A model for the findings observed in this study.

(A) In this work, wtKLF6 was found to regulate the expression of ASAH1, CCL20 and iNOS in lung cells in the absence of simvastatin (SIM).(B) SIM may induce KLF2 and KLF6 splice variant expression by binding to promoter elements and inhibition of Rho and Ras GTPase signalling. Rho and Ras GTPase signalling are also attenuated by the T3SS of P. aeruginosa, which may account for the induction of KLF2 and KLF6 by this species. The mechanism by which SIM induces IL-8 is unclear. However, the synergistic effect observed on CCL20 in this study may be a result of increased bacterial adhesion by SIM, and induction via wtKLF6. In addition, the wtKLF6-dependent reduction of iNOS by SIM may potentially be responsible for the observed increase in bacterial adhesion, Broken arrows represent mechanisms which require further elucidation.