Curious interactions between a bacterium, its virus, and predatory roundworms
Presentation Type
Oral Presentation
Category
STEM (science, technology, engineering, mathematics)
Abstract/Artist Statement
The opportunistic human pathogen Pseudomonas aeruginosa PAO1 is infected by the Pf4 bacteriophage (virus). Pf4 virions promote biofilm formation, protect bacteria from antibiotics, and modulate animal immune responses in ways that promote bacterial infection. Furthermore, bacterial strains cured of their Pf4 bacteriophage (∆Pf4) are less virulent in animal models of infection. Consistently, we find that strain ∆Pf4 is less virulent in a Caenorhabditis elegansroundworm infection model. However, our data indicate that bacterial communication, PQS quorum sensing, is activated and production of the pigment pyocyanin, a potent virulence factor, is enhanced in strain ∆Pf4. The reduced virulence of ∆Pf4 despite high levels of pyocyanin production may be explained by our finding that C. elegans mutants unable to sense bacterial pigments through the aryl hydrocarbon receptor are more susceptible to ∆Pf4 infection compared to wild-type C. elegans. Collectively, our data support a model where suppression of quorum-regulated virulence factors by Pf4 allows P. aeruginosa to evade detection by innate host immune responses.
Mentor Name
Patrick R. Secor
Curious interactions between a bacterium, its virus, and predatory roundworms
UC 330
The opportunistic human pathogen Pseudomonas aeruginosa PAO1 is infected by the Pf4 bacteriophage (virus). Pf4 virions promote biofilm formation, protect bacteria from antibiotics, and modulate animal immune responses in ways that promote bacterial infection. Furthermore, bacterial strains cured of their Pf4 bacteriophage (∆Pf4) are less virulent in animal models of infection. Consistently, we find that strain ∆Pf4 is less virulent in a Caenorhabditis elegansroundworm infection model. However, our data indicate that bacterial communication, PQS quorum sensing, is activated and production of the pigment pyocyanin, a potent virulence factor, is enhanced in strain ∆Pf4. The reduced virulence of ∆Pf4 despite high levels of pyocyanin production may be explained by our finding that C. elegans mutants unable to sense bacterial pigments through the aryl hydrocarbon receptor are more susceptible to ∆Pf4 infection compared to wild-type C. elegans. Collectively, our data support a model where suppression of quorum-regulated virulence factors by Pf4 allows P. aeruginosa to evade detection by innate host immune responses.