Alterations in the dynamics of inflammation, proliferation and apoptosis in subcutaneous implants of lupus-prone mice
Paula P. Campos1, Anilton C. Vasconcelos2, Mônica A.N.D. Ferreira2 and Silvia P. Andrade1
1Departments of Physiology and Biophysics and 2General Pathology of the Institute of Biological Sciences, Federal University of Minas Gerais/Brazil.
Offprint requests to: Silvia Passos Andrade, Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais (UFMG), Av. Antônio Carlos, 6627, Campus Pampulha, CEP 31.270-901, Belo Horizonte - Minas Gerais – Brazil. e-mail: andrades@icb.ufmg.br
Summary. Wound repair is a complex process that involves inflammation, proliferation, extracellular matrix deposition/remodeling and apoptosis. Autoimmune diseases profoundly affect the healing process. We have used histological parameters to characterize the recruitment of mast cells and the proliferative activity and apoptosis in the fibrovascular tissue induced by subcutaneous polyether-polyurethane sponge implants in lupus-prone New Zealand White (NZW) and in control Balb/c mouse strains at days 10 and 21 post implantation. Fibrovascular tissue infiltration (hematoxylin and eosin staining), mast cell number (Dominici staining) and cellular proliferation (AgNOR staining) peaked early (day 10) but collagen deposition (picrosirius red staining) and apoptosis remained high in implants of NZW mice during the experimental period. In contrast, implants of Balb/c animals showed a progressive increase in mast cell recruitment and cellular proliferation but apoptosis fell from day 10 to 21 post-implantation. This divergent response early mast cells recruitment, excessive collagen deposition and disturbed removal of apoptotic cells from the site of injury in NZW mice implies that the genotype trait of NZW mice is a determining factor in abnormal healing response. Histol Histopathol 26, 433-442 (2011)
Key words: Mast cells, Collagen deposition, AgNOR, Fibrovascular tissue
DOI: 10.14670/HH-26.433