mtDNA amplifies beryllium sulfate‐induced inflammatory responses via the cGAS‐STING pathway in 16HBE cells

Author:

Liu Xiaodong12,Jiang Tianyi12,Jin Huiyun12,Yan Chenxi12,Tong Yuqi12,Ding Jiaquan12,Li Yaqi12,Huang Lian12,Zhang Zhaohui12ORCID

Affiliation:

1. Department of Preventive Medicine, School of Public Health, Hengyang Medical School University of South China Hengyang China

2. Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, Hengyang Medical School University of South China Hengyang China

Abstract

AbstractBeryllium sulfate (BeSO4) can cause inflammation through the mechanism, which has not been elucidated. Mitochondrial DNA (mtDNA) is a key contributor of inflammation. With mitochondrial damage, released mtDNA can bind to specific receptors (e.g., cGAS) and then activate related pathway to promote inflammatory responses. To investigate the mechanism of mtDNA in BeSO4‐induced inflammatory response in 16HBE cells, we established the BeSO4‐induced 16HBE cell inflammation model and the ethidium bromide (EB)‐induced ρ016HBE cell model to detect the mtDNA content, oxidative stress‐related markers, mitochondrial membrane potential, the expression of the cGAS‐STING pathway, and inflammation‐related factors. Our results showed that BeSO4 caused oxidative stress, decline of mitochondrial membrane potential, and the release of mtDNA into the cytoplasm of 16HBE cells. In addition, BeSO4 induced inflammation in 16HBE cells by activating the cGAS‐STING pathway. Furthermore, mtDNA deletion inhibited the expression of cGAS‐STING pathway, IL‐10, TNF‐α, and IFN‐β. This study revealed a novel mechanism of BeSO4‐induced inflammation in 16HBE cells, which contributes to the understanding of the molecular mechanism of beryllium and its compounds‐induced toxicity.

Funder

Natural Science Foundation of Hunan Province

Hunan Provincial Innovation Foundation for Postgraduate

Publisher

Wiley

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