Role of Autophagy and Apoptosis in the Postinfluenza Bacterial Pneumonia

Figure 1

Autophagy and apoptosis in the early and late stage of IAV-SP mixed infection. In the figure, the orange arrows represent links of stimulation, whereas the green bars correspond to inhibitory links. (a) Autophagy and apoptosis seem to act as sequential events after IAV infection. NS1 plays a critical role in regulating IAV-induced autophagy and apoptosis. M2 is necessary for the formation of autophagosomes. The latter delays the development of apoptosis. PB1-F2 induces inflammatory response, which has a mutual promotion with apoptosis. PB1-F2 of PR8 can cause apoptosis of monocytes. Both apoptosis and inflammation contribute to secondary bacterial infection. Recognition of viral dsRNA by TLR of alveolar macrophages promotes IFN-γ production, which prevents macrophages from clearing bacteria (such as SP). (b) SP triggers autophagy by interacting with TLR4 and TLR2 through RIPI-P38 signaling and JNK signaling, respectively. By the interaction of SP and TLR2, M2 alveolar macrophages (M2 AM) polarized from monocytes help maintain the lung homeostasis. PLY stimulate autophagy through ROS hypergeneration and PI3K-I/Akt/mTOR pathway. In addition, SP causes IFN-γ increase, together with autophagy and the maintenance of lung homeostasis, which alleviates subsequent IAV infection.

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