Mast Cells, Pancreatic Stellate Cells, and Telocytes in Chronic Pancreatitis: Ultrastructural Study

Pancreatic inflammation and subsequent fibrosis drive serious disease complications. However, the pathogenesis of this process and the mechanisms underlying excessive extracellular matrix (ECM) deposition remain poorly understood. Our aim was to study intercellular interactions and ultrastructural changes in mast cells, pancreatic stellate cells, and telocytes, as well as in the extracellular matrix in various degrees of pancreatic fibrosis. Histological, immunohistochemical, and electron microscopic (EM) studies were performed on surgical materials from 17 patients. Mapping of fibrosis fields was performed on scanned images using the QuPath software v0.6.0. The IHC study was performed using a panel of antibodies: CD34, CD117, and SMA. Fluorescent IHC was performed using a panel of antibodies: CD34 and CD117. The EM study was performed on ultrathin sections with a thickness of 100-120 nm. The functional activity of mast cells (MCs) increased in pancreatic fibrosis. Most of the MCs were in a degranulation state, with the formation of intercellular contacts. The activation of pancreatic stellate cells (PaSCs), which underwent ultrastructural and functional changes in pancreatic fibrosis that developed as a result of chronic pancreatitis (CP), was noted. Multiple plasmolemma discontinuities, telopode shortenings, and nuclear fragmentations were observed among telocytes (TCs). The presence of MCs in the inflammatory infiltrate, as well as the destruction of TCs with the activation of exosomal transport, plays an important role in the pathogenesis of fibrosis in CP and provides a promising therapeutic target for the treatment of this pathology.