Abstract
ABSTRACTShigella is a leading cause of dysentery worldwide, responsible for up to 165 million cases of shigellosis each year. Shigella is also recognised as an exceptional model pathogen to study key issues in cell biology and innate immunity. Several infection models have been useful to explore Shigella biology; however, we still lack information regarding the events taking place during the Shigella infection process in vivo. Here, we discuss a selection of mechanistic insights recently gained from studying Shigella infection of zebrafish (Danio rerio), with a focus on cytoskeleton rearrangements and cellular immunity. We also discuss how infection of zebrafish can be used to investigate new concepts underlying infection control, including emergency granulopoiesis and the use of predatory bacteria to combat antimicrobial resistance. Collectively, these insights illustrate how Shigella infection of zebrafish can provide fundamental advances in our understanding of bacterial pathogenesis and vertebrate host defence. This information should also provide vital clues for the discovery of new therapeutic strategies against infectious disease in humans.
Highlights
Shigella are a pathovar of Escherichia coli that cause dysentery via inflammatory destruction of the intestinal epithelium, a disease process called shigellosis
Conclusions and emerging perspectives Here, we have illustrated how the zebrafish model can be used to study a variety of mechanisms underlying the host response to Shigella infection
Lessons learned from Shigella infection of zebrafish can be applied to other human bacterial pathogens (e.g. Listeria, mycobacteria, Salmonella), and to neglected pathogens (e.g. Burkholderia, Rickettsia, Waddlia), of which little is known
Summary
Shigella are a pathovar (see Glossary, Box 1) of Escherichia coli that cause dysentery (see Glossary, Box 1) via inflammatory destruction of the intestinal epithelium, a disease process called shigellosis. In the case of Shigella, caudal vein infection of zebrafish was first developed to study Shigella-phagocyte interactions and bacterial autophagy (see Glossary, Box 1) in vivo (Mostowy et al, 2013). Many hallmarks of shigellosis observed in humans, including epithelial cell invasion, macrophage cell death and inflammation, are reproduced in a zebrafish model of S. flexneri infection, and are strictly dependent upon the Shigella type III secretion system (T3SS; see Glossary, Box 1).
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
