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首页> 外文期刊>Cytokine >Contribution of circulating leukocytes to cytokine production in pancreatic duct obstruction-induced acute pancreatitis in rats.
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Contribution of circulating leukocytes to cytokine production in pancreatic duct obstruction-induced acute pancreatitis in rats.

机译：循环白细胞对大鼠胰管阻塞所致急性胰腺炎细胞因子产生的贡献。

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摘要

Little information is available regarding the role of circulating leukocytes in the pathogenesis of acute pancreatitis (AP). Our aim was to explore the time-course of the potential role of inflammatory peripheral blood (PB) cells during AP induced in rats by pancreatic duct obstruction (PDO). Flow cytometry immunophenotyping was used to analyse the distribution of the major circulating leukocyte subsets, the activation state of circulating monocytes as reflected by both CD11b expression and TNF-alpha production and the relative contribution of T-cell derived pro- (TNF-alpha) and anti- (IL-10) inflammatory mediators at different stages of PDO-induced AP. A progressive increase in PB neutrophils and monocytes was observed up to 6h after PDO whereas lymphocytes, as well as CD4(+) and CD8(+) T-cell subsets, rose as early as 1.5h after PDO and decreased thereafter. Monocytes were activated in PB from 6h after inducing AP as reflected by increases in both CD11b expression and spontaneous TNF-alpha production; nevertheless, they showed the capability of producing TNF-alpha at earlier AP stages by lipopolysaccharide (LPS) stimulation. In contrast, T-cells were unable to produce TNF-alpha during AP neither spontaneously nor after stimulation with PMA/Ionomycin. Therefore, only PB monocytes contribute to increase TNF-alpha levels in plasma as observed from 12h onwards after inducing AP. Interleukin-10 was produced by T-cells 6h after PDO only after PMA/Ionomycin stimulation. We conclude that systemic inflammatory events are triggered off at early stages of PDO-induced AP, with the activation of circulating monocytes, though not T-cells, playing a central role.
机译：关于循环白细胞在急性胰腺炎（AP）发病机理中的作用的信息很少。我们的目的是探讨胰腺导管阻塞（PDO）在大鼠诱发AP期间炎症性外周血（PB）细胞潜在作用的时程。流式细胞仪免疫表型分析主要循环白细胞亚群的分布，CD11b表达和TNF-α产生所反映的循环单核细胞的活化状态以及T细胞衍生的pro-（TNF-alpha）和PDO诱导的AP不同阶段的抗（IL-10）炎症介质。 PDO后直至6h观察到PB中性粒细胞和单核细胞逐渐增加，而淋巴细胞以及CD4（+）和CD8（+）T细胞亚群早在PDO后1.5h上升，此后下降。单核细胞从诱导AP后6小时开始被PB激活，这通过CD11b表达的增加和自发TNF-α的产生来反映。然而，他们显示了通过脂多糖（LPS）刺激在AP早期产生TNF-α的能力。相反，T细胞既不能自发地也不能在AP期间或在用PMA /伊诺霉素刺激后产生TNF-α。因此，从诱导AP后12小时开始，仅PB单核细胞有助于增加血浆中的TNF-α水平。仅在PMA /碘霉素刺激后，PDO后6h T细胞产生白细胞介素10。我们得出的结论是，在PDO诱导的AP的早期阶段会触发全身性炎症事件，其中循环单核细胞（而非T细胞）的激活起着核心作用。

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