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首页> 外文期刊>Cytokine >The effects of infection of thermal injury by Pseudomonas aeruginosa PAO1 on the murine cytokine response.
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The effects of infection of thermal injury by Pseudomonas aeruginosa PAO1 on the murine cytokine response.

机译：铜绿假单胞菌PAO1感染热损伤对小鼠细胞因子反应的影响。

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Pseudomonas aeruginosa infection, one of the major complications of burn wounds, may lead to sepsis and death. Using the Multi-Probe Template/RNase protection assay, we have compared the expression of different cytokine genes within the skin and livers of thermally injured mice infected with P. aeruginosa PAO1. Thermal injury alone enhanced or up-regulated certain cytokines, including macrophage colony-stimulating factor (M-CSF), interleukin 1 (IL-1)RI, IL-1 beta, macrophage inflammatory protein (MIP)-1 beta and MIP-2; while PAO1 challenge alone up-regulated tumour necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta) expression. The combination of thermal injury plus PAO1 infection enhanced the expression of several pro-inflammatory and haematopoietic cytokines [stem cell factor (SCF), leukocyte inhibitory factor (LIF), IL-6 and TNF-alpha]; induced the expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) and G-CSF by 5 h and the expression of additional cytokines, including TGF-beta, TNF-beta, lymphotoxin beta (LT-beta), interferon gamma (IFN-gamma), and IFN-beta by 40 h post-burn/infection. While the most intense cytokine expression occurred in the skin, the majority of cytokines tested were also expressed in the liver by 40 h post-burn/infection. These results suggest that in P. aeruginosa infection of burn wounds: (1) up-regulation of the expression of different cytokines, locally and within the livers of burned mice, is an indication of P. aeruginosa -induced sepsis; and (2) IL-6 and G-CSF play an important role in the host response mechanism.
机译：铜绿假单胞菌感染是烧伤创面的主要并发症之一，可能导致败血症和死亡。使用多探针模板/ RNase保护试验，我们比较了感染铜绿假单胞菌PAO1的热损伤小鼠皮肤和肝脏中不同细胞因子基因的表达。单独的热损伤会增强或上调某些细胞因子，包括巨噬细胞集落刺激因子（M-CSF），白介素1（IL-1）RI，IL-1 beta，巨噬细胞炎性蛋白（MIP）-1 beta和MIP-2 ;而PAO1单独挑战会上调肿瘤坏死因子α（TNF-alpha）和转化生长因子β（TGF-beta）的表达。热损伤加PAO1感染的结合增强了几种促炎和造血细胞因子[干细胞因子（SCF），白细胞抑制因子（LIF），IL-6和TNF-α]的表达;诱导粒细胞巨噬细胞集落刺激因子（GM-CSF）和G-CSF的表达在5 h内表达，并诱导其他细胞因子的表达，包括TGF-beta，TNF-beta，淋巴毒素beta（LT-beta），干扰素烧伤/感染后40小时后产生IFN-γ）和IFN-β。尽管最强烈的细胞因子表达发生在皮肤中，但在烧伤/感染后40小时，大多数测试的细胞因子也在肝脏中表达。这些结果表明，在烧伤创面的铜绿假单胞菌感染中：（1）局部和烧伤小鼠肝脏内不同细胞因子表达的上调是铜绿假单胞菌诱导的败血症的征兆; （2）IL-6和G-CSF在宿主反应机制中起重要作用。

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