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Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
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Rabbit intestinal xenograft model for human Encephalitozoon infections in mice
K Wasson1, K Snowden, E Didier
1Department of Pathobiology, College of Veterinary Medicine, University of Illinois, Urbana, USA.
Background And Purpose:
The gastrointestinal tract is a common portal of entry for Encephalitozoon cuniculi, one of several microsporidial organisms emerging as opportunistic pathogens in immunocompromised humans. Although most human microsporidial pathogens can be propagated in vitro and in a variety of laboratory animals, an experimental animal system to specifically study intestinal uptake and systemic spread of these organisms does not exist.
Methods:
Paired segments of near-term fetal rabbit small intestine were implanted subcutaneously into 25 athymic nude or 10 severe combined immune deficient mice. Five weeks after surgery, 65 xenografts were inoculated intraluminally with E. cuniculi (n = 14), E. intestinalis (n = 27), E. hellem (n = 20), or RK-13 cells (n = 2), or were left uninoculated (n = 2).
Results:
Intestinal xenograft infection with E. cuniculi (n = 11), E. intestinalis (n = 17), and E. hellem (n = 18) was determined by light microscopy; control xenografts remained uninfected. Extraintestinal infection with E. cuniculi developed in host mouse brain, respiratory tract, spleen, salivary glands, and gastrointestinal tract (3 of 3 mice), and infection with E. intestinalis developed in the liver (8 of 15 mice).
Conclusion:
Intestinal xenografts provide a unique, sterile, and biologically relevant animal model system for studying host enterocyte/parasite interactions, mechanisms of microsporidial pathogenicity, antimicrosporidial chemotherapeutic agents, and immune effector mechanisms. This model provides evidence for persistent graft infection with three Encephalitozoon spp., and for intestinal spread of E. cuniculi and E. intestinalis from infected enterocytes in immunoincompetent mice.
Insights
A novel intestinal xenograft model in immunocompromised mice successfully models Encephalitozoon spp. infections. This system allows study of microsporidial uptake, spread, and host-parasite interactions in a controlled environment.
Area of Science:
- Microbiology
- Immunology
- Parasitology
Background:
- Encephalitozoon cuniculi and other microsporidia are opportunistic pathogens.
- The gastrointestinal tract is a primary entry point for these pathogens.
- A dedicated animal model for studying intestinal uptake and spread is lacking.
Purpose of the Study:
- To develop and validate an experimental animal model for studying microsporidial infections.
- To investigate intestinal uptake and systemic dissemination of Encephalitozoon species.
- To provide a platform for evaluating anti-microsporidial agents and immune responses.
Main Methods:
- Fetal rabbit small intestine segments were xenografted into athymic nude or SCID mice.
- Xenografts were inoculated with Encephalitozoon cuniculi, E. intestinalis, or E. hellem.
- Infection was assessed via light microscopy and host organ analysis.
Main Results:
- Intestinal xenografts were successfully infected with E. cuniculi, E. intestinalis, and E. hellem.
- Extraintestinal spread of E. cuniculi was observed in the brain, respiratory tract, spleen, and GI tract.
- E. intestinalis infection disseminated to the liver in a subset of mice.
Conclusions:
- Intestinal xenografts offer a sterile, relevant model for studying microsporidial infections.
- The model supports research on host-enterocyte/parasite interactions and pathogenicity.
- Evidence of persistent infection and intestinal spread of Encephalitozoon spp. was demonstrated.
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