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首页> 外文OA文献 >A Neonatal Murine Escherichia coli Sepsis Model Demonstrates That Adjunctive Pentoxifylline Enhances the Ratio of Anti- vs. Pro-inflammatory Cytokines in Blood and Organ Tissues
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A Neonatal Murine Escherichia coli Sepsis Model Demonstrates That Adjunctive Pentoxifylline Enhances the Ratio of Anti- vs. Pro-inflammatory Cytokines in Blood and Organ Tissues

机译：新生儿鼠大肠杆菌Coli Sepsis模型表明，辅助化毒素碱可以增强血液和器官组织中的抗血液炎症细胞因子的比例

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Introduction: Neonatal sepsis triggers an inflammatory response that contributes to mortality and multiple organ injury. Pentoxifylline (PTX), a phosphodiesterase inhibitor which suppresses pro-inflammatory cytokines, is a candidate adjunctive therapy for newborn sepsis. We hypothesized that administration of PTX in addition to antibiotics decreases live bacteria-induced pro-inflammatory and/or enhances anti-inflammatory cytokine production in septic neonatal mice without augmenting bacterial growth.Methods: Newborn C57BL/6J mice (< 24 h old) were injected intravenously with 105 colony forming units (CFUs)/g weight of a bioluminescent derivative of the encapsulated clinical isolate Escherichia coli O18:K1. Adequacy of intravenous injections was validated using in vivo bioluminescence imaging and Evans blue. Pups were treated with gentamicin (GENT), PTX, (GENT + PTX) or saline at 0, 1.5, or 4 h after sepsis initiation, and euthanized after an additional 4 h. CFUs and cytokines were measured from blood and homogenized organ tissues.Results: GENT alone inhibited bacterial growth, IL-1β, and IL-6 production in blood and organs. Addition of PTX to GENT profoundly inhibited E. coli-induced TNF and enhanced IL-10 in blood of newborn mice at all timepoints, whereas it primarily upregulated IL-10 production in peripheral organs (lung, spleen, brain). PTX, whether alone or adjunctive to GENT, did not increase microbial colony counts in blood and organs.Conclusion: Addition of PTX to antibiotics in murine neonatal E. coli sepsis promoted an anti-inflammatory milieu through inhibition of plasma TNF and enhancement of IL-10 production in plasma and organs without increasing bacterial growth, supporting its utility as a potential adjunctive agent for newborn sepsis.
机译：介绍：新生儿脓毒症触发了有助于死亡率和多种器官损伤的炎症反应。抑制促炎细胞因子的磷酸二肽酶抑制剂，是新生脓毒症的候选辅助治疗。我们假设除了抗生素之外，PTX的给药还会降低活细菌诱导的促炎和/或增强脓毒新生小鼠的抗炎细胞因子生成，而不会增强细菌生长。方法：新生儿C57BL / 6J小鼠（<24小时旧）用105个菌落形成单元（CFU）/ g重量的包封的临床分离型大肠杆菌O18：K1的生物发光衍生物的105个菌落形成单元（CFU）/ g重量注射。使用体内生物发光成像和埃文斯蓝进行验证静脉注射的充分性。在败血症开始后，用庆大霉素（Gent），PTX，（GENT + PTX）或盐水处理幼犬，并在另外4小时后安乐死。 CFU和细胞因子由血液和均质器官组织测量。结果：GETT单独抑制血液和器官中的细菌生长，IL-1β和IL-6产生。添加PTX以在所有调节点的血液中抑制大肠杆菌诱导的大肠杆菌诱导的TNF和增强的IL-10，而它主要是上调在外周器官（肺，脾，脑）中的IL-10产生。 PTX，无论是单独使用或辅助到GENT，没有增加在血液和organs.Conclusion微生物菌落计数：加法PTX的抗生素在鼠新生儿大肠杆菌败血症通过血浆TNF的抑制和增强IL-的促进抗炎环境10在血浆和器官中生产而不增加细菌生长，支持其效用作为新生败血症的潜在辅助剂。

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