The Experts below are selected from a list of 63 Experts worldwide ranked by ideXlab platform

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.

Cory M Hogaboam - 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.