform.

  • a tlr2 s100a9 cxcl 2 signaling network is necessary for neutrophil recruitment in acute and chronic liver injury in the mouse
    Journal of Hepatology, 2014
    Co-Authors: Anna Moles, Lindsay B. Murphy, Caroline L. Wilson, Jayashree Bagchi Chakraborty, Chris Fox, Eek Joong Park, Jelena Mann, Fiona Oakley, Rachel Howarth, John G. Brain
    Abstract:

    Background & Aims Neutrophils are important immune effectors required for sterile and non-sterile inflammatory responses. However, Neutrophils are associated with pathology in drug-induced liver injury, acute alcoholic liver disease, and ischemia-reperfusion injury. An understanding of the complex mechanisms that control neutrophil recruitment to the injured liver is desirable for developing strategies aimed at limiting neutrophil-mediated cellular damage. Methods Wt, tlr2 −/− , tlr4 −/− , and s100a9 −/− mice were administered CCl 4 either acutely (8, 24, 48, or 72h) or chronically (8weeks) and livers investigated by histological (IHC for Neutrophils, fibrogenesis, proliferation, and chemotactic proteins) or molecular approaches (qRT-PCR for neutrophil chemoattractant chemokines and cytokines as well as pro-fibrogenic genes). Results Mice lacking TLR2 or S100A9 failed to recruit Neutrophils to the injured liver and had a defective hepatic induction of the neutrophil chemokine CXCL-2. Hierarchy between TLR2 and S100A9 proved to be complex. While induction of S100A9 was dependent on TLR2 in isolated Neutrophils, there was a more complicated two-way signalling cross-talk between TLR2 and S100A9 in whole liver. However, wound-healing and regenerative responses of the liver were unaffected in these genetic backgrounds as well as in wild type mice, in which Neutrophils were depleted by infusion of Ly-6G antibody. Conclusions We have identified TLR2 and S100A8/S100A9 as key regulators of hepatic CXCL-2 expression and neutrophil recruitment. This novel TLR2-S100A9-CXCL-2 pathway may be of use in development of new strategies for selectively manipulating Neutrophils in liver disease without impairing normal wound healing and regenerative responses.

  • A TLR2/S100A9/CXCL-2 signaling network is necessary for neutrophil recruitment in acute and chronic liver injury in the mouse
    Journal of Hepatology, 2013
    Co-Authors: Anna Moles, Lindsay B. Murphy, Caroline L. Wilson, Jayashree Bagchi Chakraborty, Chris Fox, Eek Joong Park, Jelena Mann, Fiona Oakley, Rachel Howarth, John G. Brain
    Abstract:

    Background & Aims Neutrophils are important immune effectors required for sterile and non-sterile inflammatory responses. However, Neutrophils are associated with pathology in drug-induced liver injury, acute alcoholic liver disease, and ischemia-reperfusion injury. An understanding of the complex mechanisms that control neutrophil recruitment to the injured liver is desirable for developing strategies aimed at limiting neutrophil-mediated cellular damage. Methods Wt, tlr2 −/− , tlr4 −/− , and s100a9 −/− mice were administered CCl 4 either acutely (8, 24, 48, or 72h) or chronically (8weeks) and livers investigated by histological (IHC for Neutrophils, fibrogenesis, proliferation, and chemotactic proteins) or molecular approaches (qRT-PCR for neutrophil chemoattractant chemokines and cytokines as well as pro-fibrogenic genes). Results Mice lacking TLR2 or S100A9 failed to recruit Neutrophils to the injured liver and had a defective hepatic induction of the neutrophil chemokine CXCL-2. Hierarchy between TLR2 and S100A9 proved to be complex. While induction of S100A9 was dependent on TLR2 in isolated Neutrophils, there was a more complicated two-way signalling cross-talk between TLR2 and S100A9 in whole liver. However, wound-healing and regenerative responses of the liver were unaffected in these genetic backgrounds as well as in wild type mice, in which Neutrophils were depleted by infusion of Ly-6G antibody. Conclusions We have identified TLR2 and S100A8/S100A9 as key regulators of hepatic CXCL-2 expression and neutrophil recruitment. This novel TLR2-S100A9-CXCL-2 pathway may be of use in development of new strategies for selectively manipulating Neutrophils in liver disease without impairing normal wound healing and regenerative responses.

Britta Engelhardt - One of the best experts on this subject based on the ideXlab platform.

