microRNA-155 Expression and Butyrylcholinesterase Activity in the Liver Tissue of Mice Infected with Toxoplasma gondii (Avirulent and Virulent Strains)
- 11 April 2021
- journal article
- research article
- Published by Springer Nature in Acta Parasitologica
- Vol. 66 (4) , 1167-1176
Abstract
Purpose Toxoplasma gondii is an apicomplexan parasite that exhibits distinct strain-related virulence patterns in mice. It can induce hepatic inflammation. The present study investigated MicroRNA-155 (miRNA-155) expression and butyrylcholinesterase (BChE) activity in the liver tissue of mice infected with virulent and avirulent strains of T. gondii. Methods Mice groups included: Group (A), uninfected controls; Group (B), infected with T. gondii avirulent strain (ME-49) and euthanized 7, 27, 47, or 67 days post-infection (pi); Group (C), infected by T. gondii virulent strain (RH) and euthanized 7 days pi; and Group (D), infected by T. gondii virulent strain (RH), treated 24 h pi with sulfamethoxazole-trimethoprim (150 mg/Kg/day and 30 mg/Kg/day, respectively) and euthanized 5, 10, or 20 days pi. miRNA-155 expression was estimated in the liver tissue using the reverse transcription real-time polymerase chain reaction and the ΔΔCt method. BChE activity was estimated in liver homogenates by Ellman’s colorimetric method. Liver sections were examined histopathologically. Results revealed a significant elevation in miRNA-155 expression and a significant reduction of BChE activity in all the infected untreated groups compared to the uninfected mice. In group B, the maximum upregulation of miRNA-155 expression and the least reduction in BChE activity were detected 7 days pi. In group D, complete restoration of normal levels occurred 20 days pi. Liver sections showed distinct histopathological patterns with detection of intracellular tachyzoites in group B. Conclusion miRNA-155 and BChE play a role in regulating host-parasite interaction in toxoplasmosis and may contribute to the pathogenesis of T. gondii induced hepatic damage.Keywords
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