Inhibition of nitric oxide production exacerbates chronic ocular toxoplasmosis
F Roberts, CW Roberts, DJP Ferguson… - Parasite …, 2000 - Wiley Online Library
F Roberts, CW Roberts, DJP Ferguson, R McLeod
Parasite immunology, 2000•Wiley Online LibraryThere 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 Lω‐nitro‐l‐arginine methyl ester …
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 Lω‐nitro‐l‐arginine methyl ester …
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 Lω‐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.
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