Caspase-12 deficiency enhances cytokine responses but does not protect against lethal Plasmodium yoelii 17XL infection

Parasite Immunol. 2010 Nov-Dec;32(11-12):773-8. doi: 10.1111/j.1365-3024.2010.01250.x.

Abstract

To investigate the effect of caspase-12 deficiency on IFN-γ- independent control of blood-stage malaria, we compared lethal Plasmodium yoelii 17XL infection in wild-type C57BL ⁄ 6J and caspase-12-/-mice. Infected caspase-12-/- mice exhibited higher parasitaemia than WT mice on days 8 and 9 post-inoculation, but all WT and caspase-12-/- mice succumbed by day 10. In addition, infected caspase-12-/-mice had significantly elevated levels of IFN-γ, TNF, IL-18,and IL-10 in sera compared to infected WT mice. At the terminal stage of disease, there were no differences in cytokine levels in the tissues of infected WT and caspase-12-/- mice. However, liver pathology was more severe in infected caspase-12-/- mice compared to infected WT mice. Together, these findings indicate that although caspase-12 deficiency results in enhanced pro-inflammatory and immunoregulatory cytokine levels in sera during P. yoelii 17XL infection, these responses are not essential for protection against lethal malaria infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caspase 12 / deficiency
  • Caspase 12 / immunology*
  • Cytokines / blood*
  • Female
  • Liver / pathology
  • Malaria / immunology*
  • Malaria / pathology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Parasitemia
  • Plasmodium yoelii / immunology*
  • Plasmodium yoelii / pathogenicity*
  • Survival Analysis

Substances

  • Cytokines
  • Casp12 protein, mouse
  • Caspase 12