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Fernando Q. Cunha - One of the best experts on this subject based on the ideXlab platform.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory pro- tein-1 (MIP-1)(CC chemokine ligand 3 (CCL3)), MIP-1(CCL4), regulated on activation, normal T expressed and secreted (RANTES)(CCL5), and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor (TNF-) and leukotriene B 4 (LTB 4 ). Herein, we show increased mRNA expression for MIP- 1(CCL3), MIP-1(CCL4), RANTES(CCL5), and CCR1 in peritoneal cells harvested from OVA-chal- lenged, immunized mice, as well as MIP-1(CCL3) and RANTES(CCL5) but not MIP-1(CCL4) proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP- 1(CCL3) / mice, but it was not inhibited by treat- ment with antibodies against RANTES(CCL5) or MIP-1(CCL4). MIP-1(CCL3) mediated neutro- phil migration in immunized mice through induc- tion of TNF- and LTB4 synthesis, as these medi- ators were detected in the exudates harvested from OVA-challenged, immunized wild-type but not MIP-1(CCL3) / mice; administration of MIP- 1(CCL3) induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF- antibody in TNF receptor 1 (p55 / )- deficient mice or by MK 886 (a 5-lipoxygenase in- hibitor); and MIP-1(CCL3) failed to induce LTB 4 production in p55 / mice. MIP-1(CCL3) used CCR1 to promote neutrophil recruitment, as OVA or MIP-1(CCL3) failed to induce neutrophil migration in CCR1 / mice, in contrast to CCR5 / mice. In summary, we have demonstrated that neutrophil mi- gration observed in this model of immune inflamma- tion is mediated by MIP-1(CCL3), which via CCR1, induces the sequential release of TNF- and LTB4. Therefore, whether a similar pathway mediates neu- trophil migration in human immune-inflammatory diseases, the development of specific CCR1 antago- nists might have a therapeutic potential. J. Leukoc. Biol. 78: 000-000; 2005.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory pro- tein-1 (MIP-1)(CC chemokine ligand 3 (CCL3)), MIP-1(CCL4), regulated on activation, normal T expressed and secreted (RANTES)(CCL5), and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor (TNF-) and leukotriene B 4 (LTB 4 ). Herein, we show increased mRNA expression for MIP- 1(CCL3), MIP-1(CCL4), RANTES(CCL5), and CCR1 in peritoneal cells harvested from OVA-chal- lenged, immunized mice, as well as MIP-1(CCL3) and RANTES(CCL5) but not MIP-1(CCL4) proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP- 1(CCL3) / mice, but it was not inhibited by treat- ment with antibodies against RANTES(CCL5) or MIP-1(CCL4). MIP-1(CCL3) mediated neutro- phil migration in immunized mice through induc- tion of TNF- and LTB4 synthesis, as these medi- ators were detected in the exudates harvested from OVA-challenged, immunized wild-type but not MIP-1(CCL3) / mice; administration of MIP- 1(CCL3) induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF- antibody in TNF receptor 1 (p55 / )- deficient mice or by MK 886 (a 5-lipoxygenase in- hibitor); and MIP-1(CCL3) failed to induce LTB 4 production in p55 / mice. MIP-1(CCL3) used CCR1 to promote neutrophil recruitment, as OVA or MIP-1(CCL3) failed to induce neutrophil migration in CCR1 / mice, in contrast to CCR5 / mice. In summary, we have demonstrated that neutrophil mi- gration observed in this model of immune inflamma- tion is mediated by MIP-1(CCL3), which via CCR1, induces the sequential release of TNF- and LTB4. Therefore, whether a similar pathway mediates neu- trophil migration in human immune-inflammatory diseases, the development of specific CCR1 antago- nists might have a therapeutic potential. J. Leukoc. Biol. 78: 000-000; 2005.