Abstract
Urticaria is characterized by wheal and flare, which usually disappear within several hours. However, there are some cases with severe and/or prolonged eruptions lasting more than 24 hours and resistant to treatments by ordinary histamine antagonists. Histology of such cases accompanies various cell infiltrations, such as eosinophils and neutrophils. In order to know the mechanism of such infiltrations, we studied the release of chemotactic activities from skin slices for neutrophils and eosinophils. The factor was identified with LTB4 by HPLC analysis and released either by antigens or substance P. Moreover, studies with skin chambers on patients with chronic urticaria revealed spontaneous release of substance P, suggesting the involvement of neuropeptides in the pathogenesis of chronic urticaria. Incubation of skin slices with dexamethasone scarcely inhibited histamine release, but almost abolished release of LTB4 in response to antigens. Recently-developed histamine H1-antagonists, called anti-allergic drugs, inhibited both degranulation and TNFα releases from rat mast cell (RBL-2H3) line, but concentrations required to inhibit TNFα release was about one tenth of those to inhibit degranulation. Inhibition of LTB4 and TNFα from mast cells may partially account for clinical efficacy of corticosteroids and some anti-allergic drugs for treatment of chronic idiopathic urticaria.
