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首页> 外文期刊>Biomaterials >The effect of chitosan on the migration of neutrophil-like HL60 cells, mediated by IL-8.
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The effect of chitosan on the migration of neutrophil-like HL60 cells, mediated by IL-8.

机译：壳聚糖对由IL-8介导的嗜中性粒细胞样HL60细胞迁移的影响。

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Research interest in chitosan stems in part from the demonstrated wound healing properties. The benefits of chitosan as a therapeutic agent appear to be paradoxical because chitosan also elicits neutrophil infiltration indicative of an inflammatory response. While the affinity between chitosan and neutrophils has been well documented, the underlying mechanism is unclear. To our knowledge, no studies have investigated the consequences of chitosan-neutrophil interaction to explain neutrophil migration. To that end, transwell migration assays to chitosan of varying extent of acetylation were conducted using a differentiated model cell line (HL60-PMN) in order to assess the effect of chitosan chemistry and the resultant physical properties such as charge and hydrophobicity on neutrophil migration. As chitosan N-acetylation increased, neutrophil migration increased and chitosan became less positively charged and more hydrophobic. Moreover, HL60-PMN cells secreted the potent neutrophil chemokine IL-8, also known as CXCL8, when exposed to chitosan and IL-8 levels increased with N-acetylation, and migration was inhibited by anti-IL-8 antibodies. Collectively these results suggest that chitosan-neutrophil interaction is encouraged by material properties, results in IL-8 secretion, and causes migration of neutrophils to chitosan. The implication is that the wound healing properties of chitosan may be enhanced through the attenuation of overabundant neutrophils, and thus the inflammatory response, simply by changing chitosan N-acetylation.
机译：对壳聚糖的研究兴趣部分源于已证明的伤口愈合特性。壳聚糖作为治疗剂的益处似乎是自相矛盾的，因为壳聚糖还引起指示炎症反应的嗜中性粒细胞浸润。尽管壳聚糖和嗜中性粒细胞之间的亲和力已得到充分证明，但其潜在机制尚不清楚。据我们所知，尚无研究调查壳聚糖-中性粒细胞相互作用来解释中性粒细胞迁移的后果。为此，使用分化的模型细胞系（HL60-PMN）对不同乙酰化程度的壳聚糖进行了跨孔迁移分析，以评估壳聚糖化学的影响以及由此产生的物理性质（如电荷和疏水性）对嗜中性白细胞迁移的影响。随着壳聚糖N-乙酰化作用的增加，中性粒细胞迁移增加，壳聚糖的带正电性降低，疏水性增加。此外，HL60-PMN细胞在暴露于壳聚糖时会分泌有效的嗜中性粒细胞趋化因子IL-8（也称为CXCL8），并且IL-8水平会随着N-乙酰化而增加，并且迁移会受到抗IL-8抗体的抑制。这些结果共同表明，壳聚糖-嗜中性粒细胞的相互作用受到物质特性的鼓励，导致IL-8分泌，并导致嗜中性粒细胞迁移至壳聚糖。这暗示着，壳聚糖的伤口愈合特性可以通过改变过量的中性粒细胞，从而通过简单地改变壳聚糖N-乙酰化来增强炎症反应。

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