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John G. Brain - One of the best experts on this subject based on the ideXlab platform.
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a tlr2 s100a9 cxcl 2 signaling network is necessary for Neutrophil recruitment in acute and chronic liver injury in the mouse
Journal of Hepatology, 2014Co-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. BrainAbstract: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.
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A TLR2/S100A9/CXCL-2 signaling network is necessary for Neutrophil recruitment in acute and chronic liver injury in the mouse
Journal of Hepatology, 2013Co-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. BrainAbstract: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.
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a tlr2 s100a9 cxcl 2 signaling network is necessary for Neutrophil recruitment in acute and chronic liver injury in the mouse
Journal of Hepatology, 2014Co-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. BrainAbstract: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.
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A TLR2/S100A9/CXCL-2 signaling network is necessary for Neutrophil recruitment in acute and chronic liver injury in the mouse
Journal of Hepatology, 2013Co-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. BrainAbstract: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.
Jayashree Bagchi Chakraborty - One of the best experts on this subject based on the ideXlab platform.
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a tlr2 s100a9 cxcl 2 signaling network is necessary for Neutrophil recruitment in acute and chronic liver injury in the mouse
Journal of Hepatology, 2014Co-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. BrainAbstract: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.
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A TLR2/S100A9/CXCL-2 signaling network is necessary for Neutrophil recruitment in acute and chronic liver injury in the mouse
Journal of Hepatology, 2013Co-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. BrainAbstract: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.
Chris Fox - One of the best experts on this subject based on the ideXlab platform.
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a tlr2 s100a9 cxcl 2 signaling network is necessary for Neutrophil recruitment in acute and chronic liver injury in the mouse
Journal of Hepatology, 2014Co-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. BrainAbstract: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.
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A TLR2/S100A9/CXCL-2 signaling network is necessary for Neutrophil recruitment in acute and chronic liver injury in the mouse
Journal of Hepatology, 2013Co-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. BrainAbstract: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.
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a tlr2 s100a9 cxcl 2 signaling network is necessary for Neutrophil recruitment in acute and chronic liver injury in the mouse
Journal of Hepatology, 2014Co-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. BrainAbstract: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.
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A TLR2/S100A9/CXCL-2 signaling network is necessary for Neutrophil recruitment in acute and chronic liver injury in the mouse
Journal of Hepatology, 2013Co-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. BrainAbstract: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.
