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Susan M. Macdonald - One of the best experts on this subject based on the ideXlab platform.

  • Pharmacologic regulation of Histamine Release by the human recombinant Histamine-releasing factor.
    Journal of Allergy and Clinical Immunology, 1999
    Co-Authors: Roy Bheekha-escura, Stacy R. Chance, Jacqueline M. Langdon, Donald W. Macglashan, Susan M. Macdonald
    Abstract:

    Abstract Background: The recently cloned human recombinant IgE-dependent Histamine releasing factor (HrHRF) was initially thought to stimulate Histamine Release from human basophils from a subpopulation of allergic donors by interacting with the IgE molecules on the surface of these cells. Additional data suggest that HrHRF exerts its biologic effects by binding to a distinct cell surface structure and not to IgE. Objective: To address the hypothesis that the HrHRF signaling pathway is distinct from the classical high-affinity IgE receptor (FcϵRI) pathway, we used pharmacologic agents known to affect basophil Histamine Release. Methods: In this report we compared the effect of staurosporine, Bis II, Go 6976, rottlerin, and pertussis toxin on Histamine Release from human basophils mediated by the following stimuli: HrHRF, polyclonal human anti-IgE antibody, and antigen, as well as the IgE-independent stimulus, FMLP. Results: None of these modulators, except rottlerin, could differentiate Histamine Release induced by anti-IgE or antigen from that induced by HrHRF. Rottlerin enhanced HrHRF-mediated Histamine Release and dose dependently blocked FMLP-mediated Release without affecting basophil activation by either anti-IgE or antigen. Conclusion: These data suggest a unique signaling pathway for HrHRF and thus strengthen the hypothesis that HrHRF binds to a specific receptor other than IgE. (J Allergy Clin Immunol 1999;103:937-43.)

  • Pharmacologic regulation of Histamine Release by the human recombinant Histamine-releasing factor.
    The Journal of allergy and clinical immunology, 1999
    Co-Authors: Roy Bheekha-escura, Stacy R. Chance, Jacqueline M. Langdon, Donald W. Macglashan, Susan M. Macdonald
    Abstract:

    The recently cloned human recombinant IgE-dependent Histamine releasing factor (HrHRF) was initially thought to stimulate Histamine Release from human basophils from a subpopulation of allergic donors by interacting with the IgE molecules on the surface of these cells. Additional data suggest that HrHRF exerts its biologic effects by binding to a distinct cell surface structure and not to IgE. To address the hypothesis that the HrHRF signaling pathway is distinct from the classical high-affinity IgE receptor (FcepsilonRI) pathway, we used pharmacologic agents known to affect basophil Histamine Release. In this report we compared the effect of staurosporine, Bis II, Gö 6976, rottlerin, and pertussis toxin on Histamine Release from human basophils mediated by the following stimuli: HrHRF, polyclonal human anti-IgE antibody, and antigen, as well as the IgE-independent stimulus, FMLP. None of these modulators, except rottlerin, could differentiate Histamine Release induced by anti-IgE or antigen from that induced by HrHRF. Rottlerin enhanced HrHRF-mediated Histamine Release and dose dependently blocked FMLP-mediated Release without affecting basophil activation by either anti-IgE or antigen. These data suggest a unique signaling pathway for HrHRF and thus strengthen the hypothesis that HrHRF binds to a specific receptor other than IgE.

Roy Bheekha-escura - One of the best experts on this subject based on the ideXlab platform.

  • Pharmacologic regulation of Histamine Release by the human recombinant Histamine-releasing factor.
    Journal of Allergy and Clinical Immunology, 1999
    Co-Authors: Roy Bheekha-escura, Stacy R. Chance, Jacqueline M. Langdon, Donald W. Macglashan, Susan M. Macdonald
    Abstract:

