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Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
Published on: July 26, 2017
Polystyrene Nanoplastics Disrupt Immune Cell Development and Suppress T Cell Activation via mTOR and ERK Signaling
Kang-Bin Dan1, Ki-Uk Kim1, Hyeyoung Min1
1College of Pharmacy, Chung-Ang University, Seoul 06974, Republic of Korea.
Abstract:
Plastics are globally recognized as widely used materials, but once discarded, they undergo physical and chemical decomposition, forming micro- and nano-sized particles that lead to adverse effects. Therefore, this study aimed to explore the impact of nanoplastics on immune cells and overall health. Experiments conducted with 100 nm polystyrene nanoparticles (PS-NPs) revealed a decrease in the proliferation of splenic CD4+ T cells, demonstrated by using the MTT assay, carboxyfluorescein succinimidyl ester dilution assay, Ki-67 staining, cell cycle analysis, and mTOR signaling pathway analysis. Furthermore, the differentiation of naïve CD4+ T cells into four CD4+ subsets (Th1, Th2, Th17, Treg cells) appeared to be reduced. PS-NPs were found to suppress the maturation of bone marrow-derived dendritic cells, as evidenced by a decrease in the expression of CD40, CD80, CD86, and major histocompatibility complex class II molecules, following lipopolysaccharide activation, which also reduced the division of T cells. PS-NPs interfered with the immune modulation of bone marrow-derived macrophages (BMDMs), which affected the differentiation of BMDMs into M1 or M2 macrophages. To investigate the in vivo effect of PS-NPs on immune cell development further, 3-week-old mice were administered water containing PS-NPs for 3 weeks. Subsequent analysis of various immune cells in the thymus, bone marrow, and spleen revealed a decrease in cell numbers in the spleen following PS-NP treatment, as well as changes in the composition of conventional dendritic cells, macrophages, and B cells. These findings suggest that PS-NPs can perturb immune cell-associated responses and homeostasis.

