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Lung Immunophenotyping of Fat-1 mice Post Chronic Organic Dust Exposure

ABSTRACT: Lung Immunophenotyping of Fat-1 mice Post Chronic Organic Dust Exposure

PROVIDER: PRJNA1076520 | ENA |

REPOSITORIES: ENA

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Lung Immunophenotyping of Fat-1 mice Post Chronic Organic Dust Exposure

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Aspirin-triggered Resolvin D1 Reduces Chronic Dust-induced Lung Pathology Without Altering Susceptibility to Dust-enhanced Carcinogenesis.

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.

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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.

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