Mast cells of human skin, but not lung, adenoids, tonsils, or intestine, release histamine in response to substance P, vasoactive intestinal polypeptide, and somatostatin. The substance P receptor of skin mast cells is not of the NK-1, NK-2 or NK-3 subtypes of smooth muscle. Time course and calcium dependency of release by peptides differed from anti-IgE. With anti-IgE, the molar ratios of histamine:PGD2:LTC4 generated by skin mast cells was 1,000:25:2, whereas with substance P these ratios were 1,000:1:0.1. Similar results were obtained with the other neuropeptides. The ability of peptides to stimulate skin mast cell histamine release suggests a mechanism whereby their release from dermal nerve endings is coupled to changes in micro-vasculature.
A technique is described for the enzymatic dispersion of mast cells in high yield from human infant foreskin. Dispersed mast cells exhibit high viability as assessed by light microscopy, low spontaneous histamine release, and survival in culture. Dispersed mast cells release histamine in response to immunological stimulation and synthetic secretagogues including ionophore A23187, compound 48/80 and poly-L-lysine. Reactivity to these stimuli indicates that cutaneous mast cells differ in their properties from human pulmonary mast cells.
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