10.1371/journal.pone.0102200.g005
Emma Hennessy
Emma
Hennessy
Julie O'Callaghan
Julie
O'Callaghan
Marlies J. Mooij
Marlies
J. Mooij
Claire Legendre
Claire
Legendre
Olga Camacho-Vanegas
Olga
Camacho-Vanegas
Sandra C. Camacho
Sandra
C. Camacho
Claire Adams
Claire
Adams
John A. Martignetti
John
A. Martignetti
Fergal O'Gara
Fergal
O'Gara
A model for the findings observed in this study.
Public Library of Science
2014
cell biology
Molecular cell biology
genetics
gene expression
immunology
Immune response
inflammation
Immune system
Innate immune system
immunity
Immune activation
microbiology
bacteriology
Gram negative bacteria
Medical microbiology
Microbial pathogens
Bacterial pathogens
Infectious diseases
Bacterial diseases
Pseudomonas infections
Pathology and laboratory medicine
pathogenesis
Host-pathogen interactions
findings
observed
2014-07-10 02:59:17
Figure
https://plos.figshare.com/articles/figure/_A_model_for_the_findings_observed_in_this_study_/1099272
<p>(<b>A</b>) 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>B</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 <i>P. aeruginosa</i>, 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.</p>