[Modeling of pemphigus vulgaris in guinea pigs]. / Modelirovanie vul'garnoi puzyrchatki na gvineiskikh svinkakh.

In 146 guinea pigs with body weight of 150-200 g pemphigus vulgaris (PV) was induced using screening techniques. The animals were injected with PV patients' IgG (IgGPV) and blister fluid (PVBF) with the PV patient mononuclears. Intraperitoneal administration of IgGPV caused dystrophy in epidermis of experimental animals while intracutaneous injection of PVBF resulted in balloon dystrophy. Clinical manifestations of -PV were obtained after two-day intraperitoneal IgGPV administration in a total dose of 1.5 g (6 mg/g) following a cycle of intracutaneous injections of 2.0 ml PVBF in 10-15 sites of guinea pig back. The presence of acantholysis, intraepidermal localization of blisters, pemphigus antibodies fixation on spinous cell surface, and almost 100% mortality of experimental animals were the major criteria for the developed model of PV in guinea pigs. Experimental PV in guinea pigs was abolished due to treatment of PVBF with dexamethasone, contrykal, heating (56 degrees C, 30 min), preincubation with human skin samples, and PVBF cell-free supernatant application. The conclusion was made that for occurrence of pemphigus in laboratory animals a combined effect of pemphigus antibodies, sensitized mononuclears, complement and endogenous proteinases is required.

[The role of kallikrein-kinin system components in the pathogenesis of bullous skin lesions in pemphigus and pemphigoid]. / Znachenie komponentov kallikrein-kininovoi sistemy v patogeneze puzyrnykh porazhenii kozhi pri puzyrchatke i pemfigoide.

Importance of kallikreinogenases in acantholysis and epidermo-dermal separation was shown, when the kallikreinkinin patterns were studied in blood plasma and blister fluids of 118 patients with pemphigus, of 78 patients with pemphigoid as well as of 224 guinea pigs. Under conditions of pemphigoid, as distinct from pemphigus, serine proteinases were mainly produced by active immunocytes responsible for destruction of epidermal basement membrane; activation of kinins was observed in skin impairments.