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Toll 样受体 7（TLR7）在脂肪细胞中表达，药理学 TLR7 激动剂咪喹莫特和脂肪细胞衍生的无细胞游离核酸（cfDNA）调节脂肪细胞功能。

Toll-like Receptor 7 (TLR7) Is Expressed in Adipocytes and the Pharmacological TLR7 Agonist Imiquimod and Adipocyte-Derived Cell-Free Nucleic Acids (cfDNA) Regulate Adipocyte Function.

机构信息

Department of Internal Medicine III, Justus-Liebig-University Giessen, 35390 Gießen, Germany.

Department of Rheumatology and Clinical Immunology, Justus-Liebig-University Giessen, Campus Kerckhoff, 61231 Bad Nauheim, Germany.

出版信息

Int J Mol Sci. 2022 Jul 30;23(15):8475. doi: 10.3390/ijms23158475.

DOI:10.3390/ijms23158475
PMID:35955609
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9369246/
Abstract

Endosome-localized Toll-like receptors (TLRs) 3 and 9 are expressed and functionally active in adipocytes. The functionality and role of TLR7 in adipocyte biology and innate immunity of adipose tissue (AT) is poorly characterized. We analyzed TLR7 mRNA and protein expression in murine 3T3-L1 and primary adipocytes, in co-cultures of 3T3-L1 adipocytes with murine J774A.1 monocytes and in human AT. The effects of TLR7 agonists imiquimod (IMQ) and cell-free nucleic acids (cfDNA) on adipokine concentration in cell-culture supernatants and gene expression profile were investigated. We found that TLR7 expression is strongly induced during adipocyte differentiation. TLR7 gene expression in adipocytes and AT stroma-vascular cells (SVC) seems to be independent of TLR9. IMQ downregulates resistin concentration in adipocyte cell-culture supernatants and modulates gene expression of glucose transporter Glut4. Adipocyte-derived cfDNA reduces adiponectin and resistin in cell-culture supernatants and potentially inhibits Glut4 gene expression. The responsiveness of 3T3-L1 adipocytes to imiquimod is preserved in co-culture with J774A.1 monocytes. Obesity-related, adipocyte-derived cfDNA engages adipocytic pattern recognition receptors (PRRs), modulating AT immune and metabolic homeostasis during adipose inflammation.

摘要

内体定位的 Toll 样受体 (TLR) 3 和 9 在脂肪细胞中表达并具有功能活性。TLR7 在脂肪细胞生物学和脂肪组织 (AT) 的固有免疫中的功能和作用尚未得到充分描述。我们分析了 TLR7 mRNA 和蛋白在小鼠 3T3-L1 和原代脂肪细胞、3T3-L1 脂肪细胞与小鼠 J774A.1 单核细胞共培养物以及人 AT 中的表达。研究了 TLR7 激动剂咪喹莫特 (IMQ) 和无细胞核酸 (cfDNA) 对细胞培养上清液中脂肪因子浓度和基因表达谱的影响。我们发现 TLR7 表达在脂肪细胞分化过程中强烈诱导。脂肪细胞和 AT 基质血管细胞 (SVC) 中的 TLR7 基因表达似乎独立于 TLR9。IMQ 下调脂肪细胞培养上清液中抵抗素的浓度，并调节葡萄糖转运蛋白 Glut4 的基因表达。脂肪细胞来源的 cfDNA 降低细胞培养上清液中的脂联素和抵抗素，并可能抑制 Glut4 基因表达。3T3-L1 脂肪细胞对咪喹莫特的反应性在与 J774A.1 单核细胞共培养时得以保留。肥胖相关的脂肪细胞衍生的 cfDNA 使脂肪细胞的模式识别受体 (PRR) 参与其中，在脂肪炎症期间调节 AT 免疫和代谢稳态。

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