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Marc Fontaine – One of the best experts on this subject based on the ideXlab platform.

  • Role of complement Anaphylatoxin receptors (C3aR, C5aR) in the development of the rat cerebellum
    Molecular Immunology, 2008
    Co-Authors: Magalie Benard, Emilie Raoult, David Vaudry, Jérôme Leprince, Anthony Falluel-morel, Bruno Gonzalez, Ludovic Galas, Hubert Vaudry, Marc Fontaine
    Abstract:

    There is now strong evidence for non-immune or inflammatory functions of complement, notably in the central nervous system. In particular, it has been recently reported that the Anaphylatoxin receptors C3aR and C5aR are transiently expressed in the cerebellar cortex of newborn rat, suggesting that Anaphylatoxins are involved in the histogenesis of the cerebellum. In the present study, we have investigated the effects of C3aR and C5aR agonists and antagonists on the development of the cerebellum of 11-12-day-old rats in vivo and in vitro. Sub-dural injection of C3aR and C5aR agonists at the surface of the cerebellum transiently modified the thickness of the cortical layers. The C5aR agonist provoked an enlargement of the external granule cell layer (EGL) that was due to increased proliferation of immature granule neurons. Conversely, the C3aR agonist decreased the thickness of the EGL and increased the thickness of the internal granule cell layer (IGL), suggesting that C3a accelerates the migration process of granule cells from the EGL to the IGL. Video-microscopy examination of cultured granule neurons confirmed the role of C3aR in cell motility. These results provide clear evidence for the involvement of Anaphylatoxin receptors in the histogenesis of the cerebellar cortex.

  • Interleukin-1β and Anaphylatoxins exert a synergistic effect on NGF expression by astrocytes
    Journal of neuroinflammation, 2006
    Co-Authors: Anne-christine Jauneau, Magalie Benard, Hubert Vaudry, Alexander Ischenko, Alexandra Chatagner, Marie-thérèse Schouft, Christine Patte, P Chan, Marc Fontaine
    Abstract:

    C3a and C5a Anaphylatoxins are proinflammatory polypeptides released during complement activation. They exert their biological activities through interaction with two G protprotein-coupled receptors named C3aR and C5aR, respectively. In the brain, these receptors are expressed on glial cells, and some recent data have suggested that Anaphylatoxins could mediate neuroprotection. In this study, we used RT-PCR and ribonuclease protection assays (RPA) to investigate the role of Anaphylatoxins on neurotrophin expression by the human glioblastoma cell line T98G and by rat astrocytes. Our data show that for both cell types, Anaphylatoxins upregulate expression of NGF mRNA. This response depended on a G protprotein-coupled pathway since pre-treatment of cells with pertussis toxin (PTX) completely blocked NGF mRNA increases. This effect was Anaphylatoxin-specific since pre-incubation with anti-C3a or anti-C5aR antibodies abolished the effects of C3a and C5a, respectively. The regulation of NGF mRNA by Anaphylatoxins was not accompanied by translation into protein expression, but there was a significant synergic effect of Anaphylatoxins/IL-1b costimulation. Our demonstration of involvement of Anaphylatoxins in the NGF release process by astrocytes suggests that C3a and C5a could modulate neuronal survival in the CNS.

  • Interleukin-1beta and Anaphylatoxins exert a synergistic effect on NGF expression by astrocytes.
    J Neuroinflammation, 2006
    Co-Authors: Anne-christine Jauneau, Magalie Benard, Hubert Vaudry, Alexander Ischenko, P Chan, Alexandra Chatagner, Marie-thérèse Schouft, Christine Patte, Marc Fontaine
    Abstract:

