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Exploring the Mechanism of Macrophages in Influenza A Virus-Induced Pneumonia through miR-1260 Targeting of Sema3A
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DOI：10.1016/j.micinf.2025.105567.png)
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Abstract
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Influenza A virus (IAV) is a global respiratory pathogen, with macrophages playing a key role in innate immunity. We established mouse models of IAV-induced pneumonia and macrophage depletion, along with an in vitro co-culture system of lung epithelial cells (MLE-12) and macrophages (RAW264.7), to study IAV infection. HE staining, immunohistochemistry, and immunofluorescence revealed IAV-induced lung damage and macrophage recruitment. In the co-culture system, IAV infection caused morphological changes in both cell types, increased viral load, and elevated inflammatory factors. High-throughput sequencing identified miR-1260 and Sema3A-mediated PI3K/AKT/mTOR pathway involvement. Transfection with miRNA mimics, inhibitors, and Sema3A-siRNA showed that miR-1260 exacerbates cell damage by targeting Sema3A via PI3K/AKT/mTOR. Macrophage-depleted mice exhibited worse outcomes (weight loss, inflammation, viral load, pathology) than IAV-infected mice, linked to miR-1260/Sema3A/PI3K/AKT/mTOR regulation. Macrophages protect against IAV by suppressing miR-1260-mediated Sema3A/PI3K/AKT/mTOR activation.
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