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Original Article |
Correspondence to: Itsuro Matsumoto, Dept. of Physiology, Nagasaki University School of Medicine, Nagasaki 852, Japan. Tel:81-95-849-7031 Fax:81-95-849-7036 E-mail:matu-itu{at}net.nagasaki-u.ac.jp.
Mast cells perform a significant role in the host defense against parasitic and some bacterial infections. Here we show that in the dog, degranulation of brain mast cells evokes hypothalamic-pituitary-adrenal responses via histamine release. A large number of mast cells were found in a circumscribed ventral region of the hypothalamus, including the pars tuberalis and median eminence. When these intracranial mast cells were passively sensitized with immunoglobulin E via either the intracerebroventricular or intravenous route, there was a marked increase in the adrenal cortisol secretion elicited by a subsequent antigenic challenge (whether this was delivered via the central or peripheral route). Comp.48/80, a mast cell secretagogue, also increased cortisol secretion when administered intracerebroventricularly. Pretreatment (intracerebroventricularly) with anti-corticotropin–releasing factor antibodies or a histamine H1 blocker, but not an H2 blocker, attenuated the evoked increases in cortisol. These data show that in the dog, degranulation of brain mast cells evokes hypothalamic-pituitary-adrenal responses via centrally released histamine and corticotrophin-releasing factor. On the basis of these data, we suggest that intracranial mast cells may act as an allergen sensor, and that the activated adrenocortical response may represent a life-saving host defense reaction to a type I allergy.
Key Words: hypersensitivity, immunoglobulin E, histamine, corticotropin-releasing factor, adrenal cortisol secretion
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