Cytokines and Fibrogenesis

Proinflammatory cytokines, such as IL-1, TNF-a, IL-6, MIP-1, PDGF, and transforming growth factor-beta 1 (TGF-^1), are expressed by inflammatory cells such as neutrophils, lymphocytes, and macrophages, and also by cen-troacinar duct cells, endothelial cells, and fibroblasts [16]. Pancreatic stellate cells are stimulated by those cytokines and then transform into myofibroblasts, crucial players in pancreatic fibrosis. Myofibroblasts also express many cytokines, growth factors and chemokines and their receptors [17]. TGF-P may

Fig. 1. Typical histology of interlobular fibrosis and intralobular fibrosis. Chronic alcoholic pancreatitis shows fibrosis between nodular pancreatic lobules with wide deposition of collagenous matrix (a), while chronic obstructive pancreatitis shows fibrosis in and around the destructive pancreatic lobules with inflammatory cells (b).

Fig. 1. Typical histology of interlobular fibrosis and intralobular fibrosis. Chronic alcoholic pancreatitis shows fibrosis between nodular pancreatic lobules with wide deposition of collagenous matrix (a), while chronic obstructive pancreatitis shows fibrosis in and around the destructive pancreatic lobules with inflammatory cells (b).

a play an important role in pancreatic fibrogenesis [18, 19]. The source of TGF-P in damaged tissue may be from neutrophils, epithelial cells, parenchymal cells or myofibroblasts [11]. This indicates the important role of autocrine and paracrine mechanisms in chronic pancreatitis and fibrosis.

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