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Interleukin-1 Receptor Type I Gene-Deficient Mice Are Less Susceptible to Staphylococcus epidermidis Biomaterial-Associated Infection than Are Wild-Type Mice

机译:与野生型小鼠相比,白细胞介素1受体I型基因缺陷小鼠对表皮葡萄球菌生物材料相关感染的敏感性较小。

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摘要

Elevated concentrations of interleukin-1 (IL-1) were found in tissue surrounding biomaterials infected with Staphylococcus epidermidis. To determine the role of IL-1 in biomaterial-associated infection (BAI), IL-1 receptor type I-deficient (IL-1R−/−) and wild-type mice received subcutaneous implants of silicon elastomer (SE) or polyvinylpyrrolidone-grafted SE (SEpvp), combined with an injection of 106 CFU of S. epidermidis or sterile saline. Neither mouse strain was susceptible to BAI around SE. IL-1R−/− mice with SEpvp implants had a no abscess formation and a reduced susceptibility to persistent S. epidermidis infection. The normal foreign body response, characterized by giant-cell formation and encapsulation, was delayed around SEpvp in wild-type mice but not in IL-1R−/− mice. This coincided with enhanced local IL-4 production in IL-1R−/− mice. These data suggest that inhibition of local IL-1 activity may be beneficial for the outcome of BAI.
机译:在被表皮葡萄球菌感染的生物材料周围的组织中发现了高浓度的白介素-1(IL-1)。为了确定IL-1在生物材料相关感染(BAI)中的作用,IL-1受体I型缺陷(IL-1R-/-)和野生型小鼠接受了硅弹性体(SE)或聚乙烯吡咯烷酮-接枝SE(SEpvp),并结合注射106 CFU的表皮葡萄球菌或无菌盐水。在SE周围,两种小鼠品系均不易感染BAI。植入SEpvp的IL-1R-/-小鼠无脓肿形成,对持久性表皮葡萄球菌感染的敏感性降低。在野生型小鼠中,SEpvp周围的正常异物反应(以巨细胞形成和封装为特征)被延迟了,但在IL-1R-/-小鼠中却没有。这与IL-1R-/-小鼠中局部IL-4产生的增加相吻合。这些数据表明,抑制局部IL-1活性可能对BAI的结果有益。

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