Project 4: The Zebrafish embryo as a model of P. aeruginosa systemic infection



Adapted from Figure 4 of Brannon et al, "Pseudomonas aeruginosa Type III secretion system interacts with phagocytes to modulate systemic infection of zebrafish embryos."
Cell Microbiol 11: 755-768" Click for link to PubMed.

We have developed the optically transparent and genetically tractable zebrafish embryo as a model for systemic P. aeruginosa infection. Despite lacking adaptive immunity at this developmental stage, zebrafish embryos are highly resistant to P. aeruginosa infection, but as in humans, phagocyte depletion dramatically increases their susceptibility.

We have shown that P. aeruginosa lacking a functional Type III secretion system (T3SS) has attenuated virulence, which can be restored through phagocyte depletion. This suggests that the T3SS influences virulence through its effects on phagocytes. Neutrophils and macrophages in zebrafish embryos rapidly phagocytose and kill P. aeruginosa, suggesting that both cell types play a role in protection against infection. Our ongoing work takes advantage of the real-time visualization capabilities and genetic tractability of the zebrafish embryo infection model to elucidate the molecular and cellular details of P. aeruginosa pathogenesis and to explore how the antibiotic resistance of this organism may be induced in vivo.

Collaborators on this project include Dr. Lalita Ramakrishnan at the University of Washington and Dr. Simon Dove at Harvard Medical School.


Click here for a page of movies from this research project.





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