• Find People
  • Campus Map
  • PiratePort
  • A-Z
    • About
    • Submit
    • Browse
    • Login
    View Item 
    •   ScholarShip Home
    • Division of Health Sciences
    • Brody School of Medicine
    • Emergency Med
    • View Item
    •   ScholarShip Home
    • Division of Health Sciences
    • Brody School of Medicine
    • Emergency Med
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of The ScholarShipCommunities & CollectionsDateAuthorsTitlesSubjectsTypeDate SubmittedThis CollectionDateAuthorsTitlesSubjectsTypeDate Submitted

    My Account

    Login

    Statistics

    View Google Analytics Statistics

    Neurogenic switching: a hypothesis for a mechanism for shifting the site of inflammation in allergy and chemical sensitivity.

    Thumbnail
    View/ Open
    Neurogenic Switching.pdf (2.515Mb)

    Show full item record
    Author
    Meggs, William J.
    Abstract
    Neurogenic switching is proposed as a hypothesis for a mechanism by which a stimulus at one site can lead to inflammation at a distant site. Neurogenic inflammation occurs when substance P and other neuropeptides released from sensory neurons produce an inflammatory response, whereas immunogenic inflammation results from the binding of antigen to antibody or leukocyte receptors. There is a crossover mechanism between these two forms of inflammation. Neurogenic switching is proposed to result when a sensory impulse from a site of activation is rerouted via the central nervous system to a distant location to produce neurogenic inflammation at the second location. Neurogenic switching is a possible explanation for systemic anaphylaxis, in which inoculation of the skin or gut with antigen produces systemic symptoms involving the respiratory and circulatory systems, and an experimental model of anaphylaxis is consistent with this hypothesis. Food-allergy-iducing asthma, urticaria, arthritis, and fibromyalgia are other possible examples of neurogenic switching. Neurogenic switching provides a mechanism to explain how allergens, infectious agents, irritants, and possibly emotional stress can exacerbate conditions such as migraine, asthma, and arthritis. Because neurogenic inflammation is known to be triggered by chemical exposures, it may play a role in the sick building syndrome and the multiple chemical sensitivity syndrome. Thus neurogenic switching would explain how the respiratory irritants lead to symptoms at other sites in these disorders. Originally published Environ Health Perspect Vol. 103, No. 1, 1995.
    URI
    http://hdl.handle.net/10342/3055
    Subject
     Allergies; Anaphylaxis; Arthritis; Asthma; Chemical sensitivity; Food allergy; Inflammation; Migraine; Neurogenic inflammation; Substance p 
    Date
    1995-01
    Citation:
    APA:
    Meggs, William J.. (January 1995). Neurogenic switching: a hypothesis for a mechanism for shifting the site of inflammation in allergy and chemical sensitivity.. , (. Retrieved from http://hdl.handle.net/10342/3055

    Display/Hide MLA, Chicago and APA citation formats.

    MLA:
    Meggs, William J.. "Neurogenic switching: a hypothesis for a mechanism for shifting the site of inflammation in allergy and chemical sensitivity.". . . (.), January 1995. February 26, 2021. http://hdl.handle.net/10342/3055.
    Chicago:
    Meggs, William J., "Neurogenic switching: a hypothesis for a mechanism for shifting the site of inflammation in allergy and chemical sensitivity.,"  , no. (January 1995), http://hdl.handle.net/10342/3055 (accessed February 26, 2021).
    AMA:
    Meggs, William J.. Neurogenic switching: a hypothesis for a mechanism for shifting the site of inflammation in allergy and chemical sensitivity.. . January 1995; () . http://hdl.handle.net/10342/3055. Accessed February 26, 2021.
    Collections
    • Emergency Med
    Publisher
    East Carolina University

    xmlui.ArtifactBrowser.ItemViewer.elsevier_entitlement

    East Carolina University has created ScholarShip, a digital archive for the scholarly output of the ECU community.

    • About
    • Contact Us
    • Send Feedback