Project description:We characterized the transcriptomic profile of whole left lung homogenate in dust exposed Fat-1 and C57Bl/6 (WT) mice in male and female mice.
Project description:Agricultural industry workers are frequently exposed to harmful dust particles and consequently have a higher risk of developing chronic lung inflammatory conditions such as chronic obstructive pulmonary disease (COPD). Lipocalin-2 (LCN-2) is an innate immune protein with paradoxical roles in both pro- and anti-inflammatory responses at mucosal sites; however, its role in the lung during homeostatic and inflammatory states, such as those induced by inhaled dusts, remain unknown. Here, we investigated the role of LCN-2 in a murine model of organic dust exposure-induced lung inflammation using wildtype C57Bl/6 (WT) and LCN-2 knockout (KO) mice exposed repetitively to extracts of dusts (DE) collected from swine confinement facilities. Repetitive DE exposure consisted of fifteen days of intranasal instillations with and without a three-day recovery period. Through these investigations, we identified an important function of LCN-2 in regulating tissue homeostasis and recovery following inflammatory injury in the lung. Additionally, compartmentalized effects on T cell and macrophage levels were observed in BALF vs. lung tissue in DE-exposed LCN-2 KO mice versus WT mice. Ablation of LCN-2 resulted in deficits in resolving histopathological markers of inflammation, and decreased levels of IL-10 after DE. Exogenous IL-10 administration partially rescued the histopathological markers of inflammation in LCN-2 KO mice after DE exposure. Taken together, these investigations highlight a novel role for LCN-2 in regulating lung homeostasis, inflammation response, and repair following organic dust-induced inflammation that may be mediated, at least in part, by IL-10.
Project description:Agricultural workers are at risk for the development of acute and chronic lung diseases due to their exposure to organic agricultural dusts. A diet intervention using the omega-3 fatty acid docosahexaenoic acid (DHA) has been shown to be an effective therapeutic approach for alleviating a dust-induced inflammatory response. We thus hypothesized a high-DHA diet would alter the dust-induced inflammatory response through the increased production of specialized pro-resolving mediators (SPMs). Mice were pre-treated with a DHA-rich diet 4 week s before being intranasally challenged with a single dose of an extract made from dust collected from a concentrated swine feeding operation (HDE ). This omega-3-fatty-acid-rich diet led to reduced arachidonic acid levels in the blood, enhanced macrophage recruitment, and increased the production of the DHA-derived SPM Resolvin D1 (RvD1) in the lung following HDE exposure. An assessment of transcript-level changes in the immune response demonstrated significant differences in immune pathway activation and alterations of numerous macrophage-associated genes among HDE-challenged mice fed a high DHA diet. Our data indicate that consuming a DHA-rich diet leads to the enhanced production of SPMs during an acute inflammatory challenge to dust, supporting a role for dietary DHA supplementation as a potential therapeutic strategy for reducing dust-induced lung inflammation.
Project description:Farm workers are at an increased risk for the development of acute and chronic lung inflammatory diseases from their everyday exposures to organic dust. Previous investigations have examined the inflammatory effects in mice from single and repetitive exposures to dust from swine confinement facilities, however, no study has explored these effects in a chronic model. To address this research gap, we established a chronic dust exposure mouse model of lung tumor-igenesis that was also used to measure the efficacy of omega-3 fatty acid-derived lipid mediators as therapeutics for mitigating these induced responses. Our results from these investigations are the first to evaluate the chronic inflammatory, and carcinogenic effects of these dusts, as well as identify a potential therapeutic strategy for mitigating the inflammatory effects by using an omega-3 fatty acid-derived bioactive lipid mediator.
Project description:Raw metaproteomic data of Chinese indoor dust derived extracellular vesicles. These dust samples were collected in the summer of 2022 and were immediately sent to the laboratory for processing. The extracellular vesicles of dust were subjected to ultracentrifugation, and they were further purified using iodixanol density gradient ultracentrifugation. After extracting the extracellular vesicles, metaproteomic sequencing was performed.
Project description:Occupational exposure to dust containing crystalline silica may result in serious adverse health effects including silicosis and cancer. Previous studies which employed animal models for inhalation exposure to crystalline silica revealed changes in blood gene expression profiles in association with the silica-induced lung toxicity. Currently, global gene expression profiles were determined in the whole blood samples obtained from control (not exposed to dust) and dust containing silica exposed individuals with or without clinically identified silicosis. Differences in the blood gene expression profiles were detected in the blood samples obtained from the control and the silica-containing dust exposed individuals. Between the two groups of the silica-containing dust exposed individuals, the number of significantly differentially expressed genes was more in the blood samples obtained from those with silicosis.