    Abstract Background: The recently cloned human recombinant IgE-dependent Histamine releasing factor (HrHRF) was initially thought to stimulate Histamine Release from human basophils from a subpopulation of allergic donors by interacting with the IgE molecules on the surface of these cells. Additional data suggest that HrHRF exerts its biologic effects by binding to a distinct cell surface structure and not to IgE. Objective: To address the hypothesis that the HrHRF signaling pathway is distinct from the classical high-affinity IgE receptor (FcϵRI) pathway, we used pharmacologic agents known to affect basophil Histamine Release. Methods: In this report we compared the effect of staurosporine, Bis II, Go 6976, rottlerin, and pertussis toxin on Histamine Release from human basophils mediated by the following stimuli: HrHRF, polyclonal human anti-IgE antibody, and antigen, as well as the IgE-independent stimulus, FMLP. Results: None of these modulators, except rottlerin, could differentiate Histamine Release induced by anti-IgE or antigen from that induced by HrHRF. Rottlerin enhanced HrHRF-mediated Histamine Release and dose dependently blocked FMLP-mediated Release without affecting basophil activation by either anti-IgE or antigen. Conclusion: These data suggest a unique signaling pathway for HrHRF and thus strengthen the hypothesis that HrHRF binds to a specific receptor other than IgE. (J Allergy Clin Immunol 1999;103:937-43.)

  • Pharmacologic regulation of Histamine Release by the human recombinant Histamine-releasing factor.
    The Journal of allergy and clinical immunology, 1999
    Co-Authors: Roy Bheekha-escura, Stacy R. Chance, Jacqueline M. Langdon, Donald W. Macglashan, Susan M. Macdonald
    Abstract:

    The recently cloned human recombinant IgE-dependent Histamine releasing factor (HrHRF) was initially thought to stimulate Histamine Release from human basophils from a subpopulation of allergic donors by interacting with the IgE molecules on the surface of these cells. Additional data suggest that HrHRF exerts its biologic effects by binding to a distinct cell surface structure and not to IgE. To address the hypothesis that the HrHRF signaling pathway is distinct from the classical high-affinity IgE receptor (FcepsilonRI) pathway, we used pharmacologic agents known to affect basophil Histamine Release. In this report we compared the effect of staurosporine, Bis II, Gö 6976, rottlerin, and pertussis toxin on Histamine Release from human basophils mediated by the following stimuli: HrHRF, polyclonal human anti-IgE antibody, and antigen, as well as the IgE-independent stimulus, FMLP. None of these modulators, except rottlerin, could differentiate Histamine Release induced by anti-IgE or antigen from that induced by HrHRF. Rottlerin enhanced HrHRF-mediated Histamine Release and dose dependently blocked FMLP-mediated Release without affecting basophil activation by either anti-IgE or antigen. These data suggest a unique signaling pathway for HrHRF and thus strengthen the hypothesis that HrHRF binds to a specific receptor other than IgE.

Martin J. Elliott - One of the best experts on this subject based on the ideXlab platform.

  • Histamine Release during paediatric cardiopulmonary bypass
    Canadian Journal of Anaesthesia, 1993
    Co-Authors: Davinia E. Withington, Martin J. Elliott
    Abstract:

    La libération d’Histamine participe à la réaction inflammatoire systémique el survient pendant la chirurgie et la circulation extra-corporelle chez l’adulte (CEC). On ne dispose que peu de données pédiatriques. La libération histaminique est étudiée chez 23 enfants qui subissent une CEC avec une technique anesthésique standard. Des échantillons de sang sont prélevés au moment d’événements anesthésiques et chirurgicaux prédéterminés, e.g., début de la CEC, déclampage aortique, réinsufflation des poumons. L’Histamine plasmatique est déterminée par la seule technique isotopique radioenzymatique. La libération d’Histamine ne survient pas de façon régulière dans la population étudiée bien que chez quelques sujets on trouve une augmentation de sa concentration plasmatique après la mise en marche de la CEC (P < 0,05) et au déclampage de l’aorte (P < 0,05). Il n’y a aucune corrélation entre la concentration d’Histamine d’une part, et la pression artérielle systolique , la température, la durée de la CEC ou la durée du clampage d’autre part. Il existe toutefois une corrélation positive avec la fréquence cardiaque. Histamine Release is part of the general inflammatory response and occurs during surgery and cardiopulmonary bypass (CPB) in adults. Few data are available for children. Histamine Release was studied in 23 children undergoing CPB with standard anaesthetic and CPB techniques. Blood sampling was performed in relation to specific anaesthetic and surgical events, e.g., start of CPB, removal of aortic clamps, reventilation of the lungs. Plasma Histamine was determined by a single isotope radioenzymatic technique. There was no consistent Histamine Release in the study population although there was an increase in plasma Histamine concentration in some subjects after initiation of CPB ( P < 0.05) and on removal of the aortic cross-clamp (P < 0.05). No correlation was demonstrated between Histamine concentration and systolic arterial pressure, temperature , duration of CPB or cross-clamp time. Histamine concentration was positively correlated with heart rate.

