Cell Adhesion on Nanofibrous Polytetrafluoroethylene (nPTFE)

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• 作者：Kristy M. Ainslie ; Eric M. Bachelder ; Sachin Borkar ; Alisar S. Zahr ; Ayusman Sen ; John V. Badding ; Michael V. Pishko
• 刊名：Langmuir
• 出版年：2007
• 出版时间：January 16, 2007
• 年：2007
• 卷：23
• 期：2
• 页码：747 - 754
• 全文大小：317K
• 年卷期：v.23,no.2(January 16, 2007)
• ISSN：1520-5827

文摘

Here, we described the in vitro biocompatibility of a novel nanostructured surface composed of PTFE as a potentialpolymer for the prevention of adverse host reactions to implanted devices. The foreign body response is characterizedat the tissue-material interface by several layers of macrophages and large multinucleated cells known as foreignbody giant cells (FBGC), and a fibrous capsule. The nanofibers of nanofibrous PTFE (nPTFE) range in size from20 to 30 nm in width and 3-4 mm in length. Glass surfaces coated with nPTFE (produced by jet-blowing of PTFE601A) were tested under in vitro conditions to characterize the amount of protein adsorption, cell adhesion, and cellviability. We have shown that nPTFE adsorbs 495 ± 100 ng of bovine serum albumin (BSA) per cm². This level wasconsiderably higher than planar PTFE, most likely due to the increase in hydrophobicity and available surface area,both a result of the nanoarchitecture. Endothelial cells and macrophages were used to determine the degree of celladsorption on the surface of the nanostructured polymer. Both cell types were significantly more round and occupiedless area on nPTFE as compared to tissue culture polystyrene (TCPS). Furthermore, a larger majority of the cells onthe nPTFE were dead compared to TCPS, at dead-to-live ratios of 778 ± 271 to 1 and 23 ± 5.6 to 1, respectively.Since there was a high amount of cell death (due to either apoptosis or necrosis), and the foreign body response isa form of chronic inflammation, an 18 cytokine Luminex panel was performed on the supernatant from macrophagesadherent on nPTFE and TCPS. As a positive control for inflammation, lipopolysaccharide (LPS) was added to macrophageson TCPS to estimate the maximum inflammation response of the macrophages. From the data presented with respectto IL-1, TNF-, IFN-, and IL-5, we concluded that nPTFE is nonimmunogenic and should not yield a huge inflammatoryresponse in vivo, and cell death observed on the surface of nPTFE was likely due to apoptosis resulting from theinability of cells to spread on these surface. On the basis of the production of IL-1, IL-6, IL-4, and GM-CSF, weconcluded that FBGC formation on nPTFE may be decreased as compared to materials known to elicit FBGC formationin vivo.