    C3a and C5a Anaphylatoxins are proinflammatory polypeptides released during complement activation. They exert their biological activities through interaction with two G protprotein-coupled receptors named C3aR and C5aR, respectively. In the brain, these receptors are expressed on glial cells, and some recent data have suggested that Anaphylatoxins could mediate neuroprotection. In this study, we used RT-PCR and ribonuclease protection assays (RPA) to investigate the role of Anaphylatoxins on neurotrophin expression by the human glioblastoma cell line T98G and by rat astrocytes. Our data show that for both cell types, Anaphylatoxins upregulate expression of NGF mRNA. This response depended on a G protprotein-coupled pathway since pre-treatment of cells with pertussis toxin (PTX) completely blocked NGF mRNA increases. This effect was Anaphylatoxin-specific since pre-incubation with anti-C3a or anti-C5aR antibodies abolished the effects of C3a and C5a, respectively. The regulation of NGF mRNA by Anaphylatoxins was not accompanied by translation into protein expression, but there was a significant synergic effect of Anaphylatoxins/IL-1b costimulation. Our demonstration of involvement of Anaphylatoxins in the NGF release process by astrocytes suggests that C3a and C5a could modulate neuronal survival in the CNS.

Anne-christine Jauneau – One of the best experts on this subject based on the ideXlab platform.

  • Interleukin-1β and Anaphylatoxins exert a synergistic effect on NGF expression by astrocytes
    Journal of neuroinflammation, 2006
    Co-Authors: Anne-christine Jauneau, Magalie Benard, Hubert Vaudry, Alexander Ischenko, Alexandra Chatagner, Marie-thérèse Schouft, Christine Patte, P Chan, Marc Fontaine
    Abstract:

    C3a and C5a Anaphylatoxins are proinflammatory polypeptides released during complement activation. They exert their biological activities through interaction with two G protein-coupled receptors named C3aR and C5aR, respectively. In the brain, these receptors are expressed on glial cells, and some recent data have suggested that Anaphylatoxins could mediate neuroprotection. In this study, we used RT-PCR and ribonuclease protection assays (RPA) to investigate the role of Anaphylatoxins on neurotrophin expression by the human glioblastoma cell line T98G and by rat astrocytes. Our data show that for both cell types, Anaphylatoxins upregulate expression of NGF mRNA. This response depended on a G protein-coupled pathway since pre-treatment of cells with pertussis toxin (PTX) completely blocked NGF mRNA increases. This effect was Anaphylatoxin-specific since pre-incubation with anti-C3a or anti-C5aR antibodies abolished the effects of C3a and C5a, respectively. The regulation of NGF mRNA by Anaphylatoxins was not accompanied by translation into protein expression, but there was a significant synergic effect of Anaphylatoxins/IL-1b costimulation. Our demonstration of involvement of Anaphylatoxins in the NGF release process by astrocytes suggests that C3a and C5a could modulate neuronal survival in the CNS.

  • Interleukin-1beta and Anaphylatoxins exert a synergistic effect on NGF expression by astrocytes.
    J Neuroinflammation, 2006
    Co-Authors: Anne-christine Jauneau, Magalie Benard, Hubert Vaudry, Alexander Ischenko, P Chan, Alexandra Chatagner, Marie-thérèse Schouft, Christine Patte, Marc Fontaine
    Abstract:

    C3a and C5a Anaphylatoxins are proinflammatory polypeptides released during complement activation. They exert their biological activities through interaction with two G protein-coupled receptors named C3aR and C5aR, respectively. In the brain, these receptors are expressed on glial cells, and some recent data have suggested that Anaphylatoxins could mediate neuroprotection. In this study, we used RT-PCR and ribonuclease protection assays (RPA) to investigate the role of Anaphylatoxins on neurotrophin expression by the human glioblastoma cell line T98G and by rat astrocytes. Our data show that for both cell types, Anaphylatoxins upregulate expression of NGF mRNA. This response depended on a G protein-coupled pathway since pre-treatment of cells with pertussis toxin (PTX) completely blocked NGF mRNA increases. This effect was Anaphylatoxin-specific since pre-incubation with anti-C3a or anti-C5aR antibodies abolished the effects of C3a and C5a, respectively. The regulation of NGF mRNA by Anaphylatoxins was not accompanied by translation into protein expression, but there was a significant synergic effect of Anaphylatoxins/IL-1b costimulation. Our demonstration of involvement of Anaphylatoxins in the NGF release process by astrocytes suggests that C3a and C5a could modulate neuronal survival in the CNS.

