Inhibition of nitric oxide production exacerbates chronic ocular toxoplasmosis

F Roberts, C W Roberts, D J Ferguson, R McLeod

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34 Citations (Scopus)


There is considerable controversy as to the roles of parasite proliferation and the inflammatory response in destruction of the retina during Toxoplasma gondii infection. A murine model was used to investigate the role of nitric oxide in pathogenesis of chronic ocular toxoplasmosis. Increased quantities of messenger RNA (mRNA) transcripts for iNOS were detected in the eyes of chronically infected C57BL/6 mice compared with noninfected control mice. Inhibition of nitric oxide (NO) by the addition of Lomega-nitro-L-arginine methyl ester (L-NAME) to the drinking water of infected mice between weeks 4-6 of infection, exacerbated ocular inflammation. The amount of inflammation was assessed semiquantitatively in histological sections of the eye. Eyes from L-NAME treated mice showed a significant increase in inflammation of the retina (P = 0.02), choroid (P = 0.03), and vitreous (P = 0.02) compared with control mice. These results demonstrate a protective role for NO in the control of chronic, ocular toxoplasmosis.
Original languageEnglish
Pages (from-to)1-5
Number of pages5
JournalParasite Immunology
Issue number1
Publication statusPublished - 2000


  • animals
  • chronic diseases
  • mice
  • mice, inbred C57BL
  • NG-ntroarginine mthyl Ester
  • nitric oxide
  • Nitric oxide synthase
  • nitric oxide synthase type II
  • RNA, messenger
  • toxoplasmosis, animal
  • toxoplasmosis, ocular


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