ABSTRACT
When Drosophila flies feed on Pseudomonas aeruginosa PA14, some bacteria cross the intestinal barrier and start proliferating intensely 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 the bacteria to elude the cellular immune response. RhlI synthesizes the auto-inducer signal that activates RhlR. Here, we have carefully compared the null mutant phenotypes of rhlR and rhlI. Surprisingly, unlike ΔrhlR mutants, ΔrhlI mutants are only modestly attenuated for virulence and are poorly phagocytosed and opsonized in a Thioester-containing Protein4-dependent manner. Likewise, ΔrhlI but not ΔrhlR mutants colonize the digestive tract of Caenorhabdtis elegans and 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, Tep4 mutant flies are more resistant to PA14 in a septic injury model, also an rhlR-dependent property. Thus, the Tep4 putative opsonin can either be protective or detrimental to host defense depending on the infection route.