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Impact of neonatal malnutrition on expression TLR-9, NF-kB and cytokines of macrophages infected in vitro with methicillin resistant Staphylococcus aureus

机译:新生儿营养不良对甲氧西林金黄色葡萄球菌体外感染巨噬细胞表达TLR-9,NF-KB和细胞因子的影响

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Early nutritional aggressions promote epigenetic adjustments that culminate in the loss of phenotype plasticity (with permanent long-term modifications). Maternal diet and inadequate neonatal nutrition can result in fetal programming that presents susceptibility to infections in adult life. Thus, it becomes essential to verify the impacts of neonatal malnutrition (even following nutritional replacement) on the immunological response to methicillin resistant Staphylococcus aureus (MRSA) infections. Male rats were divided into two distinct groups: Nourished and Malnourished. After isolation of mononuclear cells, four systems were established: negative control, positive control and two testing systems, (MSSA and MRSA). Tests were performed to analyze expression of TLR-9, NF-kB, IL-1 beta, IL-18 and IL-33. For statistical analysis, we used the Student t and ANOVA tests p 0.05. Even after nutritional replacement, malnutrition in the neonatal period compromised the animals' weight gains p 0.05. There was a reduction in the expression of the immunological response in the positive control, however deregulation was observed in the gene expression of MRSA-infected macrophages, with a reduction in TLR-9 expression, and overexpression in NF-kB and cytokines p 0.05. Puppies inflicted with protein-calorie malnutrition were compromised; (long-term) body growth and immune response. In the infectious scenario, immune collapse is reflected in inflammatory response exacerbation with a likely histolytic character. Immune disabling (resulting from gene expression deregulation) causes susceptibility to infections due to ineffective recognition, intense pro-inflammatory mediation, and cell death. It is suggested that neonatal malnutrition can program susceptibility to multiresistant bacterial infections, and generally favors a triggering of more intense confrontations with fatal outcomes.
机译:早期的营养性侵略促进表观遗传调整,这些调整终止于表型可塑性(具有永久性长期修饰)。母体饮食和新生儿营养不足可能导致胎儿编程,这呈现成年生命中感染的易感性。因此,验证新生儿营养不良(甚至营养替代)对对甲氧西林抗性金黄色葡萄球菌(MRSA)感染的免疫应答的影响是必要的。雄性大鼠分为两种截然不同的群体:营养和营养不良。在分离单核细胞后,建立了四种系统:阴性对照,阳性对照和两个测试系统(MSSA和MRSA)。进行测试以分析TLR-9,NF-KB,IL-1β,IL-18和IL-33的表达。对于统计分析,我们使用学生T和ANOVA测试P& 0.05。即使在营养替代品后,新生儿时期的营养不良均可损害动物的体重增加p& 0.05。在阳性对照中表达免疫应答的表达,然而,在MRSA感染巨噬细胞的基因表达中观察到放松管制,其TLR-9表达还原,NF-KB和细胞因子P< 0.05。用蛋白质 - 卡路里营养不良造成的小狗受到损害; (长期)身体生长和免疫应答。在感染性情景中,免疫崩溃反映在具有可能的组织特性的炎症反应恶化中。免疫致残(由基因表达放松管制引起的)导致由于无效的识别,强烈的促炎调解和细胞死亡而导致感染的易感性。建议新生儿营养不良可以针对多人细菌感染的易感性,并且普遍促使触发更强烈的对抗致命结果。

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