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory protein-1alpha (MIP-1alpha)[CC chemokine ligand 3 (CCL3)], MIP-1beta[CCL4], regulated on activation, normal T expressed and secreted (RANTES)[CCL5], and CC chemokine receptors (CCRs) on neutrophil migration in murine immune inflammation. Previously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor alpha (TNF-alpha) and leukotriene B(4)(LTB(4)). Herein, we show increased mRNA expression for MIP-1alpha[CCL3], MIP-1beta[CCL4], RANTES[CCL5], and CCR1 in peritoneal cells harvested from OVA-challenged, immunized mice, as well as MIP-1alpha[CCL3] and RANTES[CCL5] but not MIP-1beta[CCL4] proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP-1alpha[CCL3](-/-) mice, but it was not inhibited by treatment with antibodies against RANTES[CCL5] or MIP-1beta[CCL4]. MIP-1alpha[CCL3] mediated neutrophil migration in immunized mice through induction of TNF-alpha and LTB(4) synthesis, as these mediators were detected in the exudates harvested from OVA-challenged immunized wild-type but not MIP-1alpha[CCL3](-/-) mice; administration of MIP-1alpha[CCL3] induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF-alpha antibody in TNF receptor 1 (p55(-/-))-deficient mice or by MK 886 (a 5-lipoxygenase inhibitor); and MIP-1alpha[CCL3] failed to induce LTB(4) production in p55(-/-) mice. MIP-1alpha[CCL3] used CCR1 to promote neutrophil recruitment, as OVA or MIP-1alpha[CCL3] failed to induce neutrophil migration in CCR1(-/-) mice, in contrast to CCR5(-/-) mice. In summary, we have demonstrated that neutrophil migration observed in this model of immune inflammation is mediated by MIP-1alpha[CCL3], which via CCR1, induces the sequential release of TNF-alpha and LTB(4). Therefore, whether a similar pathway mediates neutrophil migration in human immune-inflammatory diseases, the development of specific CCR1 antagonists might have a therapeutic potential.

Janeusa T Souto - One of the best experts on this subject based on the ideXlab platform.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory pro- tein-1 (MIP-1)(CC chemokine ligand 3 (CCL3)), MIP-1(CCL4), regulated on activation, normal T expressed and secreted (RANTES)(CCL5), and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor (TNF-) and leukotriene B 4 (LTB 4 ). Herein, we show increased mRNA expression for MIP- 1(CCL3), MIP-1(CCL4), RANTES(CCL5), and CCR1 in peritoneal cells harvested from OVA-chal- lenged, immunized mice, as well as MIP-1(CCL3) and RANTES(CCL5) but not MIP-1(CCL4) proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP- 1(CCL3) / mice, but it was not inhibited by treat- ment with antibodies against RANTES(CCL5) or MIP-1(CCL4). MIP-1(CCL3) mediated neutro- phil migration in immunized mice through induc- tion of TNF- and LTB4 synthesis, as these medi- ators were detected in the exudates harvested from OVA-challenged, immunized wild-type but not MIP-1(CCL3) / mice; administration of MIP- 1(CCL3) induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF- antibody in TNF receptor 1 (p55 / )- deficient mice or by MK 886 (a 5-lipoxygenase in- hibitor); and MIP-1(CCL3) failed to induce LTB 4 production in p55 / mice. MIP-1(CCL3) used CCR1 to promote neutrophil recruitment, as OVA or MIP-1(CCL3) failed to induce neutrophil migration in CCR1 / mice, in contrast to CCR5 / mice. In summary, we have demonstrated that neutrophil mi- gration observed in this model of immune inflamma- tion is mediated by MIP-1(CCL3), which via CCR1, induces the sequential release of TNF- and LTB4. Therefore, whether a similar pathway mediates neu- trophil migration in human immune-inflammatory diseases, the development of specific CCR1 antago- nists might have a therapeutic potential. J. Leukoc. Biol. 78: 000-000; 2005.