Association of Toll-Like Receptor Signaling and Reactive Oxygen Species: A Potential Therapeutic Target for Posttrauma Acute Lung Injury

Figure 2

Model of shock-activated PMN in mediating the TLR4-TLR2 cross talk in AM$\varphi$ and AM$\varphi$ priming. Hemorrhagic shock-activated PMNs primarily migrate into alveoli in response to a trivial inflammatory stimulus, such as LPS, and interact with AM$\varphi$. The interaction between PMN and AM$\varphi$ enhances LPS-induced TLR2 expression (+) in the AM$\varphi$, possibly mediated by PMNs-derived oxidants and augmented NF-$\kappa$B activation. The increased TLR2 expression results in the amplified response of AM$\varphi$ to the TLR2 agonist (PGN), thereby augmenting cytokines and chemokines expression (circled +) and promoting enhanced PMN transalveolar migration. Thus, the shock-activated PMN-mediated TLR4-TLR2 cross talk activates a positive feedback signal leading to AM$\varphi$ priming and exaggerated lung inflammation in response to invading pathogens.