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Schematic model illustrating the mechanism underlying the PM2.5-mediated dampening of pneumococcus-induced macrophage activation and pulmonary infection exacerbation. PM2.5 exposure suppresses macrophage phagocytic activity and nitric oxide production during pneumococcal infection. Further, PM2.5 subverted proinflammatory cytokines and chemokines by inhibiting the PI3K/Akt and MAPK pathways in pneumococcus-infected macrophages
