Histamine secretion from human skin slices induced by anti‐IgE and artificial secretagogues and the effects of sodium cromoglycate and salbutamol

Abstract

Human cutaneous mast cells show functional differences from their counterparts in other tissues. Following passive sensitization with 1% atopic serum for 30 min at 37° C human skin slices released histamine after challenge with anti‐human IgE in a concentration dependent manner. Maximum release of 14 ± 2%, was achieved with a 1/10 dilution of anti‐IgE. Passive sensitization with 10% atopic serum increased the secretory response to anti‐IgE but histamine release was only concentration related over the entire 1/1000 to 1/10 dilution range in half of the specimens studied, the remainder showing high dose tolerance to anti‐IgE, Negligible histamine release occurred with anti‐IgE challenge of slices which had not been passively sensitized. The histamine releasing ability of A23187 in human skin slices was similar to that observed in lung and adenoidal mast cells being concentration dependent over the range 0‐1 3 μM with a maximum release of 25 ±3%. In contrast to human lung and adenoidal mast cells, poly‐L‐lysine and compound 48/80 induced histamine release from skin slices. Poly‐L‐lysine induced a concentration‐dependent release of histamine over the range 0‐01‐10 mUM with a maximum of 27 ± 3%. The response to compound 48/80 was variable, releasing in some but not all specimens. Histamine release caused by anti‐IgE. A23187 and poly‐L‐lysine was shown to be dependent upon extracellular calcium while release stimulated by compound 48/80 was calcium independent. The chemotactic peptide, formyl‐methionyl‐leucyl‐phenylalanine, over the range 0.01 10 μM failed to release histamine from skin slices. Sodium cromoglycate (100 1000 μM) failed to inhibit histamine release and the β‐adrenoceptor stimulant salbutamol (1‐10 μM) showed only weak activity at the lowest of three different concentrations of anti‐IgE used for challenge.