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Model for the role of macrophages and RNS in lung injury. Macrophages responding to ozone-induced lung injury become phenotypically polarized into M1 cells; TNFα released from M1 macrophages acts in an autocrine and paracrine manner to downregulate Cav-1, leading to activation of PI3 K/PKB signaling, NF-κB, and induction of iNOS. RNS generated via iNOS contributes to ozone-induced lung injury.
