Mast cells and pancreatic stellate cells in chronic pancreatitis with differently intensified fibrosis

BACKGROUND/AIMS: The pathogenesis of pancreatic fibrosis is unknown. Pathogenic analyses take into account the effect of oxidant stress and the increase in free radicals leading to degranulation of mast cells, which may cause inflammation and activate fibrosis. Activated pancreatic stellate cells produce abnormal components of intercellular substance and are responsible for pancreatic fibrogenesis. The aim of the study was to determine the correlation between the presence and state of mast cells and pancreatic stellate cells activation in chronic pancreatitis with varied intensity fibrosis. METHODOLOGY: We studied 27 patients with chronic pancreatitis of varied fibrosis intensity. Immunohistochemical reactions for mast cells (anti-human mast cell tryptase) and ultrastructural analyses of mast cells and pancreatic stellate cells were performed. The number of degranulated mast cells in the ultrastructural picture and the number of pancreatic stellate cells stained positive for vimentin and alpha-smooth muscle actin were counted. RESULTS: A significant increase was revealed in the number of degranulated mast cells--to 35.6% in chronic pancreatitis I degree fibrosis, 68.3% in II degree, 75.1% in III degree and IV degree (control 10.2%) and a parallel increase in the number of activated pancreatic stellate cells (stained positive for alpha-smooth muscle actin) to 328 +/- 29/mm2 in I degree fibrosis, to 978 +/- 67/mm2 in II degree and 2355 +/- 331/mm2 in III degree and IV degree (control 38.8 +/- 9/mm2). CONCLUSIONS: The increase in the number of activated pancreatic stellate cells parallel to the increase in degranulated mast cells in more pronounced pancreatic fibrosis suggests that mast cell-released chemical mediators are involved in pancreatic stellate cells activation.