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Inhibition of substance P-induced histamine release from rat peritoneal mast cells by low doses of protoporphyrin plus long-wave ultraviolet light irradiation: decreased intracellular calcium as a possible mechanism

Authors


Kurosawa Head, Division of Allergy and Clinical Immunology, Department of Dermatology, Gunma University School of Medicine, 3–39–15 Showa – machi, Maebashi 371, Japan.

Abstract

Background

A considerable amount of recent interest has been devoted to the down-regulatory effects of photosensitizers plus long-wave ultraviolet light (UVA) irradiation on multiple biologic systems. However, these effects on mast cells are controversial.

Objective

We have investigated the effect of low doses of protoporphyrin (PP) plus UVA irradiation (PP/UVA) on substance P (SP)-induced histamine release from rat mast cells.

Methods

Rat peritoneal mast cells purified on a Percoll gradient were treated with 3 ng/mL PP and/or UVA, and challenged with SP. In some experiments, IgE-sensitized mast cells were stimulated by antirat IgE in the presence of phosphatidylserine. Histamine released from mast cells and intracellular calcium concentrations ([Ca2+]i) were measured, respectively.

Results

SP at a concentration of 10−5 mol/L caused a significant histamine release with the increase in [Ca2+]i. PP or UVA irradiation alone at doses used in the present study induced no histamine release from mast cells and had no significant effects on SP-induced histamine release from the cells. On the other hand, PP/UVA inhibited SP-induced histamine release in a dose-dependent manner of UVA with the reduction of SP-induced maximal increases in [Ca2+]i. Comparing with the inhibitory effects of PP/UVA on anti-IgE-induced histamine release from IgE-sensitized mast cells and maximal increases in [Ca2+]i in the cells, the inhibitory effects of PP/UVA on the findings in SP-stimulated mast cells were less.

Conclusion

These data suggest that low doses of PP/UVA inhibits histamine release from SP-activated rat peritoneal mast cells through the suppression of [Ca2+]i.

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