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Ultrafine particles (UFPs) referred to particular matters with aerosol diameter less than 100 nm. Because of the lightweight and small size, UFPs have become an occupational inhalation risk. The UFPs will be accumulated in the deep lung through inhalation, and then reach into all the organs via circulation system; some UFPs even stay in the brain. As previous study reported, UFPs exposure is usually associated with cardiovascular disease, such as atherosclerosis (AS). In our study, we tried to understand how acute UFP exposure caused the biological dysregulation in atherosclerosis. Acute exposure of UFPs were applied to mice for 6 consecutive days, mice were sacrificed after 3, 5, 7, and 10 days post-exposure. Aorta and serum were collected for histological and biomarkers analysis. Mice aortic adventitial fibroblasts (MAFs) were isolated from mice and used to further study to understand the mechanism of UFPs induced atherosclerosis. Compared to the untreated control, the inflammation responses and nitrate stress were observed after acute exposure of UFPs, with increased IL-6, MCP-1, p47phox, and 3-NT levels in the mice serum. Besides, upregulation of microRNAs: miR-301b-3p and Let-7c-1-3p, and their downstream target: Smad2, Smad3, and TGFβ1 were also observed in mouse aorta after acute exposure of UFPs. Similar results were identified in vitro as well. Acute exposure of UFPs induced the systematic nitrate stress and inflammation responses, along with the changes of vascular permeability. Dysregulated miRNAs and TGFβ/Smads signaling pathway indicated the higher risk of atherosclerosis/vasculature remodeling when exposed to UFPs.

Chronic noise exposure has been implicated in increased risk of diabetes. However, there is limited experimental evidence of the mechanisms linking chronic noise stress and glucose metabolism. We addressed this in the present study by examining glucose metabolism, immune response, and changes in gut microbiota/host inflammatory homeostasis in rats exposed to noise for 30 consecutive days. Chronic noise exposure increased blood glucose and corticosterone levels for at least 14 days after cessation of noise. Stressed rats also exhibited elevated levels of glycogen and triglyceride in the liver and impaired hepatic insulin production via insulin-induced insulin receptor/insulin receptor substrate 1/glycogen synthase kinase 3β signalling, which persisted for 3-14 days after cessation of noise exposure. Chronic noise altered the percentage of Proteobacteria and Actinobacteria in the gut, increasing Roseburia but decreasing Faecalibacterium levels in the cecum relative to controls. Immunoglobulin A, interleukin 1β, and tumor necrosis factor α levels were also elevated in the intestine of these animals, corresponding to noise-induced abnormalities in glucose regulation and insulin sensitivity. These results suggest that lifelong environmental noise exposure could have cumulative effects on diabetes onset and development resulting from alterations in gut microbiota composition and intestinal inflammation.

Metabolites produced by the human gut microbiota play an important role in fighting and intervening in inflammatory diseases. It remains unknown whether immune homeostasis is influenced by increasing concentrations of air pollutants such as oil mist particulate matters (OMPM). Herein, we report that OMPM exposure induces a hyperlipidemia-related phenotype through microbiota dysregulation-mediated downregulation of the anti-inflammatory short-chain fatty acid (SCFA)–GPR43 axis and activation of the inflammatory pathway. A rat model showed that exposure to OMPM promoted visceral and serum lipid accumulation and inflammatory cytokine upregulation. Furthermore, our research indicated a reduction in both the "healthy" microbiome and the production of SCFAs in the intestinal contents following exposure to OMPM. The SCFA receptor GPR43 was downregulated in both the ileum and white adipose tissues (WATs). The OMPM treatment mechanism was as follows: the gut barrier was compromised, leading to increased levels of lipopolysaccharide (LPS). This increase activated the Toll-like receptor 4 Nuclear Factor-κB (TLR4-NF-κB) signaling pathway in WATs, consequently fueling hyperlipidemia-related inflammation through a positive-feedback circuit. Our findings thus imply that OMPM pollution leads to hyperlipemia-related inflammation through impairing the microbiota-SCFAs-GPR43 pathway and activating the LSP-induced TLR4-NF-κB cascade; our findings also suggest that OMPM pollution is a potential threat to humanmicrobiota dysregulation and the occurrence of inflammatory diseases. [Display omitted] • OMPM can induce hyperlipidaemia-related inflammation and macrophage infiltration. • OMPM can disturb gut microbiota to inhibit anti-inflammatory SCFAs-GPR43 signaling. • OMPM can impair the intestinal barrier to release LPS into serum. • OMPM can activate the LPS-TLR4/NF-κB pathway to induce body inflammation. [ABSTRACT FROM AUTHOR]

Growing concern has been raised over the potential hazard of nanoparticles (NPs) on human health from ambient particulate air pollution. Silicon dioxide (SiO) NPs are one of the most widely used nanoparticles in many sectors of industry. Research on NPs has focused mainly on their toxicity in organs. Meanwhile, NPs are present in the air year-round, but are more serious in winter. Thus, the aim of this study was to evaluate the inflammatory response to SiO NPs using in vivo test systems. The composition of particulate matter is complicated; however, elemental silicon accounts for a significant proportion. Cold exposure can induce many kinds of systemic reactions. Thus, the second aim of this study was also to evaluate the combined effect of NPs and cold exposure on human health. There is little research on the combined effects of nanoparticles and cold on inflammation. Sprague-Dawley rats were randomly divided into four groups: those exposed to SiO NPs by intratracheal instillation, those exposed to at 4 °C 4 h/day for 4 weeks, a combined SiO NPs and cold exposure group, and a control group. Inflammatory cell infiltration in the lungs was mainly observed after exposure to SiO NPs or cold. Hematoxylin and eosin staining revealed that inflammation of the lungs was more serious in the combined group. In the white adipose tissue and brown adipose tissue of the combined groups, the mRNA expressions of pro-inflammatory cytokines were upregulated. In conclusion, SiO NPs combined with cold exposure induced a stronger systemic inflammatory response, accompanied by more serious health hazards. [ABSTRACT FROM AUTHOR]