Acute pancreatitis (AP) is one of the leading causes of hospital admission, 20% of which could progress to the severe type with extensive acinar cell necrosis. Clinical studies have reported that diabetes is an independent risk factor of the incidence of AP and is associated with higher severity than nondiabetic subjects. However, how diabetes participates in AP progression is not well defined. To investigate this question, wild-type (wt) and diabetic db/db mice at the age of 16 weeks were used in the study. AP was induced in wt recipients by 10 injections of 50 μg/kg caerulein with a 1 h interval. One hour after the last caerulein injection, bone marrow cells (BMC) isolated from wt and db/db mice were injected intraperitoneally into the recipients (cells/recipient). The recipients with no BMC injection served as controls. Thirteen hours after BMC injection, serum lipase activity was 1.8- and 1.3-folds higher in mice that received db/db BMC, compared with those with no injection and wt BMC injection, respectively ( for both). By H&E staining, the overall severity score was 14.7 for no cell injection and 16.6 for wt BMC injection and increased to 22.6 for db/db BMC injection ( for both). In particular, mice with db/db BMC injection developed more acinar cell necrosis and vacuolization than the other groups ( for both). When sections were stained with an antibody against myeloperoxidase (MPO), the density of MPO+ cells in pancreatitis was 1.9- and 1.6-folds higher than wt BMC and no BMC injection groups, separately ( for both). Quantified by ELISA, db/db BMC produced more IL-6, GM-CSF, and IL-10 compared with wt BMC ( for all). In conclusion, BMC of db/db mice produced more inflammatory cytokines. In response to acinar cell injury, diabetic BMC aggravated the inflammation cascade and acinar cell injury, leading to the progression of acute pancreatitis.

中文翻译：

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糖尿病骨髓细胞注射加速急性胰腺炎进展

急性胰腺炎 (AP) 是住院的主要原因之一，其中 20% 可能进展为严重类型，伴有广泛的腺泡细胞坏死。临床研究报告称，糖尿病是 AP 发病的独立危险因素，并且与非糖尿病受试者相比，其严重程度更高。然而，糖尿病如何参与 AP 进展尚不明确。为了研究这个问题，研究中使用了 16 周龄的野生型 (wt) 和糖尿病 db/db 小鼠。通过 10 次注射 50 μ g/kg caerulein 以 1 小时间隔在 wt 受体中诱导 AP  。最后一次注射雨蛙素后一小时，将从 wt 和 db/db 小鼠中分离的骨髓细胞 (BMC) 腹膜内注射到受体中。细胞/受体）。未注射 BMC 的受者作为对照。BMC 注射后 13 小时，接受 db/db BMC 的小鼠的血清脂肪酶活性分别比未注射和 wt BMC 注射的小鼠高 1.8 倍和 1.3 倍（对彼此而言）。通过 H&E 染色，未注射细胞的总体严重程度评分为 14.7，注射 wt BMC 为 16.6，而注射 db/db BMC 的总体严重程度评分增加到 22.6（对彼此而言）。特别是，注射 db/db BMC 的小鼠比其他组出现更多的腺泡细胞坏死和空泡形成（对彼此而言）。当切片用抗髓过氧化物酶 (MPO) 抗体染色时，胰腺炎中 MPO+ 细胞的密度分别比 wt BMC 组和未注射 BMC 组高 1.9 倍和 1.6 倍。对彼此而言）。通过 ELISA 定量，与 wt BMC 相比，db/db BMC 产生更多的 IL-6、GM-CSF 和 IL-10（对所有人）。总之，db/db 小鼠的 BMC 产生了更多的炎性细胞因子。针对腺泡细胞损伤，糖尿病BMC加重炎症级联反应和腺泡细胞损伤，导致急性胰腺炎的进展。