急性胰腺炎的免疫发病机制

Immunopathogenesis of acute pancreatitis

急性胰腺炎一直是基础与临床医学研究的热点与难点,传统观点认为由于腺泡细胞内基因或环境异常,导致腺泡细胞损伤,进而引发胰腺内炎症反应。最近研究表明,尽管胰蛋白酶原激活可能是急性胰腺炎炎症反应重要的启动因素,但持续的炎症反应与损伤相关分子模式相关的细胞因子的激活、核因子-κB活化、细胞坏死及凋亡、肠道微生物易位等密切相关。核苷结合的寡聚作用域1的激活在核因子-κB和Ⅰ型干扰素的激活与产生中也发挥着重要作用。本文就急性胰腺炎最新免疫发病机制的研究进展作一综述。

Acute pancreatitis has been a hotspot and difficulty in basic and clinical medical research.Conventional viewpoint is that acinar cells are damaged due to abnormal gene or environment in the acinar cells,which triggers an inflammatory reaction in the pancreas.Recent studies have shown that although trypsinogen activation may be an important trigger for inflammatory responses in acute pancreatitis,but the continuous inflammatory response is closely related to the activation of cytokines associated with damage-associated molecular patterns,nuclear factor kappa B activation,cell necrosis and apoptosis,and intestinal microbial translocation.The activation of the nucleoside-binding oligomerization domain 1(NOD1)also has a critical role in the activation and production of nuclear factor kappa B and typeⅠinterferon.We reviews the latest immunopathogenesis of AP in this review.