A protective role for IL-6 during early infection with Toxoplasma gondii

H Jebbari, C W Roberts, D J P Ferguson, H Bluethmann, J Alexander, Craig Roberts

Research output: Contribution to journalArticlepeer-review

84 Citations (Scopus)

Abstract

IL-6 deficient mice were found to be signifcantly more susceptible to peroral infection with Toxoplasma gondii than their wild-type counterparts as measured by survival, brain cyst burdens and brain pathology at 28 days postinfection. The physical manifestations of disease, such as weight loss, were not observed in IL-6 deficient animals until at least seven days later than such changes occurred in wild-type mice. During this early stage of infection IL-6+/+ but not IL-6-/- mice mounted a peripheral blood neutrophilia. Furthermore, between 6-8 days post-infection there was a significant increase in plasma IFN-gamma levels in wild-type but not IL-6 deficient mice. Not until days 18-23 post-infection, concurrent with the majority of deaths in IL-6-/- mice, were plasma IFN-gamma levels substantially and significantly raised in IL-6-/- mice. At this time not only were these plasma IFN-gamma levels 20-fold higher than background but eight-fold greater than peak (6-8 clays post-infection) IFN-gamma levels in IL-6+/+ mice. IFN-gamma dependent parasite specific IgG2a levels were also significantly higher in IL-6-/- mice over this period and thereafter Overall the evidence suggests that in the absence of IL-6 mice are unable to initiate a rapid proinflammatory response against T. gondii, which allows increased parasite growth. Increased mortality in IL-6-/- mice may be directly due to this increased parasite burden and the excessive inflammatory response this induces three weeks post-infection.

Original languageEnglish
Pages (from-to)231-239
Number of pages9
JournalParasite Immunology
Volume20
Issue number5
DOIs
Publication statusPublished - May 1998

Keywords

  • transgenic/knockout
  • toxoplasma gondii
  • IL-6 immunity
  • tumor-necrosis-factor
  • listeria-monocytogenes infection
  • natural-killer-cells
  • growth-factor-beta
  • CD8+ T-cells
  • IFN-gamma
  • interleukin-6-deficient mice
  • interferon-gamma
  • immune-response
  • murine toxoplasmosis

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