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Updated: Feb 1, 2026
Phage Therapy Application to Counteract Pseudomonas aeruginosa Infection in Cystic Fibrosis Zebrafish Embryos
Published on: May 12, 2020
Dual Transcriptomics of Host-Pathogen Interaction of Cystic Fibrosis Isolate Pseudomonas aeruginosa PASS1 With
Sheemal S Kumar1, Julia I Tandberg2, Anahit Penesyan1
1Department of Molecular Sciences, Faculty of Science and Engineering, Macquarie University, Sydney, NSW, Australia.
Abstract:
Pseudomonas aeruginosa is a significant cause of mortality in patients with cystic fibrosis (CF). To explore the interaction of the CF isolate P. aeruginosa PASS1 with the innate immune response, we have used Danio rerio (zebrafish) as an infection model. Confocal laser scanning microscopy (CLSM) enabled visualization of direct interactions between zebrafish macrophages and P. aeruginosa PASS1. Dual RNA-sequencing of host-pathogen was undertaken to profile RNA expression simultaneously in the pathogen and the host during P. aeruginosa infection. Following establishment of infection in zebrafish embryos with PASS1, 3 days post infection (dpi), there were 6739 genes found to be significantly differentially expressed in zebrafish and 176 genes in PASS1. A range of virulence genes were upregulated in PASS1, including genes encoding pyoverdine biosynthesis, flagellin, non-hemolytic phospholipase C, proteases, superoxide dismutase and fimbrial subunits. Additionally, iron and phosphate acquisition genes were upregulated in PASS1 cells in the zebrafish. Transcriptional changes in the host immune response genes highlighted phagocytosis as a key response mechanism to PASS1 infection. Transcriptional regulators of neutrophil and macrophage phagocytosis were upregulated alongside transcriptional regulators governing response to tissue injury, infection, and inflammation. The zebrafish host showed significant downregulation of the ribosomal RNAs and other genes involved in translation, suggesting that protein translation in the host is affected by PASS1 infection.
Insights
Pseudomonas aeruginosa infection in cystic fibrosis (CF) patients was studied using zebrafish. Zebrafish immune cells responded to the PASS1 bacterial strain by upregulating phagocytosis genes, while bacterial virulence genes were also activated.
Area of Science:
- Infectious Diseases
- Microbiology
- Immunology
Background:
- Pseudomonas aeruginosa is a major cause of mortality in cystic fibrosis patients.
- Understanding host-pathogen interactions is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the interaction between the cystic fibrosis isolate Pseudomonas aeruginosa PASS1 and the innate immune response using a zebrafish infection model.
- To profile host and pathogen gene expression during infection using dual RNA-sequencing.
Main Methods:
- Utilized Danio rerio (zebrafish) as an infection model for Pseudomonas aeruginosa PASS1.
- Employed Confocal Laser Scanning Microscopy (CLSM) to visualize host-pathogen interactions.
- Performed dual RNA-sequencing to analyze gene expression in both zebrafish and P. aeruginosa.
Main Results:
- Significant differential gene expression observed in both zebrafish (6739 genes) and P. aeruginosa PASS1 (176 genes) at 3 days post-infection.
- Upregulation of P. aeruginosa virulence genes (e.g., pyoverdine, flagellin, phospholipase C) and iron/phosphate acquisition genes.
- Zebrafish immune response highlighted phagocytosis, with upregulation of related transcriptional regulators, alongside inflammation and tissue repair genes.
- Downregulation of ribosomal RNAs and translation-related genes in zebrafish, indicating host protein synthesis is affected.
Conclusions:
- Zebrafish serve as a valuable model for studying P. aeruginosa infections and innate immune responses.
- P. aeruginosa PASS1 activates virulence factors and nutrient acquisition mechanisms within the host.
- The host mounts a phagocytic and inflammatory response, but protein translation may be impaired during infection.
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