However, in noninfective ARDS, alveolar epithelial cell injury, pulmonary endothelial activation, and alveolar macrophage responses can recruit neutrophils and natural killer (NK) cells as well as monocytes, such as macrophages and dendritic cells, from the circulation, thus initiating the immune response during ARDS
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Mechanistically, a microglial inflammation-oxidative stress feedforward loop perpetuates injury: Activated microglia secrete neurotoxins, impairing neuronal mitochondrial function and antioxidant capacity (such as GPX4), thus increasing ROS leakage
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