Zebrafish Shigella Infection Models

Shigella, the causative agent of bacillary dysentery (also known as shigellosis), is caused by the invasion of intestinal epithelial cells and causes approximately 164,000 infections each year. Shigella infection can cause severe sequelae of infection, such as arthritis, sepsis, seizures, and hemolytic uremic syndrome. Shigella has also been recognized by the World Health Organization as a priority pathogen exhibiting antimicrobial resistance. The emergence of multidrug-resistant bacteria and the lack of effective vaccines have led to an urgent need to understand the pathogenesis of Shigella and to identify new approaches to infection control. In order to study the mechanism of Shigella infection clearly, it is urgent to use relevant animal models for in vivo studies.

With the exception of human primates, there is no mammalian model that can fully reproduce human shigellosis. Currently, zebrafish models are increasingly being used to study bacterial pathogens in humans, including S. flexneri. The major pathogenic events leading to human shigellosis (i.e., macrophage death, invasion and proliferation within the epithelium, cell-to-cell spread, inflammatory disruption of the host epithelium) can be reproduced in a zebrafish model of S. flexneri infection . Using the optical accessibility of zebrafish larvae, the development of S. flexneri innate immune responses in vivo can be studied more intuitively. In addition, S. flexneri-infected zebrafish have also helped to elucidate key roles of trained innate immunity in bacterial autophagy, bacterial predation, inflammation, and host defense in vivo.

Different injection sites of zebrafish larvae were used to study Shigella infection.

Our Zebrafish Shigella Infection Models

Our Zebrafish Shigella Infection Models have hallmarks of induction of human shigellosis, including inflammation and macrophage death. The models can thus reveal general mechanisms of host defense that are closely related to the fight against human infectious viral and fungal pathogens. In addition, our global gene expression profiling of zebrafish during infection can help you discover new mechanisms for exploring host defenses. We are dedicated to assisting you in discovering molecular determinants and events of cellular immunity to Shigella infection in vivo through these models, providing fundamental advances in your understanding of autophagy and inflammation, and screening pharmacological compounds for therapeutic advances.

Advantages

• Rapidly developing, fully annotated genome of the zebrafish (high homology to human genes)
• Optical accessibility for non-invasive live imaging.
• Innate immunity can be specifically studied without cross-interference of the adaptive immune system.
• Suitable for generation of fluorescent transgenic lines and targeted gene manipulation.

References

1. Duggan GM, et al. Use of zebrafish to study Shigella infection. Dis Model Mech. 2018, 11(2):dmm032151.
2. Torraca V, et al. Shigella sonnei infection of zebrafish reveals that O-antigen mediates neutrophil tolerance and dysentery incidence. PLoS Pathog. 2019, 15(12):e1008006.
3. Willis AR, et al. Injections of predatory bacteria work alongside host immune cells to treat Shigella infection in zebrafish larvae. Curr Biol. 2016, 26: 3343–3351.
4. Mostowy S, et al. The zebrafish as a new model for the in vivo study of Shigella flexneri interaction with phagocytes and bacterial autophagy. PLoS Pathog. 2013, 9: e1003588.

For research use only. Not intended for any clinical use.