  • Complement component Anaphylatoxins upregulate chemokine expression by human astrocytes.
    FEBS Letters, 2003
    Co-Authors: Anne-christine Jauneau, Alexander Ischenko, P Chan, Marc Fontaine
    Abstract:

    The complement (C) system, a major component of the innate immune system, has been described as a factor implicated in some brain disorders. C activation leads to the release of Anaphylatoxins, two proinflammatory polypeptides acting through specific receptors that have been detected on brain cells. Here, we examined the effect of Anaphylatoxins on chemokine expression by human astrocytes. We showed that Anaphylatoxins significantly increase chemokine mRNA expression. However, Anaphylatoxin-induced chemokine secretion (interleukin-8) was observed only in the presence of interleukin-1β. Thus, Anaphylatoxins could initiate a chemokine cascade and, at least in part, be involved in pathogenesis of the brain.

Alexander Ischenko – One of the best experts on this subject based on the ideXlab platform.

  • Interleukin-1β and Anaphylatoxins exert a synergistic effect on NGF expression by astrocytes
    Journal of neuroinflammation, 2006
    Co-Authors: Anne-christine Jauneau, Magalie Benard, Hubert Vaudry, Alexander Ischenko, Alexandra Chatagner, Marie-thérèse Schouft, Christine Patte, P Chan, Marc Fontaine
    Abstract:

    C3a and C5a Anaphylatoxins are proinflammatory polypeptides released during complement activation. They exert their biological activities through interaction with two G protein-coupled receptors named C3aR and C5aR, respectively. In the brain, these receptors are expressed on glial cells, and some recent data have suggested that Anaphylatoxins could mediate neuroprotection. In this study, we used RT-PCR and ribonuclease protection assays (RPA) to investigate the role of Anaphylatoxins on neurotrophin expression by the human glioblastoma cell line T98G and by rat astrocytes. Our data show that for both cell types, Anaphylatoxins upregulate expression of NGF mRNA. This response depended on a G protein-coupled pathway since pre-treatment of cells with pertussis toxin (PTX) completely blocked NGF mRNA increases. This effect was Anaphylatoxin-specific since pre-incubation with anti-C3a or anti-C5aR antibodies abolished the effects of C3a and C5a, respectively. The regulation of NGF mRNA by Anaphylatoxins was not accompanied by translation into protein expression, but there was a significant synergic effect of Anaphylatoxins/IL-1b costimulation. Our demonstration of involvement of Anaphylatoxins in the NGF release process by astrocytes suggests that C3a and C5a could modulate neuronal survival in the CNS.

  • Interleukin-1beta and Anaphylatoxins exert a synergistic effect on NGF expression by astrocytes.
    J Neuroinflammation, 2006
    Co-Authors: Anne-christine Jauneau, Magalie Benard, Hubert Vaudry, Alexander Ischenko, P Chan, Alexandra Chatagner, Marie-thérèse Schouft, Christine Patte, Marc Fontaine
    Abstract:

    C3a and C5a Anaphylatoxins are proinflammatory polypeptides released during complement activation. They exert their biological activities through interaction with two G protein-coupled receptors named C3aR and C5aR, respectively. In the brain, these receptors are expressed on glial cells, and some recent data have suggested that Anaphylatoxins could mediate neuroprotection. In this study, we used RT-PCR and ribonuclease protection assays (RPA) to investigate the role of Anaphylatoxins on neurotrophin expression by the human glioblastoma cell line T98G and by rat astrocytes. Our data show that for both cell types, Anaphylatoxins upregulate expression of NGF mRNA. This response depended on a G protein-coupled pathway since pre-treatment of cells with pertussis toxin (PTX) completely blocked NGF mRNA increases. This effect was Anaphylatoxin-specific since pre-incubation with anti-C3a or anti-C5aR antibodies abolished the effects of C3a and C5a, respectively. The regulation of NGF mRNA by Anaphylatoxins was not accompanied by translation into protein expression, but there was a significant synergic effect of Anaphylatoxins/IL-1b costimulation. Our demonstration of involvement of Anaphylatoxins in the NGF release process by astrocytes suggests that C3a and C5a could modulate neuronal survival in the CNS.

