The role of extracellular vesicles in murine asthma model: insights into IgE-independent mast cell activation within animal science
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Asthma, a prevalent respiratory condition in animal science, involves bronchial inflammation, leading to symptoms like coughing and difficulty breathing. Mast cells and macrophages, pivotal immune cells, contribute to the inflammatory response triggered by various factors. Extracellular vesicles (EVs), including exosomes, play crucial roles in intercellular communication and have been implicated in murine asthma. We hypothesize that murine asthma-derived EVs modulate immune cell responses in animals. Our study investigates the role of these EVs in immune cell activation, shedding light on asthma pathogenesis. Using a murine asthma model induced by ovalbumin (OVA), we assessed serum EVs via Nanoparticle Tracking Analysis (NTA). Serum EVs from normal and asthmatic mice were subjected to Enzyme-linked immunosorbent assay (ELISA) and proteomic analysis for component identification. Elevated EV concentration and inflammatory cytokines, such as Interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α, were found in asthma-derived EVs. Additionally, variations in immunoglobulin light chain types were identified. Surprisingly, murine asthma EVs failed to activate T lymphocytes, B lymphocytes, eosinophils, and macrophages but stimulated mouse bone marrow-derived mast cells (mBMMCs) via enhanced degranulation and MAP kinase phosphorylation. These results suggest murine asthma-derived EVs as potential therapeutic targets for managing asthmatic symptoms in animal science. Further research into their mechanisms and clinical applications is warranted.
Abstract
Asthma, a prevalent respiratory condition in animal science, involves bronchial inflammation, leading to symptoms like coughing and difficulty breathing. Mast cells and macrophages, pivotal immune cells, contribute to the inflammatory response triggered by various factors. Extracellular vesicles (EVs), including exosomes, play crucial roles in intercellular communication and have been implicated in murine asthma. We hypothesize that murine asthma-derived EVs modulate immune cell responses in animals. Our study investigates the role of these EVs in immune cell activation, shedding light on asthma pathogenesis. Using a murine asthma model induced by ovalbumin (OVA), we assessed serum EVs via Nanoparticle Tracking Analysis (NTA). Serum EVs from normal and asthmatic mice were subjected to Enzyme-linked immunosorbent assay (ELISA) and proteomic analysis for component identification. Elevated EV concentration and inflammatory cytokines, such as Interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α, were found in asthma-derived EVs. Additionally, variations in immunoglobulin light chain types were identified. Surprisingly, murine asthma EVs failed to activate T lymphocytes, B lymphocytes, eosinophils, and macrophages but stimulated mouse bone marrow-derived mast cells (mBMMCs) via enhanced degranulation and MAP kinase phosphorylation. These results suggest murine asthma-derived EVs as potential therapeutic targets for managing asthmatic symptoms in animal science. Further research into their mechanisms and clinical applications is warranted.