Betanzos-Cabrera G, Estrada-Luna D, Belefant-Miller H, Cancino-Díaz J C
Área Académica de Nutrición, Instituto de Ciencias de Salud, Universidad Autónoma del Estado de Hidalgo, Pachuca, Mexico.
Nutr Hosp. 2012 Jul-Aug;27(4):1196-203. doi: 10.3305/nh.2012.27.4.5842.
Pattern-recognition receptors (PRRs), which include Toll-like Receptor (TLRs) and Nacht leucine-rich repeat proteins (NLRP/NALPs), are molecules of innate immunity able to recognize a wide variety of ligands present in microorganisms and human tissues. Adipocytes (fat cells) may play an important role in the physiological regulation of their own immune responses via TLRs. During obesity, the inflammatory pathway is triggered and insulin responsiveness is altered in fat tissue as a result of TLR4 activation by dietary lipids.
Here, we investigate if other PRR family members could also participate in the inflammatory processes in the adipose tissue of obese mice.
The mRNA expression of TLRs, the NLRP3-inflammasome (NLRP3, ASC, caspase-1 and IL-lbeta), IL-6, and TNFα in the hepatic and adipose tissues of mice fed with a high fat diet (HFD) were studied by RT-PCR.
Adipose tissue from mice fed with a HFD had decreased expression levels of TLR2, TLR6 and TLR7 and was similar to the pattern in hepatic tissue HFD mice. IL-6 and TNF-α expression also were decreased in adipose tissue of mice fed with a HFD. NLRP3-inflammasome expression was not modified.
These results suggest that the low expression of TLR2, and TLR6 in the mice fed with a HFD could be regulating the inflammation induced by the diet employed in this study.
模式识别受体(PRR),包括Toll样受体(TLR)和含Nacht亮氨酸重复序列的蛋白(NLRP/NALP),是先天免疫分子,能够识别微生物和人体组织中存在的多种配体。脂肪细胞可能通过TLR在自身免疫反应的生理调节中发挥重要作用。在肥胖期间,由于膳食脂质激活TLR4,脂肪组织中的炎症途径被触发,胰岛素反应性发生改变。
在此,我们研究其他PRR家族成员是否也参与肥胖小鼠脂肪组织中的炎症过程。
通过逆转录聚合酶链反应(RT-PCR)研究高脂饮食(HFD)喂养小鼠的肝脏和脂肪组织中TLR、NLRP3炎性小体(NLRP3、ASC、半胱天冬酶-1和白细胞介素-1β)、白细胞介素-6和肿瘤坏死因子α的mRNA表达。
高脂饮食喂养小鼠的脂肪组织中TLR2、TLR6和TLR7的表达水平降低,与高脂饮食喂养小鼠肝脏组织中的模式相似。高脂饮食喂养小鼠的脂肪组织中白细胞介素-6和肿瘤坏死因子-α的表达也降低。NLRP3炎性小体表达未改变。
这些结果表明,高脂饮食喂养小鼠中TLR2和TLR6的低表达可能调节本研究中所用饮食诱导的炎症。