Dexamethasone inhibits plasminogen activator activity in experimental pemphigus in vivo but does not block acantholysis.

摘要: In vitro studies have suggested that autoantibody-stimulated increases in epidermal plasminogen activator (PA) may be an important pathogenetic mechanism pemphigus vulgaris (PV). We measured PA murine epidermis after i.p. injection of normal human IgG (NH IgG) and PV IgG, with without exposure to dexamethasone (DEX). BALB/c neonates received injections saline control or DEX (20 mg/kg). Twenty-four hours later, they a second single dose NH mg/gm body weight). After 24 hr, was obtained sequentially extracted 0.14 M NaCl, pH 6.8, 0.5% Triton X-100 0.1 Tris, 8.1. Epidermal assayed the Triton-Tris supernatant by two-stage colorimetric reaction expressed as milliPloug units per milligram protein (mPu/A280). animals injected 0.21 +/- 0.11 mPu/A280 (n = 8). increased cutaneous lesions 0.42 0.29 15). Treatment decreased levels both receiving 80%, 0.04 0.05 15) 0.09 0.07 7), respectively. Despite activity, all IgG-plus-DEX group had identical extensive disease, developed at same time points. This finding shows autoantibodies can stimulate PA, but reduction corticosteroids does not inhibit acantholysis vivo. There is no clear correlation between disease activity model pemphigus.