Abstract
Pancreatitis is an inflammatory disease of unknown causes. There are many triggers causing pancreatitis, such as alcohol, common bile duct stone, virus and congenital or acquired stenosis of main pancreatic duct, which often involve tissue injuries. Pancreatitis often occurs in sterile condition, where the dead/dying pancreatic parenchymal cells and the necrotic tissues derived from self-digested-pancreas were observed. However, the causal relationship between tissue injury and pancreatitis and how tissue injury could induce the inflammation of the pancreas were not elucidated fully until now. This study demonstrates that cytosolic double-stranded DNA increases the expression of several inflammatory genes (cytokines, chemokines, type I interferon, and major histocompatibility complex) in rat pancreatic stellate cells. Furthermore, these increase accompanied the multiple signal molecules genes, such as interferon regulatory factors, nuclear factor-kappa B, low-molecular-weight protein 2, and transporter associated with antigen processing 1. We suggest that this phenomenon is a plausible mechanism that might explain how cell damage of the pancreas or tissue injury triggers acute, chronic, and autoimmune pancreatitis; it is potentially relevant to host immune responses induced during alcohol consumption or other causes.
Highlights
In 1998, star-shaped cells in the pancreas called pancreatic stellate cells (PSCs) were identified and characterized [1, 2]
We first measured the mRNA expression of DNA-dependent activator of IFN-regulatory factors (DAI) and absent in melanoma 2 (AIM2), which recognize cytosolic doublestranded DNA (dsDNA) using real-time PCR
The synthesized dsDNA used in this study had a structure similar to that of host dsDNA, and has been widely used to imitate host dsDNA that is derived from cell and tissue injury
Summary
In 1998, star-shaped cells in the pancreas called pancreatic stellate cells (PSCs) were identified and characterized [1, 2]. PSCs are quiescent and can be identified by the presence of vitamin A-containing lipid droplets in the cytoplasm. In response to pancreatic injury or inflammation, they are transformed from their quiescent phenotype into myofibroblast-like cells, which actively proliferate, express α-smooth muscle actin (α-SMA), and produce extracellular matrix components such as type I collagen [3,4,5]. The transition from quiescent to activated PSCs is triggered by various types of molecules, recent evidence suggests that components of dead/dying host cells may trigger this transition [6]. Unmethylated CpG motifs, which are expressed at high frequency in bacterial DNA, cause
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