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. 2013 Jun 7;305(4):L282–L290. doi: 10.1152/ajplung.00112.2013

Fig. 9.

Fig. 9.

Cartoon model depicting how neonatal hyperoxia reprograms the host response to influenza A virus through different pathways. MCP-1 is involved in a pathway that promotes excessive leukocyte recruitment to the lungs following influenza virus infection in adult mice that had been exposed to hyperoxia as neonates, whereas EC-SOD is involved in a pathway that prevents the development of fibrotic lung disease.