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory pro- tein-1 (MIP-1)(CC chemokine ligand 3 (CCL3)), MIP-1(CCL4), regulated on activation, normal T expressed and secreted (RANTES)(CCL5), and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor (TNF-) and leukotriene B 4 (LTB 4 ). Herein, we show increased mRNA expression for MIP- 1(CCL3), MIP-1(CCL4), RANTES(CCL5), and CCR1 in peritoneal cells harvested from OVA-chal- lenged, immunized mice, as well as MIP-1(CCL3) and RANTES(CCL5) but not MIP-1(CCL4) proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP- 1(CCL3) / mice, but it was not inhibited by treat- ment with antibodies against RANTES(CCL5) or MIP-1(CCL4). MIP-1(CCL3) mediated neutro- phil migration in immunized mice through induc- tion of TNF- and LTB4 synthesis, as these medi- ators were detected in the exudates harvested from OVA-challenged, immunized wild-type but not MIP-1(CCL3) / mice; administration of MIP- 1(CCL3) induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF- antibody in TNF receptor 1 (p55 / )- deficient mice or by MK 886 (a 5-lipoxygenase in- hibitor); and MIP-1(CCL3) failed to induce LTB 4 production in p55 / mice. MIP-1(CCL3) used CCR1 to promote neutrophil recruitment, as OVA or MIP-1(CCL3) failed to induce neutrophil migration in CCR1 / mice, in contrast to CCR5 / mice. In summary, we have demonstrated that neutrophil mi- gration observed in this model of immune inflamma- tion is mediated by MIP-1(CCL3), which via CCR1, induces the sequential release of TNF- and LTB4. Therefore, whether a similar pathway mediates neu- trophil migration in human immune-inflammatory diseases, the development of specific CCR1 antago- nists might have a therapeutic potential. J. Leukoc. Biol. 78: 000-000; 2005.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory protein-1alpha (MIP-1alpha)[CC chemokine ligand 3 (CCL3)], MIP-1beta[CCL4], regulated on activation, normal T expressed and secreted (RANTES)[CCL5], and CC chemokine receptors (CCRs) on neutrophil migration in murine immune inflammation. Previously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor alpha (TNF-alpha) and leukotriene B(4)(LTB(4)). Herein, we show increased mRNA expression for MIP-1alpha[CCL3], MIP-1beta[CCL4], RANTES[CCL5], and CCR1 in peritoneal cells harvested from OVA-challenged, immunized mice, as well as MIP-1alpha[CCL3] and RANTES[CCL5] but not MIP-1beta[CCL4] proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP-1alpha[CCL3](-/-) mice, but it was not inhibited by treatment with antibodies against RANTES[CCL5] or MIP-1beta[CCL4]. MIP-1alpha[CCL3] mediated neutrophil migration in immunized mice through induction of TNF-alpha and LTB(4) synthesis, as these mediators were detected in the exudates harvested from OVA-challenged immunized wild-type but not MIP-1alpha[CCL3](-/-) mice; administration of MIP-1alpha[CCL3] induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF-alpha antibody in TNF receptor 1 (p55(-/-))-deficient mice or by MK 886 (a 5-lipoxygenase inhibitor); and MIP-1alpha[CCL3] failed to induce LTB(4) production in p55(-/-) mice. MIP-1alpha[CCL3] used CCR1 to promote neutrophil recruitment, as OVA or MIP-1alpha[CCL3] failed to induce neutrophil migration in CCR1(-/-) mice, in contrast to CCR5(-/-) mice. In summary, we have demonstrated that neutrophil migration observed in this model of immune inflammation is mediated by MIP-1alpha[CCL3], which via CCR1, induces the sequential release of TNF-alpha and LTB(4). Therefore, whether a similar pathway mediates neutrophil migration in human immune-inflammatory diseases, the development of specific CCR1 antagonists might have a therapeutic potential.

