Gut microbiota dysbiosis mediates mouse kidney fibrosis induced by black phosphorus quantum dots

被引:4
|
作者
Ruan, Fengkai [1 ]
Zeng, Jie [1 ]
Liu, Changqian [1 ]
Han, Jianrong [1 ]
Zheng, Naying [1 ]
Li, Kun [1 ]
Yin, Hanying [1 ]
Wu, Mingtao [1 ]
Ding, Xiaoyan [1 ]
Han, Changshun [1 ]
Yang, Lingtao [1 ]
Yang, Chunyan [1 ]
Wang, Dai [3 ]
Xiao, Nengming [1 ]
Zuo, Zhenghong [1 ,2 ]
He, Chengyong [1 ,2 ]
机构
[1] Xiamen Univ, Shenzhen Res Inst, Fac Med & Life Sci, Sch Life Sci,State Key Lab Cellular Stress Biol, Xiamen 361102, Fujian, Peoples R China
[2] Xiamen Univ, Xiangan Hosp, Fac Med & Life Sci, Sch Med,Dept Endocrinol, Xiamen 361102, Peoples R China
[3] Xiamen Univ, Sch Publ Hlth, Dept Lab Med, State Key Lab Mol Vaccinol & Mol Diagnost, Xiamen 361102, Fujian, Peoples R China
基金
中国国家自然科学基金;
关键词
Black phosphorus; Gut microbiota; Kidney injury; Lactobacillus; Nanosafety; INJURY; INFLAMMATION; SEVERITY; TOXICITY; ISCHEMIA; RECOVERY; CELLS;
D O I
10.1016/j.nantod.2024.102203
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
As a novel type of nanomaterials, black phosphorus quantum dots (BPQDs) have wide application potential, including anti-pathogenic bacteria. However, there is no information on the effects of BPQDs on the symbiotic bacteria after oral exposure. In our study, mice were daily oral administrated to 0.1 and 1 mg/kg BPQDs for 28 days. We found that BPQDs caused gut microbiota dysbiosis and decreased the abundance of Lactobacillus. From the in vitro experiments, we demonstrated that BPQDs inhibited the growth of Lactobacillus via disrupting bacterial cell membrane. Besides, we found that BPQDs oral exposure caused T cell activation, inflammation, and fibrosis in kidneys. Notably, there was no any kidney injury in BPQD-exposed germ-free mice, which proved that gut microbiota mediated BPQD-caused kidney injury. Moreover, supplementation of probiotic Lactobacillus reuteri (L. reu) and a commercial probiotic containing Lactobacillus, could rescue the kidney injury caused by BPQD exposure. As one of the beneficial metabolites of Lactobacillus, the content of acetic acid was decreased after BPQD exposure, which was recovered by probiotic supplementation. Finally, acetic acid treatment also attenuated the kidney injury. In conclusion, this study illustrates that BPQD oral exposure can cause gut microbiota dysbiosis and decrease the abundance of Lactobacillus and the content of acetic acid, all of which might mediate the renal inflammation and fibrosis. Our work suggests that the supplementation of Lactobacillus and their metabolites would be potential intervention approaches for alleviating the remote organ injury caused by nanomaterials.
引用
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页数:12
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