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Biomaterials and the foreign body reaction: Surface chemistry dependent macrophage adhesion, fusion, apoptosis, and cytokine production.

機譯：生物材料和異物反應：表面化學依賴于巨噬細胞粘附，融合，凋亡和細胞因子產生。

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The foreign body reaction has proven to be a hindrance to the functionality of implanted biomedical devices. The ability to direct this reaction, inflammation, and wound healing via the material-dependent control of key cellular components, macrophages and foreign body giant cells (FBGCs), is vital to the development of future biomedical devices. This dissertation addresses the hypothesis that surface chemistry directs adherent macrophage/FBGC behavior. Specifically, this research endeavored to elucidate the relationship of surface hydrophobicity, hydrophilicity, and ionic chemistry with macrophage adhesion, activation, fusion into FBGCs, apoptosis, and production of cytokines, chemokines, matrix metalloproteinases (MMPs), and tissue inhibitors of MMPs (TIMPs) using model material systems. In addition, a dynamic mathematical model was developed in order to further understand and predict these relationships.; Utilizing an in vitro human monocyte culture system and surface-modified biomaterials displaying hydrophobic, hydrophilic, and/or ionic chemistries, it has been demonstrated that material surface chemistry influences macrophage adhesion and fusion ultimately directing the cytokines/chemokines/MMPs/TIMPs released from biomaterial-adherent macrophages/FBGCs. Hydrophilic/neutral surfaces significantly inhibited adhesion and fusion in comparison to the hydrophobic and hydrophilic/ionic surfaces. Adherent cells on these cell-limiting hydrophilic/neutral surfaces produced greater quantities of each protein analyzed in comparison to the adhesion supporting surfaces indicating an increased activation state in these cells. This finding directly contradicts previous dogma that cell activation correlates with cellular adhesion prompting additional analysis into this phenomenon. In addition, the cytokine/chemokine profiles produced by adherent cells at earlier timepoints shifted from a more classically activated state to an alternatively activated state at later timepoints suggesting that a phenotypic switch occurs in these biomaterial-adherent cells.; Subsequent analysis using surface-modified polyurethanes confirmed that FBGC formation was promoted by hydrophobic chemistry modifications, in vitro and in vivo. Macrophage apoptosis was promoted at earlier timepoints in vivo, while fusion was promoted at later timepoints supporting the theory that macrophages fuse as a mechanism to escape apoptosis.; This pivotal study clearly presents evidence that material surface chemistry can differentially affect macrophage/FBGC adhesion, activation, fusion, and apoptosis and the cytokine/chemokine/MMP/TIMP profiles derived from activated macrophages/FBGCs adherent to biomaterial surfaces.
機譯：異物反應已被證明是對植入式生物醫(yī)學設備功能的阻礙。通過對關鍵細胞成分，巨噬細胞和異物巨細胞（FBGC）的材料依賴性控制來指導這種反應，炎癥和傷口愈合的能力，對于未來生物醫(yī)學設備的開發(fā)至關重要。本文提出了表面化學指導粘附巨噬細胞/ FBGC行為的假說。具體而言，這項研究致力于闡明表面疏水性，親水性和離子化學與巨噬細胞粘附，活化，融合到FBGC中，細胞凋亡，細胞因子，趨化因子，基質金屬蛋白酶（MMP）以及MMPs組織抑制劑（TIMPs）的關系。 ）使用模型材料系統(tǒng)。另外，開發(fā)了動態(tài)數(shù)學模型，以進一步理解和預測這些關系。利用體外人類單核細胞培養(yǎng)系統(tǒng)和表面修飾的生物材料顯示疏水，親水和/或離子化學性質，已證明材料表面化學影響巨噬細胞粘附和融合，最終指導從生物材料釋放的細胞因子/趨化因子/ MMP / TIMP -貼壁巨噬細胞/ FBGC。與疏水和親水/離子表面相比，親水/中性表面顯著抑制粘附和融合。與粘附支持表面相比，這些限制細胞的親水/中性表面上的粘附細胞產生了更多量的每種蛋白質，表明這些細胞的活化狀態(tài)增加。這一發(fā)現(xiàn)與先前的教條直接矛盾，即細胞活化與細胞粘附相關，促使對此現(xiàn)象進行進一步分析。另外，粘附細胞在較早的時間點產生的細胞因子/趨化因子譜從較經典的活化狀態(tài)轉變?yōu)檩^晚的時間的交替活化狀態(tài)，這表明在這些生物材料粘附的細胞中發(fā)生了表型轉換。隨后使用表面改性的聚氨酯進行的分析證實，通過體外和體內的疏水化學修飾，F(xiàn)BGC的形成得以促進。巨噬細胞凋亡在體內較早的時間點被促進，而融合在較晚的時間點被促進，這支持了巨噬細胞融合作為逃避凋亡的機制的理論。這項關鍵性研究清楚地表明，物質表面化學可以差異性影響巨噬細胞/ FBGC的粘附，活化，融合和凋亡，以及源自活化巨噬細胞/ FBGC的粘附于生物材料表面的細胞因子/趨化因子/ MMP / TIMP分布圖。

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  • 作者

    Jones, Jacqueline Ann.;

  • 作者單位

    Case Western Reserve University.;

  • 授予單位 Case Western Reserve University.;
  • 學科 Engineering Biomedical.
  • 學位 Ph.D.
  • 年度 2007
  • 頁碼 258 p.
  • 總頁數(shù) 258
  • 原文格式 PDF
  • 正文語種 eng
  • 中圖分類 生物醫(yī)學工程;
  • 關鍵詞

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