4.7 Article

Silicon dioxide nanoparticles induced neurobehavioral impairments by disrupting microbiota-gut-brain axis

期刊

JOURNAL OF NANOBIOTECHNOLOGY
卷 19, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12951-021-00916-2

关键词

Silicon dioxide nanoparticles; Gut-brain axis; Gut microbiota; Neurobehavioral impairments

资金

  1. National Natural Science Foundation of China [81703187, 81602820, 81903358]
  2. Natural Science Foundation of Chongqing [cstc2020jcyj-msxmX0192, cstc2020jcyj-msxmX0155]
  3. Science and Technology Research Program of Chongqing Municipal Education Commission [KJQN201800434, KJQN201900419, KJQN 201900421, KJCXZD2020020]
  4. Research Program of Basic Research and Frontier Technology of Chongqing Yuzhong district [20200105]
  5. Chongqing Talent Project [CQYC2020058650]

向作者/读者索取更多资源

The study showed that Silicon dioxide nanoparticles significantly affected the neurobehavior and gut microbiota of young mice, causing learning and memory impairments as well as tissue damage. SiO(2)NPs may induce neurotoxic effects through disrupting the gut-brain axis, with no significant impact on the gut-lung or gut-liver axis.
Background: Silicon dioxide nanoparticles (SiO(2)NPs) are widely used as additive in the food industry with controversial health risk. Gut microbiota is a new and hot topic in the field of nanotoxicity. It also contributes a novel and insightful view to understand the potential health risk of food-grade SiO(2)NPs in children, who are susceptible to the toxic effects of nanoparticles. Methods: In current study, the young mice were orally administrated with vehicle or SiO(2)NPs solution for 28 days. The effects of SiO(2)NPs on the gut microbiota were detected by 16S ribosomal RNA (rRNA) gene sequencing, and the neurobehavioral functions were evaluated by open field test and Morris water maze. The level of inflammation, tissue integrity of gut and the classical indicators involved in gut-brain, gut-liver and gut-lung axis were all assessed. Results: Our results demonstrated that SiO(2)NPs significantly caused the spatial learning and memory impairments and locomotor inhibition. Although SiO(2)NPs did not trigger evident intestinal or neuronal inflammation, they remarkably damaged the tissue integrity. The microbial diversity within the gut was unexpectedly enhanced in SiO(2)NPs-treated mice, mainly manifested by the increased abundances of Firmicutes and Patescibacteria. Intriguingly, we demonstrated for the first time that the neurobehavioral impairments and brain damages induced by SiO(2)NPs might be distinctively associated with the disruption of gut-brain axis by specific chemical substances originated from gut, such as Vipr1 and Sstr2. Unapparent changes in liver or lung tissues further suggested the absence of gut-liver axis or gut-lung axis regulation upon oral SiO(2)NPs exposure. Conclusion: This study provides a novel idea that the SiO(2)NPs induced neurotoxic effects may occur through distinctive gut-brain axis, showing no significant impact on either gut-lung axis or gut-liver axis. These findings raise the exciting prospect that maintenance and coordination of gastrointestinal functions may be critical for protection against the neurotoxicity of infant foodborne SiO(2)NPs.

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