In this issue, Matsumoto et al. 1 report that histamine exocytosed from brain mast cells (MCs) after activation by antigenic cross-linking of the high affinity IgE receptor (FcεRI) acts via Hl receptors at the hypothalamus to elicit corticotropin-releasing factor (CRF). These findings reveal a homeostatic response to a pathobiologic event in the dog. Conversely, CRF can also be proinflammatory by mediating activation of tissue MCs 2. This action is implicated in the acute immobilization stress response of the rat, in which degranulation of brain MCs is associated with a histamine H2 receptor–mediated increase in permeability of the blood–brain barrier 3. These models remind us that the inflammatory response is homeostatic in principle and pathobiologic only when the same pathways lead to an outcome that is more detrimental than beneficial to the host. Thus, the elegant demonstration that...

You do not currently have access to this content.