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A mouse model of shigellosis by intraperitoneal infection
Jin-Young Yang1, Se-Na Lee, Sun-Young Chang
1Mucosal Immunology Section, International Vaccine Institute, Seoul.
Abstract:
In human and nonhuman primates, Shigella spp. cause bacillary dysentery by invading colon epithelium and promoting a strong inflammatory response; however, adult mice are resistant to oral Shigella infection. In this study, intraperitoneal challenge with virulent S. flexneri 2a (YSH6000) resulted in diarrhea and severe body weight loss in adult B6 mice. Of note, virulent S. flexneri 2a could invade and colonize not only systemic tissues but also the serosa and lamina propria region of the large intestine. In addition, epithelial shedding, barrier integrity, and goblet cell hyperplasia were found in the large intestine by 24 hours post-intraperitoneal Shigella infection. Of note, predominant expression of proinflammatory cytokines and chemokines were found in the large intestine after intraperitoneal challenge. Monocytes played a critical role in attenuating diarrhea and in providing protective efficacy against intraperitoneal Shigella infection. Most importantly, mice prevaccinated with attenuated S. flexneri 2a (SC602) strain were protected against intraperitoneal challenge with YSH6000. When taken together, these findings show that intraperitoneal challenge with virulent S. flexneri 2a can provoke bacillary dysentery and severe pathogenesis in adult mice. This model may be helpful for understanding the induction mechanism of bacillary dysentery and for evaluating Shigella vaccine candidates.
Insights
Intraperitoneal Shigella flexneri 2a infection causes bacillary dysentery in adult mice, mimicking human disease. This new mouse model aids in understanding disease mechanisms and evaluating Shigella vaccine candidates.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Shigella spp. cause bacillary dysentery in primates by invading colon epithelium and inducing inflammation.
- Adult mice are typically resistant to oral Shigella infection, limiting disease modeling.
Purpose of the Study:
- To establish and characterize a mouse model of Shigella-induced bacillary dysentery using intraperitoneal challenge.
- To investigate the pathogenesis and immune responses following intraperitoneal Shigella infection in adult mice.
- To evaluate the protective efficacy of a pre-vaccination strategy against Shigella challenge.
Main Methods:
- Adult B6 mice were challenged intraperitoneally with virulent Shigella flexneri 2a (YSH6000).
- Disease severity, tissue colonization, histopathological changes, and cytokine/chemokine expression were assessed.
- The role of monocytes in protection was investigated.
- Mice were prevaccinated with an attenuated S. flexneri 2a (SC602) strain before challenge.
Main Results:
- Intraperitoneal challenge induced diarrhea, severe body weight loss, and colonization of systemic tissues and the large intestine.
- Histopathological analysis revealed epithelial shedding, compromised barrier integrity, and goblet cell hyperplasia.
- Pro-inflammatory cytokines and chemokines were predominantly expressed in the large intestine.
- Monocytes were critical for attenuating diarrhea and providing protective efficacy.
- Prevaccination with attenuated S. flexneri 2a conferred protection against virulent challenge.
Conclusions:
- Intraperitoneal challenge with virulent S. flexneri 2a effectively provokes bacillary dysentery and severe pathogenesis in adult mice.
- This model system is valuable for elucidating the mechanisms of bacillary dysentery induction.
- The model serves as a platform for evaluating the efficacy of novel Shigella vaccine candidates.
