Presenter Information

Autumn RobinsonFollow

Presentation Type

Presentation

Faculty Mentor’s Full Name

Patrick Secor

Faculty Mentor’s Department

Biological Sciences

Abstract

Pseudomonas aeruginosa is an opportunistic pathogen that infects diabetic ulcers and the lungs of individuals with cystic fibrosis. Most strains of P. aeruginosa are themselves infected by Pf bacteriophages. Most bacteriophages are viral parasites that kill their bacterial host. Pf bacteriophages, however, have established a more symbiotic relationship with P. aeruginosa. For example, Pf bacteriophages do not typically lyse their bacterial host and aid in bacterial adhesion and biofilm formation. Recent work demonstrates that Pf virions have immunomodulatory properties that modulate mammalian immune responses in ways that promote infection initiation. Finally, Pf bacteriophages are abundant at sites of human infection suggesting that they are clinically relevant. However, the mechanistic details for how Pf bacteriophages modulate vertebrate immune responses are poorly understood. We have discovered that key Pf-mediated infection phenotypes observed in mice are synonymous in a Caenorhabditis elegans host-pathogen model. C. elegans is an ideal and widely used model to study complex host-pathogen interactions. For example, several components of innate immunity are evolutionarily conserved between C. elegans and vertebrates. Using strains of P. aeruginosa with and without Pf bacteriophages, we found that the presence of Pf bacteriophages significantly increases P. aeruginosa virulence against C. elegans. Furthermore, we find that C. elegans predation of P. aeruginosa induces Pf replication. We hypothesize that Pf bacteriophages are a defense mechanism against predators such as C. elegans and phagocytes. Using this model, we will identify the mechanisms underlying the immunomodulatory properties of Pf bacteriophages which may reveal new therapeutic approaches to treat or prevent P. aeruginosa infections.

Category

Life Sciences

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Immunomodulation of Innate Immunity by a Bacteriophage

Pseudomonas aeruginosa is an opportunistic pathogen that infects diabetic ulcers and the lungs of individuals with cystic fibrosis. Most strains of P. aeruginosa are themselves infected by Pf bacteriophages. Most bacteriophages are viral parasites that kill their bacterial host. Pf bacteriophages, however, have established a more symbiotic relationship with P. aeruginosa. For example, Pf bacteriophages do not typically lyse their bacterial host and aid in bacterial adhesion and biofilm formation. Recent work demonstrates that Pf virions have immunomodulatory properties that modulate mammalian immune responses in ways that promote infection initiation. Finally, Pf bacteriophages are abundant at sites of human infection suggesting that they are clinically relevant. However, the mechanistic details for how Pf bacteriophages modulate vertebrate immune responses are poorly understood. We have discovered that key Pf-mediated infection phenotypes observed in mice are synonymous in a Caenorhabditis elegans host-pathogen model. C. elegans is an ideal and widely used model to study complex host-pathogen interactions. For example, several components of innate immunity are evolutionarily conserved between C. elegans and vertebrates. Using strains of P. aeruginosa with and without Pf bacteriophages, we found that the presence of Pf bacteriophages significantly increases P. aeruginosa virulence against C. elegans. Furthermore, we find that C. elegans predation of P. aeruginosa induces Pf replication. We hypothesize that Pf bacteriophages are a defense mechanism against predators such as C. elegans and phagocytes. Using this model, we will identify the mechanisms underlying the immunomodulatory properties of Pf bacteriophages which may reveal new therapeutic approaches to treat or prevent P. aeruginosa infections.