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首页> 外文期刊>Cytokine >ABSENCE OF ENDOGENOUS INTERLEUKIN-6 ENHANCES THE INFLAMMATORY RESPONSE DURING ACUTE PANCREATITIS INDUCED BY CERULEIN IN MICE.
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ABSENCE OF ENDOGENOUS INTERLEUKIN-6 ENHANCES THE INFLAMMATORY RESPONSE DURING ACUTE PANCREATITIS INDUCED BY CERULEIN IN MICE.

机译：内源性白介素6的缺乏增强了由小儿茶素诱导的急性胰腺炎期间的炎症反应。

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Interleukin-6 (IL-6) exerts a wide spectrum of regulatory activities during immune and inflammatory responses. The aim of this study was to investigate the role of endogenous IL-6 in the inflammatory response associated with acute pancreatitis. Acute pancreatitis was induced by hourly (x5) i.p. injections of cerulein (50&mgr;g/kg, suspended in saline solution) in IL-6 deficient mice (IL-6-KO) and wild-type (IL-6WT) littermates. IL-6KO mice exhibited a more severe tissue injury and a higher rate of mortality and when compared to IL-6WT mice. Acute pancreatitis was characterized by edema, neutrophil infiltration, tissue hemorrhage and cell necrosis, upregulation of P-selectin and intercellular adhesion molecule-1 (ICAM-1), as well as increases in the serum levels of amylase and lipase. The degree of oxidative and nitrosative tissue damage was significantly greater in IL-6KO mice than in wild-type littermates, as indicated by higher tissue levels of malondialdehyde and nitrosylated proteins. Plasma levels of the inflammatory cytokines tumour necrosis factor-alpha and interleukin-1beta were also greatly enhanced in IL-6KO mice when compared to wild-type mice. These events were correlated with an increase in the staining (immunoreactivity) for poly (ADP-ribose) polymerase (PARP) in the pancreas of cerulein-treated IL-6WT. The staining for PARP was more pronounced in IL-6KO mice subjected to acute pancreatitis than in the corresponding WT mice. These data demonstrate that endogenous IL-6 exerts an anti-inflammatory role during acute pancreatitis, possibly by regulating the expression of adhesion molecules, the subsequent adhesion and activation of neutrophils and finally the generation of cytokine and reactive oxygen or nitrogen species.
机译：白细胞介素6（IL-6）在免疫和炎症反应过程中发挥广泛的调节作用。这项研究的目的是调查内源性IL-6在急性胰腺炎相关炎症反应中的作用。每小时（x5）i.p.诱发急性胰腺炎。在缺乏IL-6的小鼠（IL-6-KO）和野生型（IL-6WT）的同窝小鼠中注射cerulein（50 mg / kg，悬浮于盐溶液中）。与IL-6WT小鼠相比，IL-6KO小鼠表现出更严重的组织损伤和更高的死亡率。急性胰腺炎的特征是水肿，中性粒细胞浸润，组织出血和细胞坏死，P-选择蛋白和细胞间粘附分子-1（ICAM-1）上调，以及血清淀粉酶和脂肪酶水平的升高。 IL-6KO小鼠的氧化和亚硝化组织损伤程度明显高于野生型同窝仔，这是由丙二醛和亚硝基化蛋白的较高组织水平所表明的。与野生型小鼠相比，IL-6KO小鼠的炎症细胞因子肿瘤坏死因子-α和白介素-1β的血浆水平也大大提高。这些事件与铜蓝蛋白处理过的IL-6WT胰腺中的聚（ADP-核糖）聚合酶（PARP）染色（免疫反应性）增加相关。在遭受急性胰腺炎的IL-6KO小鼠中，与相应的WT小鼠相比，PARP的染色更明显。这些数据表明内源性IL-6可能在急性胰腺炎中发挥抗炎作用，可能是通过调节粘附分子的表达，随后的嗜中性粒细胞的粘附和活化以及最终细胞因子和活性氧或氮物种的产生。

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