ICBAS - Instituto de Ciências Biomédicas de Abel Salazar, Universidade do Porto, Rua de Jorge Viterbo Ferreira n.° 228, 4050-313 Porto, Portugal; Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Portugal; INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Rua do Campo Alegre 823, 4150-180 Porto, Portugal.
ICBAS - Instituto de Ciências Biomédicas de Abel Salazar, Universidade do Porto, Rua de Jorge Viterbo Ferreira n.° 228, 4050-313 Porto, Portugal; UMIB - Unit for Multidisciplinary Biomedical Research of ICBAS - Instituto de Ciências Biomédicas de Abel Salazar, Universidade do Porto, Rua de Jorge Viterbo Ferreira n.° 228, 4050-313 Porto, Portugal.
Biomaterials. 2015;53:566-73. doi: 10.1016/j.biomaterials.2015.02.120. Epub 2015 Mar 23.
In our search for immunomodulatory biomaterials capable of modulating the inflammatory response through M2 macrophage polarization, we report here on a new strategy that resulted from the incorporation of resolvin D1 (RvD1), a pro-resolution lipid mediator in porous 3D chitosan (Ch) scaffolds, followed by its lyophilisation. We have investigated the inflammatory response caused by this biomaterial in vivo using a mouse air-pouch model of inflammation. We found that this developed material caused a decrease in inflammatory cells recruited to the implant site, together with higher numbers of F4/80(+)/CD206(+) cells (M2 macrophages) and lower numbers of F4/80(+)/CCR7(+) cells (M1 macrophages). It also induced a general decrease in pro-inflammatory cytokines, and caused a decrease in the inflammatory cells observed around and within the implanted scaffolds, when compared with Ch alone or Ch not submitted to lyophilisation after RvD1 incorporation. Our results demonstrate that we were able to develop an immunomodulating biomaterial that triggers a shift in the macrophage response towards a M2 reparative response that will be advantageous for the host.
在寻找能够通过 M2 巨噬细胞极化来调节炎症反应的免疫调节生物材料的过程中，我们在此报告了一种新策略，该策略是将促解决脂质介质分解素 D1（RvD1）掺入多孔 3D 壳聚糖（Ch）支架中，然后对其进行冻干。我们使用小鼠气囊中炎症模型在体内研究了这种生物材料引起的炎症反应。我们发现，这种材料可减少募集到植入部位的炎症细胞，同时增加 F4/80(+)/CD206(+)细胞（M2 巨噬细胞）的数量，减少 F4/80(+)/CCR7(+)细胞（M1 巨噬细胞）的数量。与单独的 Ch 或 Ch 相比，它还诱导了促炎细胞因子的普遍减少，并导致在植入支架周围和内部观察到的炎症细胞减少，而 RvD1 掺入后未经冻干的 Ch 则没有这种效果。我们的结果表明，我们能够开发出一种免疫调节生物材料，该材料可触发巨噬细胞反应向 M2 修复反应转变，这对宿主有利。
