Low-dose cadmium telluride quantum dots trigger M1 polarization in macrophages through mTOR-mediated transcription factor EB activation

Tingting Wei; Na Liu; Yongshuai Yao; Xiaoquan Huang; Zhihui Wang; Tianshu Wu; Ting Zhang; Yuying Xue; Meng Tang

doi:10.1016/j.impact.2024.100505

Low-dose cadmium telluride quantum dots trigger M1 polarization in macrophages through mTOR-mediated transcription factor EB activation

NanoImpact. 2024 Apr 3:34:100505. doi: 10.1016/j.impact.2024.100505. Online ahead of print.

Authors

Tingting Wei¹, Na Liu¹, Yongshuai Yao¹, Xiaoquan Huang¹, Zhihui Wang¹, Tianshu Wu¹, Ting Zhang¹, Yuying Xue¹, Meng Tang²

Affiliations

¹ Key Laboratory of Environmental Medicine and Engineering, Ministry of Education; School of Public Health, Southeast University, Nanjing 210009, PR China.
² Key Laboratory of Environmental Medicine and Engineering, Ministry of Education; School of Public Health, Southeast University, Nanjing 210009, PR China. Electronic address: tm@seu.edu.cn.

PMID: 38579989
DOI: 10.1016/j.impact.2024.100505

Abstract

The increasing application of quantum dots (QDs) increases interactions with organisms. The inflammatory imbalance is a significant manifestation of immunotoxicity. Macrophages maintain inflammatory homeostasis. Using macrophages differentiated by phorbol 12-myristate 13-acetate-induced THP-1 cells as models, the study found that low-dose (5 μM) cadmium telluride QDs (CdTe-QDs) hindered monocyte-macrophage differentiation. CD11b is a surface marker of macrophage, and the addition of CdTe-QDs during induction resulted in a decrease in CD11b expression. Moreover, exposure of differentiated THP-1 macrophage (dTHP-1) to 5 μM CdTe-QDs led to the initiation of M1 polarization. This was indicated by the increased surface marker CD86 expression, along with elevated level of NF-κB and IL-1β proteins. The potential mechanisms are being explored. The transcription factor EB (TFEB) plays a significant role in immune regulation and serves as a crucial regulator of the autophagic lysosomal pathway. After exposed to CdTe-QDs, TFEB activation-mediated autophagy and M1 polarization were observed to occur simultaneously in dTHP-1. The mTOR signaling pathway contributed to TFEB activation induced by CdTe-QDs. However, mTOR-independent activation of TFEB failed to promote M1 polarization. These results suggest that mTOR-TFEB is an advantageous target to enhance the biocompatibility of CdTe-QDs.

Keywords: Autophagy; Immunoregulation; Inflammation; Quantum dots.