Induction of late cutaneous reaction by kallikrein injection: comparison with allergic-like late response to compound 48/80.

Although IgE antibody is able to provoke a late cutaneous allergic response (LCAR), the mechanism of its development is not clear. It seems to involve vasoactive and clotting mediators released from mast cells and basophils. Substances biologically similar to plasma kallikrein (KK), a Hageman factor activator, have been shown to be released by basophils in the course of an IgE-dependent reaction. Because compound 48/80 induces LCAR-like responses in the skin, we compared the ability of tissue KK and compound 48/80 to induce late cutaneous reactions (LCRs). All 40 test subjects showed an immediate wheal and flare reaction (WF) after both KK and 48/80. The WF was followed by an LCR characterized by diffuse edema, pain, and erythema in 36 of 40 subjects with 48/80 and 26 of 40 with KK. The LCRs evoked by the two agents did not differ in their appearance or in their time of development. These reactions increased until the 5 hr mark, began to decrease at the 10 hr mark, and were gone after 24 hr. Histologic study showed edema and a mixed cell infiltration with fibrin deposition. Challenge of the original injection site and a new site after 1 or 2 wk showed a local refractory state lasting 2 wk. Prednisone almost totally suppressed the LCRs induced by both KK and 48/80.