We demonstrated that LPS-TLR4 signaling upregulates TLR2 expression in AMφ, and HS-activated PMN play a critical role in the mechanism of TLR2 upregulation (115) . This cross-talk between TLR4 and TLR2 in AMφ results in the amplification of expression of cytokines and chemokines in response to the bacterial products LPS and PGN, and subsequently leads to enhanced PMN sequestration in the lung. These findings reveal a novel mechanism underlying HSprimed lung injury, namely that HS-activated PMN that were initially sequestered into the alveoli can instruct AMφ to upregulate TLR2, thereby sensitizing AMφ to TLR2 ligands and promoting enhanced lung inflammation.