Department of Orthopedic, The First Affiliated Hospital, Hengyang Medical School, University of South China, No. 69, Chuanshan Road, Hengyang City, 421001, Hunan Province, China.
Institute of Orthopedics, The First Medical Center, Chinese PLA General Hospital, Beijing Key Lab of Regenerative Medicine in Orthopedics, Key Laboratory of Musculoskeletal Trauma and War Injuries PLA, No. 28 Fuxing Road, Haidian District, Beijing, 100853, China.
Arthritis Res Ther. 2021 Dec 4;23(1):294. doi: 10.1186/s13075-021-02684-8.
The use of interleukin-1 receptor-associated kinase 4 (IRAK4) inhibitor as a treatment for the inflammatory joint disease is a promising method. However, its underlying mechanism in osteoarthritis (OA) remains unclear. The purpose of this study is to look into the effects of adenovirus-mediated knockdown of IRAK4 on synovitis in the OA rabbit model.
Ad-shIRAK4 was injected two weeks after anterior cruciate ligament resection. Six weeks later, the rabbits were killed. The expression of IRAK4, TNFR-associated factor 6(TRAF6), TGF-activated kinase 1(TAK1), p-IKB kinase (p-IKK), p-nuclear factor kappa-B (p-NFκB), p38, and p-p38 in the synovial membrane was detected by western blot, qRT-PCR, and immunohistochemistry analysis. Immunohistochemistry was to detect the expression of IRAK4 proteins in articular cartilage. H&E staining was to assess the pathological changes of synovium and cartilage. The levels of interleukin (IL)-1β, tumor necrosis factor-α(TNF-α), and MMP-13 in the synovial fluid were measured by ELISA. X-ray and micro-computerized tomography (μCT) scans were used to assess knee joint conditions and microstructure of subchondral bone.
IRAK4 expression levels in synovial tissues of the OA model group exhibited a significant upward trend. Ad-shIRAK4 significantly reduced IRAK4 mRNA expression in synovium tissues. Notably, Ad-shIRAK4 suppressed the Toll-like receptor/interleukin-1 receptor (TLR/IL-1R) signaling. In addition, in the Ad-shIRAK4 treatment group, we can see less inflammatory cell infiltration and reduced hyperplasia and angiogenesis. The levels of IL-1β, TNF-α, and MMP-13 in the synovial fluid in the OA model group were significantly higher than that in the control group, which were reduced by Ad-shIRAK4 treatment. Finally, Results of HE stains, immunohistochemistry, and μCT showed that Ad-shIRAK4 treatment has a protective effect on cartilage damage.
IRAK4 is significantly upregulated in the synovium from the osteoarthritis rabbit model. In addition, Ad-shIRAK4 reduced the expression of IRAK4 and suppressed TLR/IL-1R signaling in the synovium from the osteoarthritis rabbit model. Ad-shIRAK4 could alleviate synovitis and cartilage degradation in the osteoarthritis rabbit model, and thus alleviate the symptoms of OA and prevent the progression of OA.
白细胞介素-1 受体相关激酶 4(IRAK4)抑制剂作为一种治疗炎性关节疾病的方法具有广阔的应用前景。然而,其在骨关节炎(OA)中的作用机制尚不清楚。本研究旨在探讨腺病毒介导的 IRAK4 敲低对 OA 兔模型滑膜炎的影响。
在前交叉韧带切除后两周注射 Ad-shIRAK4。6 周后处死兔子。Western blot、qRT-PCR 和免疫组化分析检测滑膜中 IRAK4、肿瘤坏死因子受体相关因子 6(TRAF6)、转化生长因子激活激酶 1(TAK1)、p-IKB 激酶(p-IKK)、p-核因子 kappa-B(p-NFκB)、p38 和 p-p38 的表达。免疫组化检测关节软骨中 IRAK4 蛋白的表达。H&E 染色评估滑膜和软骨的病理变化。ELISA 法检测滑液中白细胞介素(IL)-1β、肿瘤坏死因子-α(TNF-α)和基质金属蛋白酶 13(MMP-13)的水平。X 射线和微计算机断层扫描(μCT)扫描评估膝关节状况和软骨下骨的微观结构。
OA 模型组滑膜组织中 IRAK4 表达水平呈明显上升趋势。Ad-shIRAK4 显著降低滑膜组织中 IRAK4 mRNA 的表达。值得注意的是,Ad-shIRAK4 抑制了 Toll 样受体/白细胞介素-1 受体(TLR/IL-1R)信号通路。此外,在 Ad-shIRAK4 治疗组中,我们可以看到炎症细胞浸润减少,增生和血管生成减少。OA 模型组滑液中 IL-1β、TNF-α 和 MMP-13 的水平明显高于对照组,Ad-shIRAK4 治疗后降低。最后,HE 染色、免疫组化和 μCT 结果表明,Ad-shIRAK4 治疗对软骨损伤具有保护作用。
OA 兔模型滑膜中 IRAK4 表达显著上调。此外,Ad-shIRAK4 降低了 OA 兔模型滑膜中 IRAK4 的表达,并抑制了 TLR/IL-1R 信号通路。Ad-shIRAK4 可减轻 OA 兔模型中的滑膜炎和软骨降解,从而缓解 OA 症状并阻止 OA 的进展。