RhlR, but not RhlI, allowsP. aeruginosabacteria to evadeDrosophilaTep4-mediated opsonization

WhenDrosophilaflies feed onPseudomonas aeruginosastrain PA14, some bacteria cross the intestinal barrier and start proliferating inside the hemocoel. This process is limited by hemocytes through phagocytosis. We have previously shown that the PA14 quorum-sensing regulator RhlR is required for these bacteria to elude the cellular immune response. RhlI synthesizes the auto-inducer signal that activates RhlR. Here, we compare the null mutant phenotypes ofrhlRandrhlIin a variety of infection assays inDrosophilaand in the nematodeCaenorhabditis elegans. Surprisingly, inDrosophila, unlikeΔrhlRmutants,ΔrhlImutants are only modestly attenuated for virulence and are poorly phagocytosed and opsonized in a Thioester-containing Protein4-dependent manner. Likewise, ΔrhlIbut not ΔrhlRmutants colonize the digestive tract ofC. elegansand kill it as efficiently as wild-type PA14. Thus, RhlR has an RhlI-independent function in eluding detection or counter-acting the action of the immune system. In contrast to the intestinal infection model,Tep4mutant flies are more resistant to PA14 in a septic injury model, which also depends onrhlR. Thus, the Tep4 putative opsonin can either be protective or detrimental to host defense depending on the infection route.