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Experimental model for human intestinal microsporidiosis in interferon gamma receptor knockout mice infected by
A Achbarou1, C Ombrouck, T Gneragbe
1INSERM U. 313, CHU Pitié Salpêtrière, Paris, France.
Abstract:
Interferon gamma receptor knockout mice developed a chronic infection when inoculated with spores of Encephalitozoon intestinalis which is a cause of intestinal microsporidiosis in AIDS patients. The infection was evaluated by enumeration of the spores of the parasite shed in the stools, histological examination and follow up over a period of six months. A dose-response was demonstrated since higher numbers of spores were excreted and more infection sites were found in mice which were given an increased quantity of parasites. In infected wild type mice, the number of excreted spores decreased until day 16 post-inoculation, then spores were detected sporadically in low numbers. These data confirmed the role of IFN-gamma in the control of E. intestinalis infection. The infection was not lethal suggesting that other factors are involved in regulation of the parasite infection. This model, with the long survival time of the animals together with the measurable quantity of spores shed in the stools will be useful for testing potential therapeutical agents.
Insights
Interferon gamma (IFN-gamma) is crucial for controlling Encephalitozoon intestinalis, a cause of intestinal microsporidiosis. This study establishes a mouse model for evaluating new treatments against this chronic infection.
Area of Science:
- Immunology
- Infectious Diseases
- Parasitology
Background:
- Encephalitozoon intestinalis causes intestinal microsporidiosis, particularly in immunocompromised individuals like AIDS patients.
- Interferon gamma (IFN-gamma) signaling is a key component of the host immune response against intracellular pathogens.
Purpose of the Study:
- To investigate the role of IFN-gamma in controlling Encephalitozoon intestinalis infection.
- To establish and characterize a mouse model for studying chronic intestinal microsporidiosis and evaluating therapeutic agents.
Main Methods:
- Encephalitozoon intestinalis spores were inoculated into interferon gamma receptor knockout (KO) mice and wild-type (WT) mice.
- Infection was monitored for six months by quantifying parasite spores in feces, histological examination, and assessing infection sites.
- Dose-response effects were evaluated by varying parasite inoculation quantities.
Main Results:
- IFN-gamma receptor KO mice developed chronic E. intestinalis infections with higher spore excretion and more infection sites compared to WT mice.
- WT mice showed a decrease in spore excretion by day 16 post-inoculation, with sporadic detection thereafter.
- A clear dose-response relationship was observed, with higher parasite doses leading to increased infection severity.
Conclusions:
- IFN-gamma plays a critical role in the immune control of Encephalitozoon intestinalis infection.
- The developed mouse model, characterized by chronic infection and measurable spore shedding, is suitable for testing novel therapeutic strategies against E. intestinalis.