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二氧化钛纳米颗粒刺激海胆免疫细胞吞噬活性,涉及Toll样受体/ p38丝裂原活化蛋白激酶介导的信号通路。

Titanium dioxide nanoparticles stimulate sea urchin immune cell phagocytic activity involving TLR/p38 MAPK-mediated signalling pathway.

作者信息

Pinsino Annalisa, Russo Roberta, Bonaventura Rosa, Brunelli Andrea, Marcomini Antonio, Matranga Valeria

机构信息

Consiglio Nazionale delle Ricerche, Istituto di Biomedicina e Immunologia Molecolare "A. Monroy", Via Ugo La Malfa 153, 90146 Palermo, Italy.

Dipartimento di Scienze Ambientali, Informatica e Statistica, Università Ca' Foscari Venezia, Calle Larga S. Marta 2137, 30123 Venezia, Italy.

出版信息

Sci Rep. 2015 Sep 28;5:14492. doi: 10.1038/srep14492.

DOI:10.1038/srep14492
PMID:26412401
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4585977/
Abstract

Titanium dioxide nanoparticles (TiO2NPs) are one of the most widespread-engineered particles in use for drug delivery, cosmetics, and electronics. However, TiO2NP safety is still an open issue, even for ethical reasons. In this work, we investigated the sea urchin Paracentrotus lividus immune cell model as a proxy to humans, to elucidate a potential pathway that can be involved in the persistent TiO2NP-immune cell interaction in vivo. Morphology, phagocytic ability, changes in activation/inactivation of a few mitogen-activated protein kinases (p38 MAPK, ERK), variations of other key proteins triggering immune response (Toll-like receptor 4-like, Heat shock protein 70, Interleukin-6) and modifications in the expression of related immune response genes were investigated. Our findings indicate that TiO2NPs influence the signal transduction downstream targets of p38 MAPK without eliciting an inflammatory response or other harmful effects on biological functions. We strongly recommend sea urchin immune cells as a new powerful model for nano-safety/nano-toxicity investigations without the ethical normative issue.

摘要

二氧化钛纳米颗粒(TiO2NPs)是用于药物递送、化妆品和电子产品的应用最为广泛的工程颗粒之一。然而,即使出于伦理原因,TiO2NP的安全性仍是一个悬而未决的问题。在这项工作中,我们研究了海胆Paracentrotus lividus免疫细胞模型作为人类的替代模型,以阐明可能参与体内TiO2NP与免疫细胞持续相互作用的潜在途径。研究了细胞形态、吞噬能力、几种丝裂原活化蛋白激酶(p38 MAPK、ERK)的激活/失活变化、触发免疫反应的其他关键蛋白(类Toll样受体4、热休克蛋白70、白细胞介素-6)的变化以及相关免疫反应基因表达的改变。我们的研究结果表明,TiO2NPs影响p38 MAPK的信号转导下游靶点,而不会引发炎症反应或对生物学功能产生其他有害影响。我们强烈推荐将海胆免疫细胞作为一种新的强大模型,用于纳米安全性/纳米毒性研究,而不存在伦理规范问题。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/4a7776c1f459/srep14492-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/834787a357e3/srep14492-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/1d8dcd7bfab1/srep14492-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/5f66601115ec/srep14492-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/e71954ce9ceb/srep14492-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/76c400eafba5/srep14492-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/4a7776c1f459/srep14492-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/834787a357e3/srep14492-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/1d8dcd7bfab1/srep14492-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/5f66601115ec/srep14492-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/e71954ce9ceb/srep14492-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/76c400eafba5/srep14492-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffb0/4585977/4a7776c1f459/srep14492-f6.jpg

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