J Clin Invest. 2021 Feb 1;131(3). doi: 10.1172/JCI146210.
Due to progressive inflammation, chronic pancreatitis destroys both the exocrine and endocrine pancreas and sensitizes pancreatic nerves, leading to unremitting pain. Unfortunately, there are no treatments for pancreatic inflammation and approaches to ameliorate pain are suboptimal. Pancreatic inflammation is particularly problematic because damage to acinar cells causes local release of digestive enzymes, which initiate pancreatic autodigestion. The combination of autodigestion and inflammation is unique to pancreatitis and undoubtedly contributes to the difficulty in devising effective treatments. In this issue of the JCI, Saleh et al. describe a nonsurgical technique to ablate pancreatic acinar cells, thus eliminating the source of digestive enzymes and preventing autodigestion. In mice and a nonhuman primate model, this approach effectively reduced inflammation and pain while preserving islet cell function. These findings support the concept that ongoing acinar cell damage is at the root of chronic pancreatitis and provide a possible strategy for clinical treatment.
由于炎症的不断进展，慢性胰腺炎会破坏外分泌腺和内分泌腺，并使胰腺神经敏化，导致持续的疼痛。不幸的是，目前还没有针对胰腺炎症的治疗方法，而改善疼痛的方法也不尽如人意。胰腺炎症尤其成问题，因为腺泡细胞的损伤会导致局部释放消化酶，从而引发胰腺自身消化。这种自身消化和炎症的结合是胰腺炎所特有的，无疑对制定有效的治疗方法造成了困难。在本期 JCI 中，Saleh 等人描述了一种非手术技术来消融胰腺腺泡细胞，从而消除消化酶的来源并防止自身消化。在小鼠和非人类灵长类动物模型中，这种方法有效地减轻了炎症和疼痛，同时保留了胰岛细胞的功能。这些发现支持了持续的腺泡细胞损伤是慢性胰腺炎的根源这一概念，并为临床治疗提供了一种可能的策略。
