The Impact of Membrane Lipid Composition on Macrophage Activation in the Immune Defense against Rhodococcus equi and Pseudomonas aeruginosa
The Impact of Membrane Lipid Composition on Macrophage Activation in the Immune Defense against Rhodococcus equi and Pseudomonas aeruginosa
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DOI：
10.3390/ijms12117510
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发表时间：
2011-11-01
影响因子：
5.6
通讯作者：
Schumann, Julia
中科院分区：
文献类型：
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作者：
Schoeniger, Axel;Adolph, Stephanie;Schumann, Julia
已知营养脂肪酸对身体细胞（包括免疫系统细胞）的膜脂质组成具有影响，从而提供膳食脂肪酸摄取、炎症和免疫之间的联系。在这项研究中，我们揭示了巨噬细胞膜脂质组成对基因表达和细胞因子合成的意义，从而突出信号转导过程，巨噬细胞活化以及巨噬细胞防御机制。使用RAW264.7巨噬细胞作为模型系统，我们鉴定了n-3和n-6家族的多不饱和脂肪酸（PUFA）以下调以下的合成：（i）促炎细胞因子IL-1 β、IL-6和TNF-α;（ii）共刺激分子CD 86;以及（iii）抗微生物多肽溶菌酶。脂肪酸的作用部分取决于巨噬细胞的活化状态。特别重要的是要注意，PUFA的抗炎作用也可以在用R属的活微生物感染RAW 264.7的情况下看到。马和铜绿假单胞菌。总之，我们的数据提供了强有力的证据表明，来自n-3和n-6家族的PUFA在由持久性病原体引起的慢性感染的背景下下调炎症过程。
Nutritional fatty acids are known to have an impact on membrane lipid composition of body cells, including cells of the immune system, thus providing a link between dietary fatty acid uptake, inflammation and immunity. In this study we reveal the significance of macrophage membrane lipid composition on gene expression and cytokine synthesis thereby highlighting signal transduction processes, macrophage activation as well as macrophage defense mechanisms. Using RAW264.7 macrophages as a model system, we identified polyunsaturated fatty acids (PUFA) of both the n-3 and the n-6 family to down-regulate the synthesis of: (i) the pro-inflammatory cytokines IL-1 beta, IL-6 and TNF-alpha; (ii) the co-stimulatory molecule CD86; as well as (iii) the antimicrobial polypeptide lysozyme. The action of the fatty acids partially depended on the activation status of the macrophages. It is particularly important to note that the anti-inflammatory action of the PUFA could also be seen in case of infection of RAW264.7 with viable microorganisms of the genera R. equi and P. aeruginosa. In summary, our data provide strong evidence that PUFA from both the n-3 and the n-6 family down-regulate inflammation processes in context of chronic infections caused by persistent pathogens.