Figure 1.
Schematic overview of the complex QS systems present in P. aeruginosa.
The commanders represent the major regulatory systems, while the messengers are the signaling molecules. The soldiers represent the various virulence factors that have a function in the interaction of P. aeruginosa with the host.
Figure 2.
Effects of 3OC12HSL on P. aeruginosa, S. aureus, and C. albicans that are relevant to immune recognition.
Lines ending in arrows indicate induction and lines ending in circles indicate inhibition of the indicated process. C. albicans, in the hyphal morphology, induces phagotycosis during inflammation (1). Virulent hyphae can be inhibited and transformed to yeast cells by farnesol, the QS molecule secreted by C. albicans (2). Candida yeast cells prevent macrophages induction (3) and render C. albicans invisible for the immune system. C. albicans coexisting with P. aeruginosa exerts a double-sided reaction; farnesol inhibits Pseudomonas QS production (4), whereas 3OC12HSL secreted by P. aeruginosa prevents C. albicans filamentation without changing the growth rate (5). 3OC12HSL sensed by the host induces a pro-inflammatory response by activation of macrophages (6), but it can also give an anti-inflammatory reaction by selectively diminishing the regulation of NF-κB signaling and attenuating TLR4-dependent innate immune responses (7). P. aeruginosa 3OC12HSL influences S. aureus by inhibiting growth and hemolysin and exotoxin production (8) and by inducing protein A expression (9), which prevents recognition of S. aureus by macrophages and neutrophils (10). S. aureus detected by the immune system trigger macrophages signaling pathways (11).