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Long-term effects of neonatal malnutrition on microbicide response, production of cytokines, and survival of macrophages infected by Staphylococcus aureus sensitive/resistant to methicillin

机译:新生儿营养不良对敏感/耐甲氧西林的金黄色葡萄球菌感染的杀菌剂反应,细胞因子产生和巨噬细胞存活的长期影响

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OBJECTIVE: To assess microbicide function and macrophage viability after in vitro cellular infection by methicillin-sensitive/resistant Staphylococcus aureus in nourished rats and rats subjected to neonatal malnutrition. METHODS: Male Wistar rats (n=40) were divided in two groups: Nourished (rats suckled by dams consuming a 17% casein diet) and Malnourished (rats suckled by dams consuming an 8% casein diet). Macrophages were recovered after tracheotomy, by bronchoalveolar lavage. After mononuclear cell isolation, four systems were established: negative control composed exclusively of phagocytes; positive control composed of macrophages plus lipopolysaccharide; and two testing systems, macrophages plus methicillin-sensitive Staphylococcus aureus and macrophages plus methicillin-resistant Staphylococcus aureus. The plates were incubated in a humid atmosphere at 37 degrees Celsius containing 5% CO2 for 24 hours. After this period tests the microbicidal response, cytokine production, and cell viability were analyzed. The statistical analysis consisted of analysis of variance (p0.05). RESULTS: Malnutrition reduced weight gain, rate of phagocytosis, production of superoxide anion and nitric oxide, and macrophage viability. Production of nitrite and interleukin 18, and viability of macrophages infected with methicillin-resistant Staphylococcus aureus were lower. CONCLUSION: The neonatal malnutrition model compromised phagocyte function and reduced microbicidal response and cell viability. Interaction between malnutrition and the methicillin-resistant strain decreased the production of inflammatory mediators by effector cells of the immune response, which may compromise the immune system's defense ability.
机译:目的:评估在营养不良的大鼠和新生营养不良的大鼠中,对甲氧西林敏感/耐药的金黄色葡萄球菌体外细胞感染后的杀微生物剂功能和巨噬细胞活力。方法:雄性Wistar大鼠(n = 40)分为两组:营养丰富的(由摄入17%酪蛋白饮食的大坝哺乳的大鼠)和营养不良的(由摄入8%酪蛋白饮食的大坝哺乳的大鼠)。气管切开后通过支气管肺泡灌洗恢复巨噬细胞。在单核细胞分离后,建立了四个系统:仅由吞噬细胞组成的阴性对照;由巨噬细胞和脂多糖组成的阳性对照;和两个测试系统,巨噬细胞加对甲氧西林敏感的金黄色葡萄球菌和巨噬细胞加对耐甲氧西林的金黄色葡萄球菌。将板在37℃,含有5%CO 2的潮湿气氛中温育24小时。经过这段时间的测试后,对杀菌反应,细胞因子产生和细胞活力进行了分析。统计分析包括方差分析(p <0.05)。结果:营养不良减少了体重增加,吞噬作用,超氧阴离子和一氧化氮的产生以及巨噬细胞的生存能力。亚硝酸盐和白介素18的产生以及感染耐甲氧西林金黄色葡萄球菌的巨噬细胞的活力较低。结论:新生儿营养不良模型损害吞噬细胞功能,降低了杀微生物反应和细胞活力。营养不良和耐甲氧西林的菌株之间的相互作用降低了免疫反应的效应细胞产生的炎症介质,这可能会损害免疫系统的防御能力。

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