When feeds on, some bacteria cross the intestinal barrier and eventually proliferate in the hemocoel. This process is limited by hemocytes through phagocytosis. requires the quorum-sensing regulator RhlR to elude the cellular immune response of the fly. RhlI synthesizes the autoinducer signal that activates RhlR. Here, we show that mutants are unexpectedly more virulent than mutants, both in fly and in nematode intestinal infection models, suggesting that RhlR has RhlI-independent functions. We also report that RhlR protects from opsonization mediated by the thioester-containing protein 4 (Tep4). mutant bacteria show higher levels of mediated opsonization, as compared to mutants, which prevents lethal bacteremia in the hemocoel. In contrast, in a septic model of infection, in which bacteria are introduced directly into the hemocoel, mutant flies are more resistant to wild-type but not to the mutant. Thus, depending on the infection route, the Tep4 opsonin can either be protective or detrimental to host defense.

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