Acute pancreatitis is an inflammatory condition of the pancreas that can occur for many reasons, most commonly gallstones, alcohol, hypertriglyceridemia, etc. Recently, It has become one of the major causes of gastrointestinal disease-related hospital admissions. Most patients with acute pancreatitis have mild and self-limited symptoms, while as many as 20% of patients will develop a severe disease that needs intensive care monitoring and organ failure support.
Growing evidence suggests that the severity and prognosis of acute pancreatitis are associated with an uncontrolled or deregulated activation of the immune system. Injured acinar cells recruit and mediate the infiltration of immune cells (neutrophils, monocytes, and macrophages represent the majority of infiltrating cells) into the site of injury by releasing various chemokines, cytokines, and adhesion molecules. Recent data noted that damage-associated molecular patterns (DAMPs) derived from damaged cells could increase pancreatic damage and contribute to systemic inflammation by binding to Toll-like receptors or acting as immune activators. Activated neutrophils expel nuclear DNA and histones, which could enhance the immune response during acute pancreatitis by forming extracellular web-like structures called neutrophil extracellular traps (NET).
However, despite the above-mentioned understanding of advances in pathogenesis, no effective immunotherapy agents exist to treat acute pancreatitis currently. Therefore, further studies shedding light on the role of immune dysfunction during disease progression may open up new avenues for immune-modulating therapy in acute pancreatitis.
The goal of this focused research topic is to provide a forum to advance research and disseminate knowledge about the role of immune cells, chemokines, and cytokines, and their interaction in the mechanisms and treatment of progress and prognosis in acute pancreatitis. In addition, we intend to publish data on the ex-vivo and in-vivo studies on the topic.
- Immune mechanisms of pancreatic cellular injury and local and systemic complications
- Role of the adaptive immune cells (T lymphocytes, B lymphocytes, and NK cells) in the inflammatory processes occurring in acute pancreatitis
- Role of the innate immune system (such as macrophages, dendritic cells, neutrophils, and mast cells) in the inflammatory processes occurring in acute pancreatitis
- Relationship between immune response and cellular events such as impaired autophagy, impaired unfolded protein response (UPR), and various signaling pathways during acute pancreatitis
- Various immune cells (such as neutrophils, monocytes, macrophages, dendritic, and mast cells) are used as potential prognostic markers or predictors of severity
- Immune response and prevention of secondary infection of pancreatic or peripancreatic necrosis
- Treatment of pancreatitis by regulating immune responses or inhibiting pro-inflammatory cytokines
Acute pancreatitis is an inflammatory condition of the pancreas that can occur for many reasons, most commonly gallstones, alcohol, hypertriglyceridemia, etc. Recently, It has become one of the major causes of gastrointestinal disease-related hospital admissions. Most patients with acute pancreatitis have mild and self-limited symptoms, while as many as 20% of patients will develop a severe disease that needs intensive care monitoring and organ failure support.
Growing evidence suggests that the severity and prognosis of acute pancreatitis are associated with an uncontrolled or deregulated activation of the immune system. Injured acinar cells recruit and mediate the infiltration of immune cells (neutrophils, monocytes, and macrophages represent the majority of infiltrating cells) into the site of injury by releasing various chemokines, cytokines, and adhesion molecules. Recent data noted that damage-associated molecular patterns (DAMPs) derived from damaged cells could increase pancreatic damage and contribute to systemic inflammation by binding to Toll-like receptors or acting as immune activators. Activated neutrophils expel nuclear DNA and histones, which could enhance the immune response during acute pancreatitis by forming extracellular web-like structures called neutrophil extracellular traps (NET).
However, despite the above-mentioned understanding of advances in pathogenesis, no effective immunotherapy agents exist to treat acute pancreatitis currently. Therefore, further studies shedding light on the role of immune dysfunction during disease progression may open up new avenues for immune-modulating therapy in acute pancreatitis.
The goal of this focused research topic is to provide a forum to advance research and disseminate knowledge about the role of immune cells, chemokines, and cytokines, and their interaction in the mechanisms and treatment of progress and prognosis in acute pancreatitis. In addition, we intend to publish data on the ex-vivo and in-vivo studies on the topic.
- Immune mechanisms of pancreatic cellular injury and local and systemic complications
- Role of the adaptive immune cells (T lymphocytes, B lymphocytes, and NK cells) in the inflammatory processes occurring in acute pancreatitis
- Role of the innate immune system (such as macrophages, dendritic cells, neutrophils, and mast cells) in the inflammatory processes occurring in acute pancreatitis
- Relationship between immune response and cellular events such as impaired autophagy, impaired unfolded protein response (UPR), and various signaling pathways during acute pancreatitis
- Various immune cells (such as neutrophils, monocytes, macrophages, dendritic, and mast cells) are used as potential prognostic markers or predictors of severity
- Immune response and prevention of secondary infection of pancreatic or peripancreatic necrosis
- Treatment of pancreatitis by regulating immune responses or inhibiting pro-inflammatory cytokines
