The anti-inflammatory adipokine CTRP-3 might affect innate immune reactions such as NOD1. The impact of CTRP-3 on NOD1-mediated inflammation in adipocytes and monocytic cells as well as on NOD1 expression was investigated. Murine 3T3-L1 pre-adipocytes and adipocytes as well as human THP-1 monocyte-like cells were co-stimulated with the synthetic NOD1 agonist Tri-DAP and recombinant CTRP-3. Gonadal adipose tissue and primary adipocytes were obtained from a murine model carrying a knockout (KO) of CTRP-3 in adipocytes but not in stroma-vascular cells. Wildtype mice with lipopolysaccharide (LPS)-induced elevated NOD1 expression were treated with CTRP-3. Secreted inflammatory cytokines in cell supernatants were measured by ELISA and mRNA levels were quantified by RT-PCR. Pro-inflammatory chemokine and cytokine secretion (MCP-1, RANTES, TNFα) was induced by NOD1 activation in adipocytes and monocyte-like cells, and MCP-1 and RANTES release was effectively inhibited by pre-incubation of cells with CTRP-3. CTRP-3 also antagonized LPS-triggered induction of NOD1 gene expression in murine adipose tissue, whereas adipocyte CTRP-3 deficiency upregulated NOD1 expression in adipose tissue. CTRP-3 is an effective antagonist of peptidoglycan-induced, NOD1-mediated inflammation and of LPS-induced NOD1 expression. Since basal NOD1 expression is increased by adipocyte CTRP-3 deficiency, there have to be also inflammation-independent mechanisms of NOD1 expression regulation by CTRP-3.

抗炎脂肪因子 CTRP-3 可能影响先天免疫反应，如 NOD1。研究了 CTRP-3 对脂肪细胞和单核细胞中 NOD1 介导的炎症以及对 NOD1 表达的影响。用合成的 NOD1 激动剂 Tri-DAP 和重组 CTRP-3 共同刺激小鼠 3T3-L1 前脂肪细胞和脂肪细胞以及人 THP-1 单核细胞样细胞。性腺脂肪组织和原代脂肪细胞是从携带 CTRP-3 敲除 (KO) 在脂肪细胞中但不在基质血管细胞中的小鼠模型中获得的。用 CTRP-3 治疗具有脂多糖 (LPS) 诱导的 NOD1 表达升高的野生型小鼠。通过ELISA测量细胞上清液中分泌的炎性细胞因子，并通过RT-PCR定量mRNA水平。促炎趋化因子和细胞因子分泌（MCP-1、RANTES、脂肪细胞和单核细胞样细胞中的 NOD1 激活可诱导 TNFα)，而细胞与 CTRP-3 的预孵育可有效抑制 MCP-1 和 RANTES 的释放。CTRP-3 还拮抗 LPS 引发的小鼠脂肪组织中 NOD1 基因表达的诱导，而脂肪细胞 CTRP-3 缺乏会上调脂肪组织中 NOD1 的表达。CTRP-3 是肽聚糖诱导的、NOD1 介导的炎症和 LPS 诱导的 NOD1 表达的有效拮抗剂。由于脂肪细胞 CTRP-3 缺乏会增加基础 NOD1 表达，因此 CTRP-3 对 NOD1 表达的调节也必须存在炎症非依赖性机制。CTRP-3 还拮抗 LPS 引发的小鼠脂肪组织中 NOD1 基因表达的诱导，而脂肪细胞 CTRP-3 缺乏会上调脂肪组织中 NOD1 的表达。CTRP-3 是肽聚糖诱导的、NOD1 介导的炎症和 LPS 诱导的 NOD1 表达的有效拮抗剂。由于脂肪细胞 CTRP-3 缺乏会增加基础 NOD1 表达，因此 CTRP-3 对 NOD1 表达的调节也必须存在炎症非依赖性机制。CTRP-3 还拮抗 LPS 引发的小鼠脂肪组织中 NOD1 基因表达的诱导，而脂肪细胞 CTRP-3 缺乏会上调脂肪组织中 NOD1 的表达。CTRP-3 是肽聚糖诱导的、NOD1 介导的炎症和 LPS 诱导的 NOD1 表达的有效拮抗剂。由于脂肪细胞 CTRP-3 缺乏会增加基础 NOD1 表达，因此 CTRP-3 对 NOD1 表达的调节也必须存在炎症非依赖性机制。