Polystyrene nanoplastics deteriorate LPS-modulated duodenal permeability and inflammation in mice via ROS drived-NF-κB/NLRP3 pathway. (November 2022)

• Record Type: Journal Article
• Authors: He, Yujiao; Li, Zhe; Xu, Tong; Luo, Dongliu; Chi, Qianru; Zhang, Yiming; Li, Shu
• Is Part Of: Chemosphere. Volume 307:Part 1(2022)
• Publication Date: 2022-11
• Subjects: Polystyrene nanoplastics -- NF-κB/NLRP3 -- Oxidative stress -- Duodenum -- Inflammation; Pollution -- Periodicals; Pollution -- Physiological effect -- Periodicals; Environmental sciences -- Periodicals; Atmospheric chemistry -- Periodicals; 551.511
• DOI: 10.1016/j.chemosphere.2022.135662
• Languages: English
• ISSNs: 0045-6535

Abstract

Abstract: The widespread occurrence of nanoplastics (NPs), has markedly affected the ecosystem and has become a global threat to animals and human health. There is growing evidence showing that polystyrene nanoparticles (PSNPs) exposure induced enteritis and the intestinal barrier disorder. Lipopolysaccharide (LPS) can trigger the inflammation burden of various tissues. Whether PSNPs deteriorate LPS-induced intestinal damage via ROS drived-NF-κB/NLRP3 pathway is remains unknown. In this study, PSNPs exposure/PSNPs and LPS co-exposure mice model were duplicated by intraperitoneal injection. The results showed that exposure to PSNPs/LPS caused duodenal inflammation and increased permeability. We evaluated the change of duodenum structure, oxidative stress parameters, inflammatory factors, and tight junction protein in the duodenum. We found that PSNPs/LPS could aggravate the production of ROS and oxidative stress in cells, activate NF-κB/NLRP3 pathway, decrease the expression tight junction proteins (ZO-1, Claudin 1, and Occludin) levels, promote inflammatory factors (TNF-α, IL-6, and IFN-γ) expressions. Duodenal oxidative stress and inflammation in PS + LPS group were more serious than those in single exposure group, which could be alleviated by NF-kB inhibitor QNZ. Collectively, the results verified that PSNPs deteriorated LPS-induced inflammation and increasing permeability in mice duodenum via ROS drived-NF-κB/NLRP3 pathway. The current study indicated the relationship and molecular mechanism between PSNPs and intestinal injury, providing novel insights into the adverse effects of PSNPs exposure on mammals and humans. Graphical abstract: Image 1 Highlights: PSNPs exposure can damage intestinal epithelial barrier function. PSNPs exposure promoted LPS-induced intestinal inflammation. In vitro, PSNPs exposure induced the production of ROS, causing cellular damage. PSNPs exposure can induce oxidative stress and activate NF-κB/NLRP3 pathway.