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Updated: Feb 13, 2026

Author Spotlight: Advancing Therapeutics to Treat Vibriosis in Humans and Aquatic Organisms
Published on: May 31, 2024
Quorum-sensing regulator RhlR but not its autoinducer RhlI enables Pseudomonas to evade opsonization
Samantha Haller1, Adrien Franchet1, Abdul Hakkim2,3
1CNRS, M3I UPR 9022, Université de Strasbourg, Strasbourg, France.
Abstract:
When Drosophila melanogaster feeds on Pseudomonas aeruginosa, some bacteria cross the intestinal barrier and eventually proliferate in the hemocoel. This process is limited by hemocytes through phagocytosis. P. aeruginosa 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 rhlI mutants are unexpectedly more virulent than rhlR mutants, both in fly and in nematode intestinal infection models, suggesting that RhlR has RhlI-independent functions. We also report that RhlR protects P. aeruginosa from opsonization mediated by the Drosophila thioester-containing protein 4 (Tep4). RhlR mutant bacteria show higher levels of Tep4-mediated opsonization, as compared to rhlI mutants, which prevents lethal bacteremia in the Drosophila hemocoel. In contrast, in a septic model of infection, in which bacteria are introduced directly into the hemocoel, Tep4 mutant flies are more resistant to wild-type P. aeruginosa, but not to the rhlR mutant. Thus, depending on the infection route, the Tep4 opsonin can either be protective or detrimental to host defense.
Insights
Pseudomonas aeruginosa virulence relies on RhlR, but RhlR has functions independent of its signal RhlI. RhlR protects bacteria from fly immune responses, with Tep4 opsonization playing a complex role in host defense.
Area of Science:
- * Microbiology
- * Immunology
- * Genetics
Background:
- * *Pseudomonas aeruginosa* can infect *Drosophila melanogaster* by crossing the intestinal barrier.
- * Hemocytes provide cellular immunity against bacterial proliferation in the hemocoel.
- * Quorum-sensing regulators like RhlR are crucial for bacterial evasion of host immune responses.
Purpose of the Study:
- * To investigate the role of *Pseudomonas aeruginosa* quorum-sensing regulator RhlR and its signal RhlI in *Drosophila* infection models.
- * To elucidate RhlR-independent functions and its interaction with the *Drosophila* immune system, specifically Tep4.
- * To determine the dual role of Tep4 opsonization in different infection routes.
Main Methods:
- * Intestinal and septic infection models using *Drosophila melanogaster* and nematodes.
- * Genetic manipulation of *Pseudomonas aeruginosa* (rhlI and rhlR mutants).
- * Assessment of bacterial virulence, hemocyte phagocytosis, and Tep4-mediated opsonization.
Main Results:
- * *rhlI* mutants exhibited higher virulence than *rhlR* mutants in intestinal infection models, indicating RhlR's RhlI-independent functions.
- * RhlR protects *P. aeruginosa* from Tep4-mediated opsonization, with *rhlR* mutants showing increased opsonization.
- * In septic infections, Tep4-mutant flies were more resistant to wild-type *P. aeruginosa*, but not *rhlR* mutants, highlighting context-dependent opsonin function.
Conclusions:
- * RhlR possesses significant RhlI-independent virulence functions in *P. aeruginosa* infections.
- * RhlR actively protects bacteria from Tep4-mediated opsonization, impacting bacteremia.
- * The immune protein Tep4's role is context-dependent, acting as protective or detrimental based on the infection route.
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