Figure 1

TLR4 signalling. Of all the radioresistant stromal cells (SCs), epithelial cells (ECs) that line the airways are the most likely to mediate the effects of LPS, given their exposed position, their known and confirmed expression of TLR4 and their activation of TLR4 dependent signalling cascades upon exposure to TLR4 ligands (LPS, DAMPs, HDM). The intracellular compartmentalization of TLR4 may prevent "inopportune" activation of pulmonary ECs. Whereas TRL4 signalling via MyD88 is essential for the LPS-induced acute pulmonary inflammation response, TRL4 signalling via TRIF is dispensable [9]. MyD88 and TIRAP are involved in early activation of NF-κB and MAPK, whereas TRIF and TRAM are critical for late activation of NF-κB as well as the activation of IRF-3 [9]. There is no consensus about the expression and role of CD14 in LPS-induced lung epithelial activation.