Comparative Effects of Graphene and Molybdenum Disulfide on Human Macrophage Toxicity

Autor: Paolo Samorì, Alberto Bianco, Ding-Kun Ji, Hazel Lin, Matteo Andrea Lucherelli, Giacomo Reina, Stefano Ippolito
Přispěvatelé: Immunopathologie et chimie thérapeutique (ICT), Institut de biologie moléculaire et cellulaire (IBMC), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Zdroj: Small
Small, Wiley-VCH Verlag, 2020, 16 (35), pp.2002194. ⟨10.1002/smll.202002194⟩
ISSN: 1613-6810
1613-6829
Popis: International audience; Graphene and other two-dimensional (2D) materials, such as molybdenum disulfide, have been increasingly used in electronics, composites and biomedicine. In particular, MoS2 and graphene hybrids have attracted a great interest for applications in the biomedical research, therefore stimulating a pertinent investigation on their safety in immune cells like macrophages, which commonly engulf these materials. In our study, M1 and M2 macrophage viability and activation were mainly found to be unaffected by few-layer graphene (FLG) and MoS2 at doses up to 50 µg/mL. The uptake of both materials was confirmed by transmission electron microscopy, inductively coupled plasma mass spectrometry and inductively coupled plasma atomic emission spectroscopy. Notably, both 2D materials increased the secretion of inflammatory cytokines in M1 macrophages. At the highest dose, FLG decreased CD206 expression while MoS2 decreased CD80 expression. CathB and CathL gene expression were dose-dependently increased by both materials. Despite a minimal impact on the autophagic pathway, FLG was found to increase the expression of Atg5 and autophagic flux, as observed by western blotting of LC3-II, in M1 macrophages. Overall, FLG and MoS2 are little toxic in human macrophages even though they were found to trigger cell stress and inflammatory responses. 2
Databáze: OpenAIRE