Claudio Canetti - One of the best experts on this subject based on the ideXlab platform.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory pro- tein-1 (MIP-1)(CC chemokine ligand 3 (CCL3)), MIP-1(CCL4), regulated on activation, normal T expressed and secreted (RANTES)(CCL5), and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor (TNF-) and leukotriene B 4 (LTB 4 ). Herein, we show increased mRNA expression for MIP- 1(CCL3), MIP-1(CCL4), RANTES(CCL5), and CCR1 in peritoneal cells harvested from OVA-chal- lenged, immunized mice, as well as MIP-1(CCL3) and RANTES(CCL5) but not MIP-1(CCL4) proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP- 1(CCL3) / mice, but it was not inhibited by treat- ment with antibodies against RANTES(CCL5) or MIP-1(CCL4). MIP-1(CCL3) mediated neutro- phil migration in immunized mice through induc- tion of TNF- and LTB4 synthesis, as these medi- ators were detected in the exudates harvested from OVA-challenged, immunized wild-type but not MIP-1(CCL3) / mice; administration of MIP- 1(CCL3) induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF- antibody in TNF receptor 1 (p55 / )- deficient mice or by MK 886 (a 5-lipoxygenase in- hibitor); and MIP-1(CCL3) failed to induce LTB 4 production in p55 / mice. MIP-1(CCL3) used CCR1 to promote neutrophil recruitment, as OVA or MIP-1(CCL3) failed to induce neutrophil migration in CCR1 / mice, in contrast to CCR5 / mice. In summary, we have demonstrated that neutrophil mi- gration observed in this model of immune inflamma- tion is mediated by MIP-1(CCL3), which via CCR1, induces the sequential release of TNF- and LTB4. Therefore, whether a similar pathway mediates neu- trophil migration in human immune-inflammatory diseases, the development of specific CCR1 antago- nists might have a therapeutic potential. J. Leukoc. Biol. 78: 000-000; 2005.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory pro- tein-1 (MIP-1)(CC chemokine ligand 3 (CCL3)), MIP-1(CCL4), regulated on activation, normal T expressed and secreted (RANTES)(CCL5), and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor (TNF-) and leukotriene B 4 (LTB 4 ). Herein, we show increased mRNA expression for MIP- 1(CCL3), MIP-1(CCL4), RANTES(CCL5), and CCR1 in peritoneal cells harvested from OVA-chal- lenged, immunized mice, as well as MIP-1(CCL3) and RANTES(CCL5) but not MIP-1(CCL4) proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP- 1(CCL3) / mice, but it was not inhibited by treat- ment with antibodies against RANTES(CCL5) or MIP-1(CCL4). MIP-1(CCL3) mediated neutro- phil migration in immunized mice through induc- tion of TNF- and LTB4 synthesis, as these medi- ators were detected in the exudates harvested from OVA-challenged, immunized wild-type but not MIP-1(CCL3) / mice; administration of MIP- 1(CCL3) induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF- antibody in TNF receptor 1 (p55 / )- deficient mice or by MK 886 (a 5-lipoxygenase in- hibitor); and MIP-1(CCL3) failed to induce LTB 4 production in p55 / mice. MIP-1(CCL3) used CCR1 to promote neutrophil recruitment, as OVA or MIP-1(CCL3) failed to induce neutrophil migration in CCR1 / mice, in contrast to CCR5 / mice. In summary, we have demonstrated that neutrophil mi- gration observed in this model of immune inflamma- tion is mediated by MIP-1(CCL3), which via CCR1, induces the sequential release of TNF- and LTB4. Therefore, whether a similar pathway mediates neu- trophil migration in human immune-inflammatory diseases, the development of specific CCR1 antago- nists might have a therapeutic potential. J. Leukoc. Biol. 78: 000-000; 2005.