Parasitology Research

, Volume 111, Issue 3, pp 1093–1101

Organ-specific testosterone-insensitive response of miRNA expression of C57BL/6 mice to Plasmodium chabaudi malaria

Authors

    • Department of Zoology, College of ScienceKing Saud University
  • Mohamed A. Dkhil
    • Department of Zoology, College of ScienceKing Saud University
    • Department of Zoology and Entomology, Faculty of ScienceHelwan University
  • Denis Delic
    • Department of Molecular ParasitologyHeinrich-Heine University
    • Max Planck Institute for Neurological Research
  • Abdel Azeem Abdel-Baki
    • Department of Zoology, College of ScienceKing Saud University
    • Department of Zoology, Faculty of ScienceBeni-Suef University
  • Frank Wunderlich
    • Department of Molecular ParasitologyHeinrich-Heine University
Original Paper

DOI: 10.1007/s00436-012-2937-3

Cite this article as:
Al-Quraishy, S., Dkhil, M.A., Delic, D. et al. Parasitol Res (2012) 111: 1093. doi:10.1007/s00436-012-2937-3

Abstract

Increasing evidence critically implicates miRNAs in the pathogenesis of diseases, but little is known in context with infectious diseases. This study investigates as to whether the testosterone-induced persistent susceptibility to blood-stage malaria of Plasmodium chabaudi coincides with changes in miRNA expression of the anti-malaria effectors sites spleen and liver. Female C57BL/6 mice were treated with vehicle or testosterone (T) for 3 weeks. Then, T treatment was discontinued for 12 weeks before challenge with 106P. chabaudi-parasitized erythrocytes. The miRNA expression was examined after 12 weeks of T withdrawal and during infections at peak parasitemia on day 8 p.i. using miRXplore™ microarray technology. P. chabaudi infections induce an organ-specific response of miRNA expression. We can identify 25 miRNA species to be downregulated by more than 2-fold in the spleen and 169 miRNA species in the liver. Among these 194 miRNA species, there are 12 common miRNA species that are downregulated by 0.48–0.14-fold in both spleen and liver, which are miR-194, miR-192, miR-193A-3P, miR-145, miR-16, miR-99A, miR-99B, miR-15A, miR-152, let-7G, let-7B, and miR-455-3P. Only in the liver, there is an upregulation of the miR-142-5p by 2.5-fold and miR-342-3p by 5.1-fold. After 12 weeks of T withdrawal, the spleen exhibits only the miR-200A that is upregulated by 2.7-fold. In the liver, miR-376B, miR-493*, and miR-188-3P are upregulated by 2.4-fold, 2.2-fold, and 2.1-fold, respectively, and miR-347, miR-200A, and miR-200B are downregulated by approximately 0.4-fold. Upon infection, however, these changes are not sustained, i.e., the miRNA expressions of both spleen and liver of T-pretreated mice exhibit the same response to P. chabaudi malaria as that of vehicle-treated control mice. Our data suggest (1) that the P. chabaudi-induced downregulation of miRNA expression in spleen and liver is required to allow the upregulation of their numerous target genes in response to infection, and (2) that the T-induced persistent susceptibility to P. chabaudi does not affect the responsiveness of miRNA expression in spleen and liver to blood-stage malaria.

Supplementary material

436_2012_2937_MOESM1_ESM.tif (550 kb)
High resolution image (TIFF 550 kb)
436_2012_2937_MOESM2_ESM.xlsx (16 kb)
Table S1Liver-specific deregulation of miRNA expression of unknown function induced by P. chabaudi malaria in vehicle-treated control mice (XLSX 16 kb)
436_2012_2937_MOESM3_ESM.xlsx (12 kb)
Table S2MicroRNA expression of spleen and liver of T-pretreated and vehicle-treated mice during P. chabaudi malaria on day 8 p.i. (XLSX 12 kb)

Copyright information

© Springer-Verlag 2012