首页> 外文OA文献 >Chitosan polysaccharide suppress toll like receptor dependent immune response Çitosan polisakkaridi toll benzeri reseptöre bağlı bağışıklık yanıtını baskılar
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Chitosan polysaccharide suppress toll like receptor dependent immune response Çitosan polisakkaridi toll benzeri reseptöre bağlı bağışıklık yanıtını baskılar

机译:壳聚糖多糖抑制通行费样受体依赖性免疫反应壳聚糖多糖抑制通行费样受体引起的免疫反应

摘要

Objectives: Chitosan is a widely used vaccine or anti-cancer delivery vehicle. In this study, we investigated the immunomodulatory effect of chitosan/pIC nanocomplexes on mouse immune cells. Materials and methods: Proliferative and cytotoxic features of chitosan were tested via CCK-8 assay on RAW 264. 7. IL-1β production was assessed via ELISA from PEC supernatants. TNF-α, and NO induction from chitosan treated RAW cells detected by ELISA and Griess assay, respectively. mRNA message levels of TLRs and cytokines on macrophages in response to chitosan/pIC nanocomplex treatments were evaluated by RT-PCR. Results: Results revealed that chitosan is non-toxic to cells, however, proliferative capacities of macrophages were reduced by chitosan administration. Mouse PECs treated with chitosan, led to NLRP3 dependent inflammasome activation as evidenced by dose-dependent IL-1β secretion. Chitosan/pIC nanocomplexes did not improve immunostimulatory action of pIC on RAW cells, since TNF-α and NO productions remained unaltered. Expression levels of several TLRs, CXCL-16 and IFN-α messages from mouse splenocytes were down regulated in response to chitosan/pIC nanocomplex treatment. Conclusion: Our results revealed that chitosan is an anti-proliferative and inflammasome triggering macromolecule on immune cells. Utilization of chitosan as a carrier system is of concern for immunotherapeutic applications. © 2015 Turkish Journal of Immunology.
机译:目的:壳聚糖是一种广泛使用的疫苗或抗癌载体。在这项研究中,我们调查了壳聚糖/ pIC纳米复合物对小鼠免疫细胞的免疫调节作用。材料和方法:通过在RAW 264上进行CCK-8分析,测试了壳聚糖的增殖和细胞毒性特征。7.通过ELISA从PEC上清液中评估了IL-1β的产生。通过ELISA和Griess分析分别检测了壳聚糖处理的RAW细胞的TNF-α和NO诱导。通过RT-PCR评估响应壳聚糖/ pIC纳米复合物处理的巨噬细胞上TLR和细胞因子的mRNA信息水平。结果:结果表明,壳聚糖对细胞无毒,但是,施用壳聚糖可降低巨噬细胞的增殖能力。壳聚糖处理的小鼠PEC导致NLRP3依赖性炎性小体活化,如剂量依赖性IL-1β分泌所证明。壳聚糖/ pIC纳米复合物不能改善pIC对RAW细胞的免疫刺激作用,因为TNF-α和NO的产生保持不变。响应于壳聚糖/ pIC纳米复合物处理,来自小鼠脾细胞的几种TLR,CXCL-16和IFN-α信息的表达水平被下调。结论:我们的结果表明,壳聚糖是一种抗增殖和炎症小体,触发免疫细胞上的大分子。对于免疫治疗应用而言,壳聚糖作为载体系统的使用是令人关注的。 ©2015土耳其免疫学杂志。

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