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory protein-1alpha (MIP-1alpha)[CC chemokine ligand 3 (CCL3)], MIP-1beta[CCL4], regulated on activation, normal T expressed and secreted (RANTES)[CCL5], and CC chemokine receptors (CCRs) on neutrophil migration in murine immune inflammation. Previously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor alpha (TNF-alpha) and leukotriene B(4)(LTB(4)). Herein, we show increased mRNA expression for MIP-1alpha[CCL3], MIP-1beta[CCL4], RANTES[CCL5], and CCR1 in peritoneal cells harvested from OVA-challenged, immunized mice, as well as MIP-1alpha[CCL3] and RANTES[CCL5] but not MIP-1beta[CCL4] proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP-1alpha[CCL3](-/-) mice, but it was not inhibited by treatment with antibodies against RANTES[CCL5] or MIP-1beta[CCL4]. MIP-1alpha[CCL3] mediated neutrophil migration in immunized mice through induction of TNF-alpha and LTB(4) synthesis, as these mediators were detected in the exudates harvested from OVA-challenged immunized wild-type but not MIP-1alpha[CCL3](-/-) mice; administration of MIP-1alpha[CCL3] induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF-alpha antibody in TNF receptor 1 (p55(-/-))-deficient mice or by MK 886 (a 5-lipoxygenase inhibitor); and MIP-1alpha[CCL3] failed to induce LTB(4) production in p55(-/-) mice. MIP-1alpha[CCL3] used CCR1 to promote neutrophil recruitment, as OVA or MIP-1alpha[CCL3] failed to induce neutrophil migration in CCR1(-/-) mice, in contrast to CCR5(-/-) mice. In summary, we have demonstrated that neutrophil migration observed in this model of immune inflammation is mediated by MIP-1alpha[CCL3], which via CCR1, induces the sequential release of TNF-alpha and LTB(4). Therefore, whether a similar pathway mediates neutrophil migration in human immune-inflammatory diseases, the development of specific CCR1 antagonists might have a therapeutic potential.

Cleber D L Ramos - One of the best experts on this subject based on the ideXlab platform.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory pro- tein-1 (MIP-1)(CC chemokine ligand 3 (CCL3)), MIP-1(CCL4), regulated on activation, normal T expressed and secreted (RANTES)(CCL5), and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor (TNF-) and leukotriene B 4 (LTB 4 ). Herein, we show increased mRNA expression for MIP- 1(CCL3), MIP-1(CCL4), RANTES(CCL5), and CCR1 in peritoneal cells harvested from OVA-chal- lenged, immunized mice, as well as MIP-1(CCL3) and RANTES(CCL5) but not MIP-1(CCL4) proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP- 1(CCL3) / mice, but it was not inhibited by treat- ment with antibodies against RANTES(CCL5) or MIP-1(CCL4). MIP-1(CCL3) mediated neutro- phil migration in immunized mice through induc- tion of TNF- and LTB4 synthesis, as these medi- ators were detected in the exudates harvested from OVA-challenged, immunized wild-type but not MIP-1(CCL3) / mice; administration of MIP- 1(CCL3) induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF- antibody in TNF receptor 1 (p55 / )- deficient mice or by MK 886 (a 5-lipoxygenase in- hibitor); and MIP-1(CCL3) failed to induce LTB 4 production in p55 / mice. MIP-1(CCL3) used CCR1 to promote neutrophil recruitment, as OVA or MIP-1(CCL3) failed to induce neutrophil migration in CCR1 / mice, in contrast to CCR5 / mice. In summary, we have demonstrated that neutrophil mi- gration observed in this model of immune inflamma- tion is mediated by MIP-1(CCL3), which via CCR1, induces the sequential release of TNF- and LTB4. Therefore, whether a similar pathway mediates neu- trophil migration in human immune-inflammatory diseases, the development of specific CCR1 antago- nists might have a therapeutic potential. J. Leukoc. Biol. 78: 000-000; 2005.