  • Regulation by complement C3a and C5a Anaphylatoxins of cytokine production in human umbilical vein endothelial cells
    FASEB Journal, 2003
    Co-Authors: Tiphaine Monsinjon, Alexander Ischenko, P Chan, Philippe Gasque, Jennifer Brady, Marc Fontaine
    Abstract:

    C3a and C5a Anaphylatoxins are cytokine-like polypeptides generated during complement (C) system activation and released at the inflammatory site. They exert several biological activities through binding to the G-protein-coupled receptors C3aR and C5aR, respectively. Cloning and Northern blot experiments have indicated that both receptors are expressed by myeloid as well as nonmyeloid cells (e.g., endothelial and epithelial cells). To better understand the roles of C Anaphylatoxins during inflammation, we investigated their effects on the expression of cytokine and chemokine genes by cultured human umbilical cord endothelial cells (HUVEC). HUVEC constitutively expressed both Anaphylatoxin receptors, and addition of physiological concentrations of C3a or C5a (nM range) caused a strong up-regulation of IL-8, IL-1beta, and RANTES mRNA in a time- and dose-dependent manner. Conversely, a decrease in IL-6 mRNA was observed, but only with C5a stimulation. These variations in mRNA levels were inhibited by pretreatment with anti-C5aR and anti-C3aR antibodies as well as pertussis toxin, indicating that G-proteins are involved in Anaphylatoxin-activated signal transduction pathways. Finally, we showed that C3a and C5a both strongly activate downstream MAP kinase signaling pathways (p44 and p42 Erk kinases).

P Chan – One of the best experts on this subject based on the ideXlab platform.

  • Interleukin-1beta and Anaphylatoxins exert a synergistic effect on NGF expression by astrocytes.
    J Neuroinflammation, 2006
    Co-Authors: Anne-christine Jauneau, Magalie Benard, Hubert Vaudry, Alexander Ischenko, P Chan, Alexandra Chatagner, Marie-thérèse Schouft, Christine Patte, Marc Fontaine
    Abstract:

    C3a and C5a Anaphylatoxins are proinflammatory polypeptides released during complement activation. They exert their biological activities through interaction with two G protein-coupled receptors named C3aR and C5aR, respectively. In the brain, these receptors are expressed on glial cells, and some recent data have suggested that Anaphylatoxins could mediate neuroprotection. In this study, we used RT-PCR and ribonuclease protection assays (RPA) to investigate the role of Anaphylatoxins on neurotrophin expression by the human glioblastoma cell line T98G and by rat astrocytes. Our data show that for both cell types, Anaphylatoxins upregulate expression of NGF mRNA. This response depended on a G protein-coupled pathway since pre-treatment of cells with pertussis toxin (PTX) completely blocked NGF mRNA increases. This effect was Anaphylatoxin-specific since pre-incubation with anti-C3a or anti-C5aR antibodies abolished the effects of C3a and C5a, respectively. The regulation of NGF mRNA by Anaphylatoxins was not accompanied by translation into protein expression, but there was a significant synergic effect of Anaphylatoxins/IL-1b costimulation. Our demonstration of involvement of Anaphylatoxins in the NGF release process by astrocytes suggests that C3a and C5a could modulate neuronal survival in the CNS.