  • β2 integrin mediated crawling on endothelial icam 1 and icam 2 is a prerequisite for transcellular neutrophil diapedesis across the inflamed blood brain barrier
    Journal of Immunology, 2014
    Co-Authors: Roser Gorina, Ruth Lyck, Dietmar Vestweber, Britta Engelhardt
    Abstract:

    In acute neuroinflammatory states such as meningitis, Neutrophils cross the blood–brain barrier (BBB) and contribute to pathological alterations of cerebral function. The mechanisms that govern neutrophil migration across the BBB are ill defined. Using live-cell imaging, we show that LPS-stimulated BBB endothelium supports neutrophil arrest, crawling, and diapedesis under physiological flow in vitro. Investigating the interactions of Neutrophils from wild-type, CD11a−/−, CD11b−/−, and CD18null mice with wild-type, junctional adhesion molecule-A−/−, ICAM-1null, ICAM-2−/− , or ICAM-1null/ICAM-2−/− primary mouse brain microvascular endothelial cells, we demonstrate that neutrophil arrest, polarization, and crawling required G-protein–coupled receptor–dependent activation of β2 integrins and binding to endothelial ICAM-1. LFA-1 was the prevailing ligand for endothelial ICAM-1 in mediating neutrophil shear resistant arrest, whereas Mac-1 was dominant over LFA-1 in mediating neutrophil polarization on the BBB in vitro. Neutrophil crawling was mediated by endothelial ICAM-1 and ICAM-2 and neutrophil LFA-1 and Mac-1. In the absence of crawling, few Neutrophils maintained adhesive interactions with the BBB endothelium by remaining either stationary on endothelial junctions or displaying transient adhesive interactions characterized by a fast displacement on the endothelium along the direction of flow. Diapedesis of stationary Neutrophils was unchanged by the lack of endothelial ICAM-1 and ICAM-2 and occurred exclusively via the paracellular pathway. Crawling Neutrophils, although preferentially crossing the BBB through the endothelial junctions, could additionally breach the BBB via the transcellular route. Thus, β2 integrin–mediated neutrophil crawling on endothelial ICAM-1 and ICAM-2 is a prerequisite for transcellular neutrophil diapedesis across the inflamed BBB.

  • β2 Integrin–Mediated Crawling on Endothelial ICAM-1 and ICAM-2 Is a Prerequisite for Transcellular Neutrophil Diapedesis across the Inflamed Blood–Brain Barrier
    Journal of Immunology, 2013
    Co-Authors: Roser Gorina, Ruth Lyck, Dietmar Vestweber, Britta Engelhardt
    Abstract:

    In acute neuroinflammatory states such as meningitis, Neutrophils cross the blood–brain barrier (BBB) and contribute to pathological alterations of cerebral function. The mechanisms that govern neutrophil migration across the BBB are ill defined. Using live-cell imaging, we show that LPS-stimulated BBB endothelium supports neutrophil arrest, crawling, and diapedesis under physiological flow in vitro. Investigating the interactions of Neutrophils from wild-type, CD11a−/−, CD11b−/−, and CD18null mice with wild-type, junctional adhesion molecule-A−/−, ICAM-1null, ICAM-2−/− , or ICAM-1null/ICAM-2−/− primary mouse brain microvascular endothelial cells, we demonstrate that neutrophil arrest, polarization, and crawling required G-protein–coupled receptor–dependent activation of β2 integrins and binding to endothelial ICAM-1. LFA-1 was the prevailing ligand for endothelial ICAM-1 in mediating neutrophil shear resistant arrest, whereas Mac-1 was dominant over LFA-1 in mediating neutrophil polarization on the BBB in vitro. Neutrophil crawling was mediated by endothelial ICAM-1 and ICAM-2 and neutrophil LFA-1 and Mac-1. In the absence of crawling, few Neutrophils maintained adhesive interactions with the BBB endothelium by remaining either stationary on endothelial junctions or displaying transient adhesive interactions characterized by a fast displacement on the endothelium along the direction of flow. Diapedesis of stationary Neutrophils was unchanged by the lack of endothelial ICAM-1 and ICAM-2 and occurred exclusively via the paracellular pathway. Crawling Neutrophils, although preferentially crossing the BBB through the endothelial junctions, could additionally breach the BBB via the transcellular route. Thus, β2 integrin–mediated neutrophil crawling on endothelial ICAM-1 and ICAM-2 is a prerequisite for transcellular neutrophil diapedesis across the inflamed BBB.