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory pro- tein-1 (MIP-1)(CC chemokine ligand 3 (CCL3)), MIP-1(CCL4), regulated on activation, normal T expressed and secreted (RANTES)(CCL5), and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor (TNF-) and leukotriene B 4 (LTB 4 ). Herein, we show increased mRNA expression for MIP- 1(CCL3), MIP-1(CCL4), RANTES(CCL5), and CCR1 in peritoneal cells harvested from OVA-chal- lenged, immunized mice, as well as MIP-1(CCL3) and RANTES(CCL5) but not MIP-1(CCL4) proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP- 1(CCL3) / mice, but it was not inhibited by treat- ment with antibodies against RANTES(CCL5) or MIP-1(CCL4). MIP-1(CCL3) mediated neutro- phil migration in immunized mice through induc- tion of TNF- and LTB4 synthesis, as these medi- ators were detected in the exudates harvested from OVA-challenged, immunized wild-type but not MIP-1(CCL3) / mice; administration of MIP- 1(CCL3) induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF- antibody in TNF receptor 1 (p55 / )- deficient mice or by MK 886 (a 5-lipoxygenase in- hibitor); and MIP-1(CCL3) failed to induce LTB 4 production in p55 / mice. MIP-1(CCL3) used CCR1 to promote neutrophil recruitment, as OVA or MIP-1(CCL3) failed to induce neutrophil migration in CCR1 / mice, in contrast to CCR5 / mice. In summary, we have demonstrated that neutrophil mi- gration observed in this model of immune inflamma- tion is mediated by MIP-1(CCL3), which via CCR1, induces the sequential release of TNF- and LTB4. Therefore, whether a similar pathway mediates neu- trophil migration in human immune-inflammatory diseases, the development of specific CCR1 antago- nists might have a therapeutic potential. J. Leukoc. Biol. 78: 000-000; 2005.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory protein-1alpha (MIP-1alpha)[CC chemokine ligand 3 (CCL3)], MIP-1beta[CCL4], regulated on activation, normal T expressed and secreted (RANTES)[CCL5], and CC chemokine receptors (CCRs) on neutrophil migration in murine immune inflammation. Previously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor alpha (TNF-alpha) and leukotriene B(4)(LTB(4)). Herein, we show increased mRNA expression for MIP-1alpha[CCL3], MIP-1beta[CCL4], RANTES[CCL5], and CCR1 in peritoneal cells harvested from OVA-challenged, immunized mice, as well as MIP-1alpha[CCL3] and RANTES[CCL5] but not MIP-1beta[CCL4] proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP-1alpha[CCL3](-/-) mice, but it was not inhibited by treatment with antibodies against RANTES[CCL5] or MIP-1beta[CCL4]. MIP-1alpha[CCL3] mediated neutrophil migration in immunized mice through induction of TNF-alpha and LTB(4) synthesis, as these mediators were detected in the exudates harvested from OVA-challenged immunized wild-type but not MIP-1alpha[CCL3](-/-) mice; administration of MIP-1alpha[CCL3] induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF-alpha antibody in TNF receptor 1 (p55(-/-))-deficient mice or by MK 886 (a 5-lipoxygenase inhibitor); and MIP-1alpha[CCL3] failed to induce LTB(4) production in p55(-/-) mice. MIP-1alpha[CCL3] used CCR1 to promote neutrophil recruitment, as OVA or MIP-1alpha[CCL3] failed to induce neutrophil migration in CCR1(-/-) mice, in contrast to CCR5(-/-) mice. In summary, we have demonstrated that neutrophil migration observed in this model of immune inflammation is mediated by MIP-1alpha[CCL3], which via CCR1, induces the sequential release of TNF-alpha and LTB(4). Therefore, whether a similar pathway mediates neutrophil migration in human immune-inflammatory diseases, the development of specific CCR1 antagonists might have a therapeutic potential.

João S. Silva - One of the best experts on this subject based on the ideXlab platform.

