The distribution of mast cells (MCs) containing tryptase (T) and chymase (C) was studied in the non-lesional and lesional skin of 26 patients with atopic dermatitis (AD) and 23 patients with non-atopic nummular eczema (NE), and in the skin of eight healthy controls. T and C activities were demonstrated enzymehistochemically using Z-Gly-Pro-Arg-MNA and Suc-Val-Pro-Phe-MNA as substrates, respectively. The T- and C-containing MCs were counted separately in the epidermis, in contact with the basement membrane, in the papillary dermis and in different dermal levels (0.2 mm each). Also, the C protein was determined immunohistochemically.
T-positive MCs were similarly distributed in non-lesional and lesional skin of both AD and NE. The MC number was relatively high in the upper dermis (papillary dermis and levels I and II) of non-lesional and lesional skin of AD. In the upper dermis of non-lesional AD and NE skin and in normal skin, about 50% of T-positive MCs displayed C activity, whereas the percentage in lesional AD and NE skin was only about 30%. In this respect, the non-lesional and lesional samples differed significantly from each other in both dermatoses (in AD p = 0.003; in NE p = 0.002, Students' t-test).
In all samples the MC number decreased in the deeper dermal levels, although numerous T-containing MCs were still counted in the deeper dermis (dermal levels IV-VII) of lesional AD and NE skin, differing significantly from the MC number in normal skin (in AD p = 0.005, in NE p = 0.041). In the deeper dermis, the percentage of MCs containing active C was about 70% in non-lesional and lesional AD and NE, and about 90% in normal healthy skin. However, in the upper dermis of non-lesional and lesional skin of both AD and NE, about 80% of all MCs contained the C protein, which differed significantly from the value of 100% in normal skin (p<0.05).
In conclusion, the increased number of T-positive MCs in the upper dermis of non-lesional and lesional AD contributes to promoting inflammation. C apparently loses its activity in the upper dermis of lesional AD and especially in NE. Thus, the enzyme partially lacks its capability to suppress inflammation, such as degradation of neuropeptides and proteins. The dysregulation of these proteinases exists already in non-lesional skin of AD and NE.