Titanium surface hydrophilicity modulates the human macrophage inflammatory cytokine response
Titanium surface hydrophilicity modulates the human macrophage inflammatory cytokine response
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DOI：
10.1002/jbm.a.34666
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发表时间：
2014-01-01
影响因子：
4.9
通讯作者：
Ivanovski, Saso
中科院分区：
文献类型：
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作者：
Alfarsi, Mohammed A.;Hamlet, Stephen M.;Ivanovski, Saso
增加钛表面亲水性已被证明可以加速牙种植体骨整合。巨噬细胞在外科植入物放置的早期炎症反应中很重要，并影响随后的愈合反应。本研究探讨了亲水性钛表面对人巨噬细胞系（THP-1）中炎性细胞因子表达谱的调节作用。在暴露于（1）抛光（SMO）、（2）微粗糙喷砂、酸蚀刻（SLA）和（3）抛光改性SLA（modSLA）钛表面1天和3天后，分析了84种细胞因子、趋化因子及其受体的基因。到第3天，与SMO表面相比，SLA表面引起促炎反应，其中16个基因[肿瘤坏死因子（TNF）、白细胞介素（IL）-1、趋化因子（TNF-α）、白细胞介素（IL）-1、白细胞介素（IL）-2、白细胞介素（IL）-1、白细胞介素（IL-1）、白细胞介素（（C-C基序）配体（CCL）-1，2，3，4，18，19和20，趋化因子（C-X-C基序）配体（CXCL）-1，5，8和12，趋化因子（C-C基序）受体（CCR）-7，趋化因子-β（LTB）和白三烯B4受体（LTB 4 R）]。这种作用被modSLA表面抵消，与SLA表面相比，modSLA表面下调了10种基因（TNF，IL-1和CCL-1，3，19和20，CXCL-1和8，以及IL-1受体1型）的表达，而两种基因（骨桥蛋白和CCR 5）的表达上调。这些细胞因子基因表达的变化证实了相应的蛋白质分泌水平的降低，响应于modSLA相比，SLA。这些结果表明，亲水性钛表面可以调节人巨噬细胞促炎细胞因子基因表达和蛋白质分泌。减弱的促炎反应可能是更快和/或改善伤口愈合的重要分子机制。(c)2013 Wiley Periodicals，Inc. J Biomed Mater Res Part A：102A：60-67，2014.
Increased titanium surface hydrophilicity has been shown to accelerate dental implant osseointegration. Macrophages are important in the early inflammatory response to surgical implant placement and influence the subsequent healing response. This study investigated the modulatory effect of a hydrophilic titanium surface on the inflammatory cytokine expression profile in a human macrophage cell line (THP-1). Genes for 84 cytokines, chemokines, and their receptors were analyzed following exposure to (1) polished (SMO), (2) micro-rough sand blasted, acid etched (SLA), and (3) hydrophilic-modified SLA (modSLA) titanium surfaces for 1 and 3 days. By day 3, the SLA surface elicited a pro-inflammatory response compared to the SMO surface with statistically significant up-regulation of 16 genes [Tumor necrosis factor (TNF) Interleukin (IL)-1, Chemokine (C-C motif) ligand (CCL)-1, 2, 3, 4, 18, 19, and 20, Chemokine (C-X-C motif) ligand (CXCL)-1, 5, 8 and 12, Chemokine (C-C motif) receptor (CCR)-7, Lymphotoxin-beta (LTB), and Leukotriene B4 receptor (LTB4R)]. This effect was countered by the modSLA surface, which down-regulated the expression of 10 genes (TNF, IL-1 and , CCL-1, 3, 19 and 20, CXCL-1 and 8, and IL-1 receptor type 1), while two were up-regulated (osteopontin and CCR5) compared to the SLA surface. These cytokine gene expression changes were confirmed by decreased levels of corresponding protein secretion in response to modSLA compared to SLA. These results show that a hydrophilic titanium surface can modulate human macrophage pro-inflammatory cytokine gene expression and protein secretion. An attenuated pro-inflammatory response may be an important molecular mechanism for faster and/or improved wound healing. (c) 2013 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 102A: 60-67, 2014.