  • Histamine Release during paediatric cardiopulmonary
    1993
    Co-Authors: Davinia E. Withington, Frca Mrcp, K. Man, Martin J. Elliott
    Abstract:

    Histamine Release is part of the general inflammatory response and occurs during surgery and cardiopulmonary bypass (CPB) in adults. Few data are available for children. Histamine Release was studied in 23 children undergoing CPB with standard an- aesthetic and CPB techniques. Blood sampling was performed in relation to specific anaesthetic and surgical events, e.g., start of CPB, removal of aortic clamps, reventilation of the lungs. Plasma Histamine was determined by a single isotope radioen- zymatic technique. There was no consistent Histamine Release in the study population although there was an increase in plasma Histamine concentration in some subjects after initiation of CPB (P < 0.05) and on removal of the aortic cross-clamp (P < 0.05). No correlation was demonstrated between hista- mine concentration and systolic arterial pressure, temperature, duration of CPB or cross-clamp time. Histamine concentration was positively correlated with heart rate.

Stacy R. Chance - One of the best experts on this subject based on the ideXlab platform.

  • Pharmacologic regulation of Histamine Release by the human recombinant Histamine-releasing factor.
    Journal of Allergy and Clinical Immunology, 1999
    Co-Authors: Roy Bheekha-escura, Stacy R. Chance, Jacqueline M. Langdon, Donald W. Macglashan, Susan M. Macdonald
    Abstract:

    Abstract Background: The recently cloned human recombinant IgE-dependent Histamine releasing factor (HrHRF) was initially thought to stimulate Histamine Release from human basophils from a subpopulation of allergic donors by interacting with the IgE molecules on the surface of these cells. Additional data suggest that HrHRF exerts its biologic effects by binding to a distinct cell surface structure and not to IgE. Objective: To address the hypothesis that the HrHRF signaling pathway is distinct from the classical high-affinity IgE receptor (FcϵRI) pathway, we used pharmacologic agents known to affect basophil Histamine Release. Methods: In this report we compared the effect of staurosporine, Bis II, Go 6976, rottlerin, and pertussis toxin on Histamine Release from human basophils mediated by the following stimuli: HrHRF, polyclonal human anti-IgE antibody, and antigen, as well as the IgE-independent stimulus, FMLP. Results: None of these modulators, except rottlerin, could differentiate Histamine Release induced by anti-IgE or antigen from that induced by HrHRF. Rottlerin enhanced HrHRF-mediated Histamine Release and dose dependently blocked FMLP-mediated Release without affecting basophil activation by either anti-IgE or antigen. Conclusion: These data suggest a unique signaling pathway for HrHRF and thus strengthen the hypothesis that HrHRF binds to a specific receptor other than IgE. (J Allergy Clin Immunol 1999;103:937-43.)

  • Pharmacologic regulation of Histamine Release by the human recombinant Histamine-releasing factor.
    The Journal of allergy and clinical immunology, 1999
    Co-Authors: Roy Bheekha-escura, Stacy R. Chance, Jacqueline M. Langdon, Donald W. Macglashan, Susan M. Macdonald
    Abstract:

    The recently cloned human recombinant IgE-dependent Histamine releasing factor (HrHRF) was initially thought to stimulate Histamine Release from human basophils from a subpopulation of allergic donors by interacting with the IgE molecules on the surface of these cells. Additional data suggest that HrHRF exerts its biologic effects by binding to a distinct cell surface structure and not to IgE. To address the hypothesis that the HrHRF signaling pathway is distinct from the classical high-affinity IgE receptor (FcepsilonRI) pathway, we used pharmacologic agents known to affect basophil Histamine Release. In this report we compared the effect of staurosporine, Bis II, Gö 6976, rottlerin, and pertussis toxin on Histamine Release from human basophils mediated by the following stimuli: HrHRF, polyclonal human anti-IgE antibody, and antigen, as well as the IgE-independent stimulus, FMLP. None of these modulators, except rottlerin, could differentiate Histamine Release induced by anti-IgE or antigen from that induced by HrHRF. Rottlerin enhanced HrHRF-mediated Histamine Release and dose dependently blocked FMLP-mediated Release without affecting basophil activation by either anti-IgE or antigen. These data suggest a unique signaling pathway for HrHRF and thus strengthen the hypothesis that HrHRF binds to a specific receptor other than IgE.

Jacqueline M. Langdon - One of the best experts on this subject based on the ideXlab platform.

  • Pharmacologic regulation of Histamine Release by the human recombinant Histamine-releasing factor.
    Journal of Allergy and Clinical Immunology, 1999
    Co-Authors: Roy Bheekha-escura, Stacy R. Chance, Jacqueline M. Langdon, Donald W. Macglashan, Susan M. Macdonald
    Abstract:

    Abstract Background: The recently cloned human recombinant IgE-dependent Histamine releasing factor (HrHRF) was initially thought to stimulate Histamine Release from human basophils from a subpopulation of allergic donors by interacting with the IgE molecules on the surface of these cells. Additional data suggest that HrHRF exerts its biologic effects by binding to a distinct cell surface structure and not to IgE. Objective: To address the hypothesis that the HrHRF signaling pathway is distinct from the classical high-affinity IgE receptor (FcϵRI) pathway, we used pharmacologic agents known to affect basophil Histamine Release. Methods: In this report we compared the effect of staurosporine, Bis II, Go 6976, rottlerin, and pertussis toxin on Histamine Release from human basophils mediated by the following stimuli: HrHRF, polyclonal human anti-IgE antibody, and antigen, as well as the IgE-independent stimulus, FMLP. Results: None of these modulators, except rottlerin, could differentiate Histamine Release induced by anti-IgE or antigen from that induced by HrHRF. Rottlerin enhanced HrHRF-mediated Histamine Release and dose dependently blocked FMLP-mediated Release without affecting basophil activation by either anti-IgE or antigen. Conclusion: These data suggest a unique signaling pathway for HrHRF and thus strengthen the hypothesis that HrHRF binds to a specific receptor other than IgE. (J Allergy Clin Immunol 1999;103:937-43.)

  • Pharmacologic regulation of Histamine Release by the human recombinant Histamine-releasing factor.
    The Journal of allergy and clinical immunology, 1999
    Co-Authors: Roy Bheekha-escura, Stacy R. Chance, Jacqueline M. Langdon, Donald W. Macglashan, Susan M. Macdonald
    Abstract:

    The recently cloned human recombinant IgE-dependent Histamine releasing factor (HrHRF) was initially thought to stimulate Histamine Release from human basophils from a subpopulation of allergic donors by interacting with the IgE molecules on the surface of these cells. Additional data suggest that HrHRF exerts its biologic effects by binding to a distinct cell surface structure and not to IgE. To address the hypothesis that the HrHRF signaling pathway is distinct from the classical high-affinity IgE receptor (FcepsilonRI) pathway, we used pharmacologic agents known to affect basophil Histamine Release. In this report we compared the effect of staurosporine, Bis II, Gö 6976, rottlerin, and pertussis toxin on Histamine Release from human basophils mediated by the following stimuli: HrHRF, polyclonal human anti-IgE antibody, and antigen, as well as the IgE-independent stimulus, FMLP. None of these modulators, except rottlerin, could differentiate Histamine Release induced by anti-IgE or antigen from that induced by HrHRF. Rottlerin enhanced HrHRF-mediated Histamine Release and dose dependently blocked FMLP-mediated Release without affecting basophil activation by either anti-IgE or antigen. These data suggest a unique signaling pathway for HrHRF and thus strengthen the hypothesis that HrHRF binds to a specific receptor other than IgE.