  • Regulation by complement C3a and C5a Anaphylatoxins of cytokine production in human umbilical vein endothelial cells
    FASEB Journal, 2003
    Co-Authors: Tiphaine Monsinjon, Alexander Ischenko, P Chan, Philippe Gasque, Jennifer Brady, Marc Fontaine
    Abstract:

    C3a and C5a Anaphylatoxins are cytokine-like polypeptides generated during complement (C) system activation and released at the inflammatory site. They exert several biological activities through binding to the G-protein-coupled receptors C3aR and C5aR, respectively. Cloning and Northern blot experiments have indicated that both receptors are expressed by myeloid as well as nonmyeloid cells (e.g., endothelial and epithelial cells). To better understand the roles of C Anaphylatoxins during inflammation, we investigated their effects on the expression of cytokine and chemokine genes by cultured human umbilical cord endothelial cells (HUVEC). HUVEC constitutively expressed both Anaphylatoxin receptors, and addition of physiological concentrations of C3a or C5a (nM range) caused a strong up-regulation of IL-8, IL-1beta, and RANTES mRNA in a time- and dose-dependent manner. Conversely, a decrease in IL-6 mRNA was observed, but only with C5a stimulation. These variations in mRNA levels were inhibited by pretreatment with anti-C5aR and anti-C3aR antibodies as well as pertussis toxin, indicating that G-proteins are involved in Anaphylatoxin-activated signal transduction pathways. Finally, we showed that C3a and C5a both strongly activate downstream MAP kinase signaling pathways (p44 and p42 Erk kinases).

  • Complement component Anaphylatoxins upregulate chemokine expression by human astrocytes.
    FEBS Letters, 2003
    Co-Authors: Anne-christine Jauneau, Alexander Ischenko, P Chan, Marc Fontaine
    Abstract:

    The complement (C) system, a major component of the innate immune system, has been described as a factor implicated in some brain disorders. C activation leads to the release of Anaphylatoxins, two proinflammatory polypeptides acting through specific receptors that have been detected on brain cells. Here, we examined the effect of Anaphylatoxins on chemokine expression by human astrocytes. We showed that Anaphylatoxins significantly increase chemokine mRNA expression. However, Anaphylatoxin-induced chemokine secretion (interleukin-8) was observed only in the presence of interleukin-1β. Thus, Anaphylatoxins could initiate a chemokine cascade and, at least in part, be involved in pathogenesis of the brain.

Dimitrios Mougiakakos – One of the best experts on this subject based on the ideXlab platform.

  • mesenchymal stromal cells engage complement and complement receptor bearing innate effector cells to modulate immune responses
    PLOS ONE, 2011
    Co-Authors: Guido Moll, Dimitrios Mougiakakos, Regina Jitschin, Lena Von Bahr, Ida Rasmussonduprez, Birgitta Sundberg, Lena Lonnies, Graciela Elgue, Kristina Nilssonekdahl
    Abstract:

    Infusion of human third-party mesenchymal stromal cells (MSCs) appears to be a promising therapy for acute graft-versus-hosthost disease (aGvHD). To date, little is known about how MSCs interact with the body’s innate immune system after clinical infusion. This study shows, that exposure of MSCs to blood type ABO-matched human blood activates the complement system, which triggers complement-mediated lymphoid and myeloid effector cell activation in blood. We found deposition of complement component C3-derived fragments iC3b and C3dg on MSCs and fluid-phase generation of the chemotactic Anaphylatoxins C3a and C5a. MSCs bound low amounts of immunoglobulins and lacked expression of complement regulatory proteins MCP (CD46) and DAF (CD55), but were protected from complement lysis via expression of protectin (CD59). Cell-surface-opsonization and Anaphylatoxin-formation triggered complement receptor 3 (CD11b/CD18)-mediated effector cell activation in blood. The complement-activating properties of individual MSCs were furthermore correlated with their potency to inhibit PBMC-proliferation in vitro, and both effector cell activation and the immunosuppressive effect could be blocked either by using complement inhibitor Compstatin or by depletion of CD14/CD11b-high myeloid effector cells from mixed lymphocyte reactions. Our study demonstrates for the first time a major role of the complement system in governing the immunomodulatory activity of MSCs and elucidates how complement activation mediates the interaction with other immune cells.