A rat model to study Blastocytis subtype 1 infections
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Blastocytis sp. is the most common enteric protozoan in human, but its pathogenesis is still unclear. To study the infectious effects of Blastocytis sp. on tissue damage, we orally challenged the Sprague Dawley (SD) rats with different doses of Blastocytis subtype1 (ST1) and examined the histological changes. We found that there was no difference of disease incidence among the Blastocytis ST1-infected groups challenged with different doses of the protozoan. Histological results showed that the lamina propria was infected by Blastocytis ST1 in the vacuolar form, along with the mucus membrane slough and inflammatory cell infiltration into the lamina propria. Compared to the uninfected group, the histological scores were significantly higher in the infected groups. However, groups infected with various doses of Blastocystis ST1 showed no difference in terms of histological scores. In conclusion, this study indicates that the SD rats can be easily infected with Blastocytis ST1 even with low dose of cysts, and the histopathological effects of the infection in the intestine of the infected rats show individual differences.
KeywordsHistopathology Change Cyst Form Sprague Dawley Infected Group Granule Form
This work was supported by the Natural Science Foundation of China (no. 30860254) and Natural Science Foundation of Jiangxi Province of China (no. 2009GZY0003). The experiments comply with the current regulations of People’s Republic of China. Ting Deng and Xiaohua Li contributed equally to this work. The authors would like to thank Dr. Syed Ahmad Moosa, faculty of international education, Gannan Medical University, for his suggestion and critically reading the manuscript.
- Noël C, Dufernez F, Gerbod D, Edgcomb VP, Delgado-Viscogliosi P, Ho LC, Singh M, Wintjens R, Sogin ML, Capron M, Pierce R, Zenner L, Viscogliosi E (2005) Molecular phylogenies of Blastocystis isolates from different hosts: implications for genetic diversity, identification of species, and zoonosis. J Clin Microbiol 43:348–355PubMedCrossRefGoogle Scholar