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Updated: Aug 9, 2025

Author Spotlight: Investigating Bacteriophage-Induced Immune Responses in Gnotobiotic Mice
Published on: January 26, 2024
Tripartite interactions between filamentous Pf4 bacteriophage, Pseudomonas aeruginosa, and bacterivorous nematodes
Caleb M Schwartzkopf1, Autumn J Robinson1, Mary Ellenbecker1
1Division of Biological Sciences, University of Montana, Missoula, Montana, United States of America.
Abstract:
The opportunistic pathogen Pseudomonas aeruginosa PAO1 is infected by the filamentous bacteriophage Pf4. Pf4 virions promote biofilm formation, protect bacteria from antibiotics, and modulate animal immune responses in ways that promote infection. Furthermore, strains cured of their Pf4 infection (ΔPf4) are less virulent in animal models of infection. Consistently, we find that strain ΔPf4 is less virulent in a Caenorhabditis elegans nematode infection model. However, our data indicate that PQS quorum sensing is activated and production of the pigment pyocyanin, a potent virulence factor, is enhanced in strain ΔPf4. The reduced virulence of ΔPf4 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 ΔPf4 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.
Insights
Pseudomonas aeruginosa bacteriophage Pf4 suppresses bacterial virulence factors, aiding infection. Removing Pf4 increases pyocyanin pigment but reduces overall bacterial virulence in C. elegans.
Area of Science:
- Microbiology
- Infectious Diseases
- Bacteriophage Research
Background:
- * Pseudomonas aeruginosa is an opportunistic pathogen.
- * The filamentous bacteriophage Pf4 infects P. aeruginosa PAO1.
- * Pf4 infection influences biofilm formation, antibiotic resistance, and host immune responses.
Purpose of the Study:
- * To investigate the role of Pf4 infection in P. aeruginosa virulence.
- * To understand the mechanisms underlying P. aeruginosa virulence modulation by Pf4.
- * To explore the interaction between P. aeruginosa, Pf4, and host immune responses.
Main Methods:
- * Comparative analysis of wild-type P. aeruginosa PAO1 and Pf4-cured (ΔPf4) strains.
- * Utilization of a Caenorhabditis elegans nematode infection model.
- * Measurement of pyocyanin production and PQS quorum sensing activation.
- * Assessment of host immune response in C. elegans mutants lacking aryl hydrocarbon receptor.
Main Results:
- * Pf4-cured ΔPf4 strains exhibited reduced virulence in the C. elegans model.
- * ΔPf4 strains showed activated PQS quorum sensing and enhanced pyocyanin production.
- * C. elegans mutants lacking aryl hydrocarbon receptor were more susceptible to ΔPf4 infection.
- * Pf4 suppression of quorum-regulated virulence factors was implicated in immune evasion.
Conclusions:
- * Pf4 infection of P. aeruginosa PAO1 plays a significant role in modulating bacterial virulence.
- * The interplay between Pf4, pyocyanin, and host aryl hydrocarbon receptor influences infection outcomes.
- * Pf4 may facilitate P. aeruginosa pathogenesis by suppressing virulence factors, enabling evasion of host immunity.
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