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Effects of bβ‐endorphin on nasal allergic inflammation
Author(s) -
Baumgarten C. R.,
Schmitz P.,
O'Connor A.,
Kunkel G.
Publication year - 2002
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.2002.01284.x
Subject(s) - histamine , allergy , medicine , nasal provocation test , nasal administration , immunology , antigen , allergic inflammation , provocation test , endocrinology , mast cell , desensitization (medicine) , receptor , allergen , pathology , alternative medicine
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.