Caroline L. Wilson - One of the best experts on this subject based on the ideXlab platform.

  • a tlr2 s100a9 cxcl 2 signaling network is necessary for neutrophil recruitment in acute and chronic liver injury in the mouse
    Journal of Hepatology, 2014
    Co-Authors: Anna Moles, Lindsay B. Murphy, Caroline L. Wilson, Jayashree Bagchi Chakraborty, Chris Fox, Eek Joong Park, Jelena Mann, Fiona Oakley, Rachel Howarth, John G. Brain
    Abstract:

    Background & Aims Neutrophils are important immune effectors required for sterile and non-sterile inflammatory responses. However, Neutrophils are associated with pathology in drug-induced liver injury, acute alcoholic liver disease, and ischemia-reperfusion injury. An understanding of the complex mechanisms that control neutrophil recruitment to the injured liver is desirable for developing strategies aimed at limiting neutrophil-mediated cellular damage. Methods Wt, tlr2 −/− , tlr4 −/− , and s100a9 −/− mice were administered CCl 4 either acutely (8, 24, 48, or 72h) or chronically (8weeks) and livers investigated by histological (IHC for Neutrophils, fibrogenesis, proliferation, and chemotactic proteins) or molecular approaches (qRT-PCR for neutrophil chemoattractant chemokines and cytokines as well as pro-fibrogenic genes). Results Mice lacking TLR2 or S100A9 failed to recruit Neutrophils to the injured liver and had a defective hepatic induction of the neutrophil chemokine CXCL-2. Hierarchy between TLR2 and S100A9 proved to be complex. While induction of S100A9 was dependent on TLR2 in isolated Neutrophils, there was a more complicated two-way signalling cross-talk between TLR2 and S100A9 in whole liver. However, wound-healing and regenerative responses of the liver were unaffected in these genetic backgrounds as well as in wild type mice, in which Neutrophils were depleted by infusion of Ly-6G antibody. Conclusions We have identified TLR2 and S100A8/S100A9 as key regulators of hepatic CXCL-2 expression and neutrophil recruitment. This novel TLR2-S100A9-CXCL-2 pathway may be of use in development of new strategies for selectively manipulating Neutrophils in liver disease without impairing normal wound healing and regenerative responses.

  • A TLR2/S100A9/CXCL-2 signaling network is necessary for neutrophil recruitment in acute and chronic liver injury in the mouse
    Journal of Hepatology, 2013
    Co-Authors: Anna Moles, Lindsay B. Murphy, Caroline L. Wilson, Jayashree Bagchi Chakraborty, Chris Fox, Eek Joong Park, Jelena Mann, Fiona Oakley, Rachel Howarth, John G. Brain
    Abstract:

    Background & Aims Neutrophils are important immune effectors required for sterile and non-sterile inflammatory responses. However, Neutrophils are associated with pathology in drug-induced liver injury, acute alcoholic liver disease, and ischemia-reperfusion injury. An understanding of the complex mechanisms that control neutrophil recruitment to the injured liver is desirable for developing strategies aimed at limiting neutrophil-mediated cellular damage. Methods Wt, tlr2 −/− , tlr4 −/− , and s100a9 −/− mice were administered CCl 4 either acutely (8, 24, 48, or 72h) or chronically (8weeks) and livers investigated by histological (IHC for Neutrophils, fibrogenesis, proliferation, and chemotactic proteins) or molecular approaches (qRT-PCR for neutrophil chemoattractant chemokines and cytokines as well as pro-fibrogenic genes). Results Mice lacking TLR2 or S100A9 failed to recruit Neutrophils to the injured liver and had a defective hepatic induction of the neutrophil chemokine CXCL-2. Hierarchy between TLR2 and S100A9 proved to be complex. While induction of S100A9 was dependent on TLR2 in isolated Neutrophils, there was a more complicated two-way signalling cross-talk between TLR2 and S100A9 in whole liver. However, wound-healing and regenerative responses of the liver were unaffected in these genetic backgrounds as well as in wild type mice, in which Neutrophils were depleted by infusion of Ly-6G antibody. Conclusions We have identified TLR2 and S100A8/S100A9 as key regulators of hepatic CXCL-2 expression and neutrophil recruitment. This novel TLR2-S100A9-CXCL-2 pathway may be of use in development of new strategies for selectively manipulating Neutrophils in liver disease without impairing normal wound healing and regenerative responses.

