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Mediator release during nasal provocation: A model to investigate the pathophysiology of rhinitis

  • Alkis Togias
    Affiliations
    Division of Clinical Immunology, Departments of Medicine and Otorynolaryngology, Johns Hopkins University School of Medicine at Good Samaritan Hospital, Baltimore, Maryland, USA
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  • Robert M. Naclerio
    Footnotes
    Affiliations
    Division of Clinical Immunology, Departments of Medicine and Otorynolaryngology, Johns Hopkins University School of Medicine at Good Samaritan Hospital, Baltimore, Maryland, USA
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  • David Proud
    Affiliations
    Division of Clinical Immunology, Departments of Medicine and Otorynolaryngology, Johns Hopkins University School of Medicine at Good Samaritan Hospital, Baltimore, Maryland, USA
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  • Claus Baumgarten
    Affiliations
    Division of Clinical Immunology, Departments of Medicine and Otorynolaryngology, Johns Hopkins University School of Medicine at Good Samaritan Hospital, Baltimore, Maryland, USA
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  • Stephen Peters
    Footnotes
    Affiliations
    Division of Clinical Immunology, Departments of Medicine and Otorynolaryngology, Johns Hopkins University School of Medicine at Good Samaritan Hospital, Baltimore, Maryland, USA
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  • Peter S. Creticos
    Affiliations
    Division of Clinical Immunology, Departments of Medicine and Otorynolaryngology, Johns Hopkins University School of Medicine at Good Samaritan Hospital, Baltimore, Maryland, USA
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  • Jane Warner
    Affiliations
    Division of Clinical Immunology, Departments of Medicine and Otorynolaryngology, Johns Hopkins University School of Medicine at Good Samaritan Hospital, Baltimore, Maryland, USA
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  • Anne Kagey-sobotka
    Affiliations
    Division of Clinical Immunology, Departments of Medicine and Otorynolaryngology, Johns Hopkins University School of Medicine at Good Samaritan Hospital, Baltimore, Maryland, USA
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  • N.Franklin Adkinson Jr.
    Affiliations
    Division of Clinical Immunology, Departments of Medicine and Otorynolaryngology, Johns Hopkins University School of Medicine at Good Samaritan Hospital, Baltimore, Maryland, USA
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  • Philip S. Norman
    Affiliations
    Division of Clinical Immunology, Departments of Medicine and Otorynolaryngology, Johns Hopkins University School of Medicine at Good Samaritan Hospital, Baltimore, Maryland, USA
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  • Lawrence M. Lichtenstein
    Correspondence
    Requests for reprints should be addressed to Dr. Lawrence M. Lichtenstein, Division of Clinical Immunology, Johns Hopkins University School of Medicine, Good Samaritan Hospital, 5601 Loch Raven Boulevard, Baltimore, Maryland 21239.
    Affiliations
    Division of Clinical Immunology, Departments of Medicine and Otorynolaryngology, Johns Hopkins University School of Medicine at Good Samaritan Hospital, Baltimore, Maryland, USA
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  • Author Footnotes
    1 Dr. Naclerio is recipient of Teacher Development Investigator Award 1K07-NS00811-01 from the National Institute of Neurological and Communicative Disorders and Stroke
    2 Dr. Peters is recipient of Clinical Investigator Award 1 K08-HL-01034 from the National Heart, Lung and Blood Institute, National Institutes of Health.
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      Abstract

      The pathogenesis of rhinitis was investigated using a model of nasal provocation with different types of stimuli. Allergic subjects had an immediate response to antigenic challenge with symptoms of rhinitis highly correlated with increments in the concentrations of histamine, prostaglandin D2, kinins and kininogens, leukotrienes, and toluene sulfonyl arginine methyl ester esterase activity in their nasal secretions. This reaction was abated by a tricyclic antihistamine also capable of inhibiting mediator release from human mast cells in vitro and, in some subjects, by disodium cromoglycate. In a number of patients, symptoms reappeared three to 12 hours after nasal provocation. This late reaction also involves release of all of the aforementioned mediators except for prostaglandin D2, and preliminary data suggest that it can be inhibited by oral or topical steroids. Cold; dry air can induce rhinitis with mast cell mediator release from selected subjects. The pathogenesis of this reaction is unclear, but there are indications that osmolarity changes are responsible for mast cell activation. Thus, mast cells can be induced to release mediators and cause nasal symptoms by both immunologic and physical mechanisms, which may account for the pathophysiology of several types of rhinitis.
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