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Clinical & Experimental Allergy

Effects of bβ-endorphin on nasal allergic inflammation

Authors

  • C. R. Baumgarten,

    Corresponding author
    1. Charité, Campus Virchow-Klinikum, Allergy and Asthma Clinic, Humboldt University, Berlin, Germany
      Claus R. Baumgarten, Charité, Campus Virchow-Klinikum, Allergy and Asthma Clinic, Humboldt University Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. E-mail: claus.baumgarten @charite.de
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  • P. Schmitz,

    1. Charité, Campus Virchow-Klinikum, Allergy and Asthma Clinic, Humboldt University, Berlin, Germany
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  • A. O'Connor,

    1. Charité, Campus Virchow-Klinikum, Allergy and Asthma Clinic, Humboldt University, Berlin, Germany
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  • G. Kunkel

    1. Charité, Campus Virchow-Klinikum, Allergy and Asthma Clinic, Humboldt University, Berlin, Germany
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Claus R. Baumgarten, Charité, Campus Virchow-Klinikum, Allergy and Asthma Clinic, Humboldt University Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. E-mail: claus.baumgarten @charite.de

Abstract

Background πβ-endorphin is a derivative of pro-opiomelanocortin. Cells of the immune system can also synthesize and secrete β-endorphin. Its concentration is increased during the allergic reaction and during stress. Increased reactivity during psychological stress of allergic subjects is also well known.

Objective Is β-endorphin one physiological link between stress and an exacerbation of the allergic reaction?

Methods First, intranasal β-endorphin challenges with subsequent lavages to determine histamine and albumin levels and measurements of nasal flow and resistance in dose-response and time course experiments were performed. Secondly, we examined whether β-endorphin pre-treatment increased the antigen-induced release of histamine and albumin in nasal lavages and the clinical symptoms.

Results Exogenous β-endorphin (100 pM−10 µM/mL) induced a dose-dependent increase in nasal symptoms in asymptomatic allergic subjects with rhinitis (n = 14) as well as in non-allergic controls (n = 10), but did not release any mediators into nasal secretion. However, comparing the antigen-evoked release of mediators into nasal secretions with that of a β-endorphin pre-treated antigen challenge we could note a significant enhancement of human serum albumin influx (P < 0.05) and histamine liberation (P < 0.05) 10 min after antigen challenge compared with the allergen challenge alone, with also a correlation with the more pronounced decrease in nasal flow (P < 0.05).

Conclusion These results suggest that β-endorphin-induced increase in nasal congestion is mediated through direct neuroendocrine receptor activation independent of mast cell activation and that during the allergic reaction there is a β-endorphin/mast cell interaction that enhances the mediator response to nasal allergen challenge.

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