Meriläinen Sanna, Mäkelä Jyrki, Jensen Hanna Alaoja, Dahlbacka Sebastian, Lehtonen Siri, Karhu Toni, Herzig Karl-Heinz, Kröger Meeri, Koivukangas Vesa, Koskenkari Juha, Ohtonen Pasi, Karttunen Tuomo, Lehenkari Petri, Juvonen Tatu
Department of Surgery, Oulu University Hospital, Oulu, Finland.
Scand J Gastroenterol. 2012 Nov;47(11):1375-85. doi: 10.3109/00365521.2012.722675. Epub 2012 Sep 7.
Cytokines initiate and modify systemic inflammatory response in early acute pancreatitis. The aim of this study was to analyze which cytokines are released from the pancreas to portal venous blood in the early phase of acute experimental necrotizing and oedematous pancreatitis and which of those cytokines are correlated with the more severe form of the disease.
Fifteen pigs were randomized to develop mild oedematous pancreatitis (n = 5, saline infusion to pancreatic duct), severe necrotizing pancreatitis (n = 5, taurocholic acid infusion) along with a control group (n = 5). Arterial and venous blood samples were drawn and cytokine levels were measured from portal vein blood at 0, 120, 240 and 360 min after the induction of pancreatitis. Tissue samples from the pancreas were harvested at 0 and 360 min.
White blood cell count increased in necrotizing pancreatitis and the control group. The amount of neutrophils increased (p < 0.001) and the lymphocyte and eosinophil counts decreased in all groups (p < 0.001, p < 0.001). The monocyte count, as well as PDGF and IL-6 concentrations, increased only in necrotizing pancreatitis. IL-8 and eotaxin increased both in oedematous and necrotizing pancreatitis. MCP-1 increased in all groups. IL-9, IL-4, MIP-1α, IFN- γ concentrations did not change. Eotaxin and MCP-1 plasma levels from a previous series between portal venous and pulmonary arterial blood were not significantly different.
The initial inflammatory process was diverse in oedematous and necrotizing pancreatitis. Increased monocyte count in combination with elevated PDGF and IL-6 are characteristic of necrotizing pancreatitis in our model.
细胞因子在早期急性胰腺炎中启动并改变全身炎症反应。本研究旨在分析在急性实验性坏死性和水肿性胰腺炎早期,哪些细胞因子从胰腺释放至门静脉血中,以及这些细胞因子中哪些与更严重的疾病形式相关。
15只猪被随机分为三组,分别为轻度水肿性胰腺炎组(n = 5,向胰管内注入生理盐水)、严重坏死性胰腺炎组(n = 5,向胰管内注入牛磺胆酸)以及对照组(n = 5)。在诱导胰腺炎后的0、120、240和360分钟采集动脉和静脉血样,并测定门静脉血中的细胞因子水平。在0和360分钟采集胰腺组织样本。
坏死性胰腺炎组和对照组的白细胞计数增加。所有组中性粒细胞数量增加(p < 0.001),淋巴细胞和嗜酸性粒细胞计数减少(p < 0.001,p < 0.001)。仅坏死性胰腺炎组的单核细胞计数以及血小板衍生生长因子(PDGF)和白细胞介素-6(IL-6)浓度增加。白细胞介素-8(IL-8)和嗜酸性粒细胞趋化因子在水肿性和坏死性胰腺炎中均增加。所有组的单核细胞趋化蛋白-1(MCP-1)均增加。白细胞介素-9(IL-9)、白细胞介素-4(IL-4)、巨噬细胞炎性蛋白-1α(MIP-1α)、干扰素-γ(IFN-γ)浓度未发生变化。先前系列研究中门静脉血和肺动脉血之间的嗜酸性粒细胞趋化因子和MCP-1血浆水平无显著差异。
水肿性和坏死性胰腺炎的初始炎症过程各不相同。在我们的模型中,单核细胞计数增加以及PDGF和IL-6升高是坏死性胰腺炎的特征。