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首页> 外文期刊>The Journal of Nutritional Biochemistry >Fish-oil-derived n-3 polyunsaturated fatty acids reduce NLRP3 inflammasome activity and obesity-related inflammatory cross-talk between adipocytes and CD11b(+) macrophages
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Fish-oil-derived n-3 polyunsaturated fatty acids reduce NLRP3 inflammasome activity and obesity-related inflammatory cross-talk between adipocytes and CD11b(+) macrophages

机译：鱼油衍生的N-3多不饱和脂肪酸降低NLRP3炎症组和肥胖相关的炎症串扰脂肪细胞和CD11b（+）巨噬细胞

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摘要

Adipocyte-macrophage cross-talk propagates immune responses in obese adipose tissue (AT). Long-chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) mitigate inflammation, partly through up-regulation of adiponectin; however, specific mechanisms are unclear. We determined if adipocyte-macrophage crosstalk could be mitigated by dietary LC n-3 PUFA and if this was dependent on adiponectin-mediated signaling. We utilized an in vitro co-culture model mimicking the ratio of adipocytes:macrophages in obese AT, whereby 3T3-L1 adipocytes were co-cultured with splenic CD11b(+) macrophages from C57BL/6 mice fed high fat control (HF-CON; 34% w/w fat) or fish oil diets (HF-FO; 34% w/w fat containing 7.6% w/w FO), as well as mice fed low-fat control (LF-CON; 10% w/w fat) or FO diets (LF-FO; 10% w/w fat containing 3% w/w FO). Co-culture conditions tested effects of soluble mediator-driven mechanisms (trans-well system), cell contact and low-dose lipopolysaccharide (LPS) mimicking acute or chronic inflammatory conditions. HF-FO macrophages from acute LPS-stimulated trans-well co-cultures had decreased mRNA expression of Casp1, Il1 beta and Il18, as well as cellular caspase-1 activity compared to HF-CON macrophages (P =.05). Moreover, adipocytes from acute LPS-stimulated HF-FO co-cultures had decreased caspase-1 activity and decreased IL-1 beta/IL-18 levels following chronic LPS pretreatment compared to HF-CON co-cultures (P =.05). Additionally, in contact co-cultures with adiponectin-neutralizing antibody, the FO-mediated modulation of NF kappa B activity and decrease in phosphorylated p65 NF kappa B, expression of NLRP3 inflammasome genes, M1 macrophage marker genes and inflammatory cytokine/chemokine secretion were controlled partly through adiponectin, while cellular caspase-1 activity and IL-1 beta/IL-18 levels were decreased independently of adiponectin (P =.05). LC n-3 PUFA may decrease the intensity of adipocyte-macrophage cross-talk to mitigate obesity-associated pathologies. (C) 2016 Published by Elsevier Inc.
机译：脂肪细胞 - 巨噬细胞串扰在肥胖脂肪组织（AT）中繁殖免疫应答。长链N-3多不饱和脂肪酸（LC N-3 PUFA）减轻炎症，部分通过脂联素的上调;但是，具体机制尚不清楚。我们确定是否可以通过膳食LC N-3 PUFA减轻脂肪细胞 - 巨噬细胞串扰，如果这取决于脂联素介导的信号传导。我们利用体外共培养模型模仿脂肪细胞的比例：肥胖的巨噬细胞在肥胖的脂肪组织中，由C57BL / 6小鼠与喂养高脂肪对照的C57BL / 6小鼠共培养（HF-Con; 34％w / w脂肪）或鱼油饮食（Hf-fo; 34％w / w含有7.6％w / w fo的脂肪），以及喂养低脂肪对照的小鼠（lf-con; 10％w / w脂肪）或饮食（LF-FO; 10％w / w含有3％w / w fo的脂肪）。共培养条件可溶性介质驱动机构（反式井系统），细胞接触和低剂量脂多糖（LPS）模拟急性或慢性炎症条件的综合培养条件。与HF-CON巨噬细胞相比，来自急性LPS刺激的转孔阱共培养物的HF-FO血栓血液的HF-FO巨噬细胞对CasP1，IL1β和IL18的mRNA表达，以及细胞胱天蛋白酶-1活性（P <。05）。此外，与HF-CON共培养物相比，急性LPS刺激的HF-FO-培养物的脂肪细胞来自慢性LPS预处理后的Caspase-1活性降低，降低了慢性LPS预处理后的IL-1β/ IL-18水平（P <。05 ）。另外，在具有脂联素中和抗体的接触共培养物中，控制NFκB活性的FO介导的调节和磷酸化的P65 NF Kappa B的降低，NLRP3炎症组基因的表达，M1巨噬细胞标记基因和炎症细胞因子/趋化因子分泌。部分通过脂联素，而细胞胱天蛋白酶-1活性和IL-1β/ IL-18水平独立于脂联素（P <= 05）。 LC N-3 PUFA可能会降低脂肪细胞巨噬细胞串扰的强度，以减轻肥胖相关的病理学。 （c）2016年由elsevier公司发布

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