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Scleroderma-like remodeling induced by type V collagen.

Authors
  • Bezerra, Mailze Campos
  • Teodoro, Walcy Rosolia
  • de Oliveira, Cristiane Carla
  • Velosa, Ana Paula Pereira
  • Ogido, Luciana Tsuzuki Ichicawa
  • Gauditano, Giancarla
  • Parra, Edwin Roger
  • Capelozzi, Vera Luiza
  • Yoshinari, Natalino Hajime
Type
Published Article
Journal
Archives of dermatological research
Publication Date
Jul 01, 2006
Volume
298
Issue
2
Pages
51–57
Identifiers
PMID: 16710740
Source
Medline
License
Unknown

Abstract

Recently, we discovered that New Zealand rabbits immunized with human type V collagen plus Freund's adjuvant present fibrosis and vasculitis of organs usually affected by systemic sclerosis. In this way, we studied the fibrillogenesis process to identify possible factors involved in altered remodeling observed in this scleroderma-like model. Additionally, we have done a very preliminary comparison with human skins obtained from scleroderma patients (n=3). Female New Zealand rabbits (n=10) were immunized subcutaneously with two doses of 1 mg collagen V (COL V) plus complete Freund's adjuvant for a 30-day interval, followed by two additional intramuscular booster immunizations in incomplete Freund's adjuvant for a 15-day interval. Animals from control group (n=10), were only inoculated with complete and incomplete Freund's adjuvant given at same conditions of COL V. Histological analysis of skins from animals and patients were done by Masson's trichrome staining, and immunofluorescence method to detect collagen fibers and interactions of types I, III and V collagen in the remodeling process. The analysis of animal skins showed collagen fibril deposits in the dermis after 7 days of sensibilization and an increase in these deposits after 75 and 120 days, respectively. Skin thickness and atrophy of sebaceous and sweat glands were progressively more intense in late sacrificed animals and correlated with increased amount of collagen deposition. Surprisingly, type V collagen was overexpressed both in animals and patients, forming dense and atypical collagen fibers in the dermis. We suggest that this anomalous expression of morphologically different type V collagen could justify the remodeling observed in scleroderma plaque.

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