  • evidences of the cooperative role of the chemokines ccl3 ccl4 and CCL5 and its receptors ccr1 and ccr5 in rankl cell migration throughout experimental periodontitis in mice
    Bone, 2010
    Co-Authors: Carlos Eduardo Repeke, Samuel B Ferreira, Elcia Maria Varize Silveira, Mario Julio Avilacampos, Marcela Claudino, João S. Silva, Gerson Francisco De Assis, Gustavo Pompermaier Garlet
    Abstract:

    Periodontal disease (PD) is characterized by the inflammatory bone resorption in response to the bacterial challenge, in a host response that involves a series of chemokines supposed to control cell influx into periodontal tissues and determine disease outcome. In this study, we investigated the role of chemokines and its receptors in the immunoregulation of experimental PD in mice. Aggregatibacter actinomycetemcomitans-infected C57Bl/6 (WT) mice developed an intense inflammatory reaction and severe alveolar bone resorption, associated with a high expression of CCL3 and the migration of CCR5+, CCR1+ and RANKL+ cells to periodontal tissues. However, CCL3KO-infected mice developed a similar disease phenotype than WT strain, characterized by the similar expression of cytokines (TNF-α, IFN-γ and IL-10), osteoclastogenic factors (RANKL and OPG) and MMPs (MMP-1, MMP-2, MMP-3, TIMP-1 and TIMP-3), and similar patterns of CCR1+, CCR5+ and RANKL+ cell migration. The apparent lack of function for CCL3 is possible due the relative redundancy of chemokine system, since chemokines such as CCL4 and CCL5, which share the receptors CCR1 and CCR5 with CCL3, present a similar kinetics of expression than CCL3. Accordingly, CCL4 and CCL5 kinetics of expression after experimental periodontal infection remain unaltered regardless the presence/absence of CCL3. Conversely, the individual absence of CCR1 and CCR5 resulted in a decrease of leukocyte infiltration and alveolar bone loss. When CCR1 and CCR5 were simultaneously inhibited by met-RANTES treatment a significantly more effective attenuation of periodontitis progression was verified, associated with lower values of bone loss and decreased counts of leukocytes in periodontal tissues. Our results suggest that the absence of CCL3 does not affect the development of experimental PD in mice, probably due to the presence of homologous chemokines CCL4 and CCL5 that overcome the absence of this chemokine. In addition, our data demonstrate that the absence of chemokine receptors CCR1+ and CCR5+ attenuate of inflammatory bone resorption. Finally, our data shows data the simultaneous blockade of CCR1 and CCR5 with MetRANTEs presents a more pronounced effect in the arrest of disease progression, demonstrating the cooperative role of such receptors in the inflammatory bone resorption process throughout experimental PD.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory pro- tein-1 (MIP-1)(CC chemokine ligand 3 (CCL3)), MIP-1(CCL4), regulated on activation, normal T expressed and secreted (RANTES)(CCL5), and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor (TNF-) and leukotriene B 4 (LTB 4 ). Herein, we show increased mRNA expression for MIP- 1(CCL3), MIP-1(CCL4), RANTES(CCL5), and CCR1 in peritoneal cells harvested from OVA-chal- lenged, immunized mice, as well as MIP-1(CCL3) and RANTES(CCL5) but not MIP-1(CCL4) proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP- 1(CCL3) / mice, but it was not inhibited by treat- ment with antibodies against RANTES(CCL5) or MIP-1(CCL4). MIP-1(CCL3) mediated neutro- phil migration in immunized mice through induc- tion of TNF- and LTB4 synthesis, as these medi- ators were detected in the exudates harvested from OVA-challenged, immunized wild-type but not MIP-1(CCL3) / mice; administration of MIP- 1(CCL3) induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF- antibody in TNF receptor 1 (p55 / )- deficient mice or by MK 886 (a 5-lipoxygenase in- hibitor); and MIP-1(CCL3) failed to induce LTB 4 production in p55 / mice. MIP-1(CCL3) used CCR1 to promote neutrophil recruitment, as OVA or MIP-1(CCL3) failed to induce neutrophil migration in CCR1 / mice, in contrast to CCR5 / mice. In summary, we have demonstrated that neutrophil mi- gration observed in this model of immune inflamma- tion is mediated by MIP-1(CCL3), which via CCR1, induces the sequential release of TNF- and LTB4. Therefore, whether a similar pathway mediates neu- trophil migration in human immune-inflammatory diseases, the development of specific CCR1 antago- nists might have a therapeutic potential. J. Leukoc. Biol. 78: 000-000; 2005.