Institute for Experimental Surgery, Rostock University Medical Center, Rostock 18057, Germany.
Division of Gastroenterology, Department of Medicine II, Rostock University Medical Center, Rostock 18057, Germany.
World J Gastroenterol. 2018 Jul 28;24(28):3120-3129. doi: 10.3748/wjg.v24.i28.3120.
To evaluate the influence of hyperglycemia on the progression of autoimmune pancreatitis.
We induced hyperglycemia by repetitive intraperitoneal (ip) injection of 50 mg/kg streptozotocin in MRL/MpJ mice, which develop autoimmune pancreatitis due to a genetic predisposition. We compared the extent of inflammation (histological score, CD3 lymphocytes, CD8 T-cells, CD4 T-cells, Foxp3 T-helper cells) in the pancreas of hyperglycemic and normoglycemic mice. We also analyzed the number of leukocytes, lymphocytes, granulocytes and monocytes in the blood. In addition, we determined the percentage of CD3 lymphocytes, CD8 T-cells, CD4 T-cells, Foxp3 T-helper cells, Foxp3 CD25 T-helper and Foxp3 T-helper cells in the spleen by flow cytometry.
Treatment with streptozotocin caused a strong induction of hyperglycemia and a reduction in body weight ( < 0.001). Severe hyperglycemia did not, however, lead to an aggravation, but rather to a slight attenuation of autoimmune pancreatitis. In the pancreas, both the histological score of the pancreas as well as the number of CD3 lymphocytes ( < 0.053) were decreased by hyperglycemia. No major changes in the percentage of CD8 T-cells, CD4 T-cells, Foxp3 T-helper cells were observed between hyperglycemic and normoglycemic mice. Hyperglycemia increased the numbers of leukocytes ( < 0.001), lymphocytes ( = 0.016), granulocytes and monocytes ( = 0.001) in the blood. Hyperglycemia also moderately reduced the percentage of CD3 lymphocytes ( = 0.057), significantly increased the percentage of Foxp3 T-helper cells ( = 0.018) and Foxp3 CD25 T-helper cells ( = 0.021) and reduced the percentage of Foxp3 T-helper cells ( = 0.034) in the spleen.
Hyperglycemia does not aggravate but moderately attenuates autoimmune pancreatitis, possibly by increasing the percentage of regulatory T-cells in the spleen.
评估高血糖对自身免疫性胰腺炎进展的影响。
我们通过重复腹腔内（ip）注射 50mg/kg链脲佐菌素（streptozotocin）诱导 MRL/MpJ 小鼠发生高血糖，该模型由于遗传易感性而发生自身免疫性胰腺炎。我们比较了高血糖和正常血糖小鼠胰腺中的炎症程度（组织学评分、CD3 淋巴细胞、CD8 T 细胞、CD4 T 细胞、Foxp3 T 辅助细胞）。我们还分析了血液中的白细胞、淋巴细胞、粒细胞和单核细胞数量。此外，我们通过流式细胞术测定了脾脏中 CD3 淋巴细胞、CD8 T 细胞、CD4 T 细胞、Foxp3 T 辅助细胞、Foxp3 CD25 T 辅助细胞和 Foxp3 T 辅助细胞的百分比。
链脲佐菌素治疗导致强烈的高血糖诱导和体重减轻（<0.001）。然而，严重的高血糖并没有导致自身免疫性胰腺炎的加重，而是轻微减轻。在胰腺中，高血糖导致胰腺组织学评分和 CD3 淋巴细胞数量减少（<0.053）。高血糖和正常血糖小鼠之间 CD8 T 细胞、CD4 T 细胞、Foxp3 T 辅助细胞的百分比没有明显变化。高血糖增加了血液中的白细胞（<0.001）、淋巴细胞（=0.016）、粒细胞和单核细胞（=0.001）。高血糖还适度降低了 CD3 淋巴细胞的百分比（=0.057），显著增加了 Foxp3 T 辅助细胞的百分比（=0.018）和 Foxp3 CD25 T 辅助细胞的百分比（=0.021），并降低了 Foxp3 T 辅助细胞的百分比（=0.034）脾脏中的细胞。
高血糖不会加重自身免疫性胰腺炎，而是适度减轻，可能是通过增加脾脏中调节性 T 细胞的百分比。
