Figure 2: Agr-controlled PSMα peptides and lipopeptides are required for strong TLR2 activity.
From: Toll-like receptor 2 activation depends on lipopeptide shedding by bacterial surfactants
Inactivation of PSMα genes in S. aureus USA300 has a similar impact on IL-8 induction in HEK-TLR2 cells as deletion of the lipoprotein diacylglyceryl transferase gene (lgt) (a) and this phenotype can be complemented by recombinant expression of the PSMα cluster (b). Stimulation of HEK-TLR2 with live S. aureus leads to decreased IL-8 induction by the PSM mutant compared with USA300 wild-type, which can be restored by PSMα expression (c). The capacity of S. aureus Δlgt to stimulate IL-8 release in HEK-TLR2 cells can be restored by transformation with an lgt-expressing plasmid (d). A USA300 mutant lacking PSMs and Lgt requires complementation with both, PSM genes and lgt to regain TLR2-stimulating activity (e). The synthetic lipopeptide Pam2CSK4 and TSB medium were used as positive and negative controls, respectively. Data represent means +/− s.e.m. of at least three independent experiments. ***P<0.001; ****P<0.0001 significantly different versus USA300 wild-type (a,c,d), pTXΔα1-4 versus empty plasmid (b), or as indicated (e) as calculated by Student’s t test.