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory pro- tein-1 (MIP-1)(CC chemokine ligand 3 (CCL3)), MIP-1(CCL4), regulated on activation, normal T expressed and secreted (RANTES)(CCL5), and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor (TNF-) and leukotriene B 4 (LTB 4 ). Herein, we show increased mRNA expression for MIP- 1(CCL3), MIP-1(CCL4), RANTES(CCL5), and CCR1 in peritoneal cells harvested from OVA-chal- lenged, immunized mice, as well as MIP-1(CCL3) and RANTES(CCL5) but not MIP-1(CCL4) proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP- 1(CCL3) / mice, but it was not inhibited by treat- ment with antibodies against RANTES(CCL5) or MIP-1(CCL4). MIP-1(CCL3) mediated neutro- phil migration in immunized mice through induc- tion of TNF- and LTB4 synthesis, as these medi- ators were detected in the exudates harvested from OVA-challenged, immunized wild-type but not MIP-1(CCL3) / mice; administration of MIP- 1(CCL3) induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF- antibody in TNF receptor 1 (p55 / )- deficient mice or by MK 886 (a 5-lipoxygenase in- hibitor); and MIP-1(CCL3) failed to induce LTB 4 production in p55 / mice. MIP-1(CCL3) used CCR1 to promote neutrophil recruitment, as OVA or MIP-1(CCL3) failed to induce neutrophil migration in CCR1 / mice, in contrast to CCR5 / mice. In summary, we have demonstrated that neutrophil mi- gration observed in this model of immune inflamma- tion is mediated by MIP-1(CCL3), which via CCR1, induces the sequential release of TNF- and LTB4. Therefore, whether a similar pathway mediates neu- trophil migration in human immune-inflammatory diseases, the development of specific CCR1 antago- nists might have a therapeutic potential. J. Leukoc. Biol. 78: 000-000; 2005.

  • mip 1α ccl3 acting on the ccr1 receptor mediates neutrophil migration in immune inflammation via sequential release of tnf α and ltb4
    Journal of Leukocyte Biology, 2005
    Co-Authors: Cleber D L Ramos, Janeusa T Souto, Cory M Hogaboam, Claudio Canetti, Sergio H Ferreira, João S. Silva, Fernando Q. Cunha
    Abstract:

    In the present study, we investigated the involvement of macrophage-inflammatory protein-1alpha (MIP-1alpha)[CC chemokine ligand 3 (CCL3)], MIP-1beta[CCL4], regulated on activation, normal T expressed and secreted (RANTES)[CCL5], and CC chemokine receptors (CCRs) on neutrophil migration in murine immune inflammation. Previously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor alpha (TNF-alpha) and leukotriene B(4)(LTB(4)). Herein, we show increased mRNA expression for MIP-1alpha[CCL3], MIP-1beta[CCL4], RANTES[CCL5], and CCR1 in peritoneal cells harvested from OVA-challenged, immunized mice, as well as MIP-1alpha[CCL3] and RANTES[CCL5] but not MIP-1beta[CCL4] proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP-1alpha[CCL3](-/-) mice, but it was not inhibited by treatment with antibodies against RANTES[CCL5] or MIP-1beta[CCL4]. MIP-1alpha[CCL3] mediated neutrophil migration in immunized mice through induction of TNF-alpha and LTB(4) synthesis, as these mediators were detected in the exudates harvested from OVA-challenged immunized wild-type but not MIP-1alpha[CCL3](-/-) mice; administration of MIP-1alpha[CCL3] induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF-alpha antibody in TNF receptor 1 (p55(-/-))-deficient mice or by MK 886 (a 5-lipoxygenase inhibitor); and MIP-1alpha[CCL3] failed to induce LTB(4) production in p55(-/-) mice. MIP-1alpha[CCL3] used CCR1 to promote neutrophil recruitment, as OVA or MIP-1alpha[CCL3] failed to induce neutrophil migration in CCR1(-/-) mice, in contrast to CCR5(-/-) mice. In summary, we have demonstrated that neutrophil migration observed in this model of immune inflammation is mediated by MIP-1alpha[CCL3], which via CCR1, induces the sequential release of TNF-alpha and LTB(4). Therefore, whether a similar pathway mediates neutrophil migration in human immune-inflammatory diseases, the development of specific CCR1 antagonists might have a therapeutic potential.