Rachel Howarth - One of the best experts on this subject based on the ideXlab platform.

  • a tlr2 s100a9 cxcl 2 signaling network is necessary for neutrophil recruitment in acute and chronic liver injury in the mouse
    Journal of Hepatology, 2014
    Co-Authors: Anna Moles, Lindsay B. Murphy, Caroline L. Wilson, Jayashree Bagchi Chakraborty, Chris Fox, Eek Joong Park, Jelena Mann, Fiona Oakley, Rachel Howarth, John G. Brain
    Abstract:

    Background & Aims Neutrophils are important immune effectors required for sterile and non-sterile inflammatory responses. However, Neutrophils are associated with pathology in drug-induced liver injury, acute alcoholic liver disease, and ischemia-reperfusion injury. An understanding of the complex mechanisms that control neutrophil recruitment to the injured liver is desirable for developing strategies aimed at limiting neutrophil-mediated cellular damage. Methods Wt, tlr2 −/− , tlr4 −/− , and s100a9 −/− mice were administered CCl 4 either acutely (8, 24, 48, or 72h) or chronically (8weeks) and livers investigated by histological (IHC for Neutrophils, fibrogenesis, proliferation, and chemotactic proteins) or molecular approaches (qRT-PCR for neutrophil chemoattractant chemokines and cytokines as well as pro-fibrogenic genes). Results Mice lacking TLR2 or S100A9 failed to recruit Neutrophils to the injured liver and had a defective hepatic induction of the neutrophil chemokine CXCL-2. Hierarchy between TLR2 and S100A9 proved to be complex. While induction of S100A9 was dependent on TLR2 in isolated Neutrophils, there was a more complicated two-way signalling cross-talk between TLR2 and S100A9 in whole liver. However, wound-healing and regenerative responses of the liver were unaffected in these genetic backgrounds as well as in wild type mice, in which Neutrophils were depleted by infusion of Ly-6G antibody. Conclusions We have identified TLR2 and S100A8/S100A9 as key regulators of hepatic CXCL-2 expression and neutrophil recruitment. This novel TLR2-S100A9-CXCL-2 pathway may be of use in development of new strategies for selectively manipulating Neutrophils in liver disease without impairing normal wound healing and regenerative responses.

  • A TLR2/S100A9/CXCL-2 signaling network is necessary for neutrophil recruitment in acute and chronic liver injury in the mouse
    Journal of Hepatology, 2013
    Co-Authors: Anna Moles, Lindsay B. Murphy, Caroline L. Wilson, Jayashree Bagchi Chakraborty, Chris Fox, Eek Joong Park, Jelena Mann, Fiona Oakley, Rachel Howarth, John G. Brain
    Abstract:

    Background & Aims Neutrophils are important immune effectors required for sterile and non-sterile inflammatory responses. However, Neutrophils are associated with pathology in drug-induced liver injury, acute alcoholic liver disease, and ischemia-reperfusion injury. An understanding of the complex mechanisms that control neutrophil recruitment to the injured liver is desirable for developing strategies aimed at limiting neutrophil-mediated cellular damage. Methods Wt, tlr2 −/− , tlr4 −/− , and s100a9 −/− mice were administered CCl 4 either acutely (8, 24, 48, or 72h) or chronically (8weeks) and livers investigated by histological (IHC for Neutrophils, fibrogenesis, proliferation, and chemotactic proteins) or molecular approaches (qRT-PCR for neutrophil chemoattractant chemokines and cytokines as well as pro-fibrogenic genes). Results Mice lacking TLR2 or S100A9 failed to recruit Neutrophils to the injured liver and had a defective hepatic induction of the neutrophil chemokine CXCL-2. Hierarchy between TLR2 and S100A9 proved to be complex. While induction of S100A9 was dependent on TLR2 in isolated Neutrophils, there was a more complicated two-way signalling cross-talk between TLR2 and S100A9 in whole liver. However, wound-healing and regenerative responses of the liver were unaffected in these genetic backgrounds as well as in wild type mice, in which Neutrophils were depleted by infusion of Ly-6G antibody. Conclusions We have identified TLR2 and S100A8/S100A9 as key regulators of hepatic CXCL-2 expression and neutrophil recruitment. This novel TLR2-S100A9-CXCL-2 pathway may be of use in development of new strategies for selectively manipulating Neutrophils in liver disease without impairing normal wound healing and regenerative responses.