Mast cell tryptase and chymase are potential regulators of neurogenic inflammation in psoriatic skin
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Updated: Aug 17, 2026

Investigating Mast Cell Secretory Granules; from Biosynthesis to Exocytosis
Published on: January 26, 2015
A Naukkarinen1, I T Harvima, M L Aalto
1Department of Pathology, University of Kuopio, Finland.
Background:
Tryptase and chymase are proteinases present only in mast cells. In psoriatic lesions, mast cells are increased in number. Certain neuropeptides are also more abundant in lesional than nonlesional psoriatic skin. Based on some earlier results as well as the results of the present study, a hypothesis is presented concerning the regulatory action of mast cell tryptase and chymase on neuropeptides in psoriatic inflammation.
Methods:
Forty patients were biopsied, 13 for a mature psoriatic plaque and 9 patients of 27 for a developing (1-3 weeks) psoriatic lesion induced by tape stripping (Koebner reaction). Each lesion had its nonlesional control from the same patient. Mast cell tryptase and chymase, and the neuropeptides Substance P (SP) vasoactive intestinal polypeptide (VIP), and calcitonin-gene-related peptide (CGRP) were stained by enzyme- and immunohistochemical methods. Morphological contacts between mast cells and neuropeptides were visualized using double stains and quantitated in the upper dermis.
Results:
As the lesion aged, MCTC mast cells displaying tryptase activity increased in number, whereas chymase activity in these cells decreased. All neuropeptides showed some increase along with the development of the lesion, but SP was most abundant in mature lesions. Substance P-positive nerves had also more contacts with mast cells compared to VIP- or CGRP-containing fibers, the contact count being highest in mature lesions.
Conclusions:
Tryptase is known to degrade VIP and CGRP, but not SP. Chymase is capable of cleaving both SP and VIP, but is rendered partially inactive in psoriatic skin. These data together with the results of the present study strongly suggest that SP has potency to act as an important mediator in different stages of the psoriatic inflammation.
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