Roberts, F and Roberts, C W and Ferguson, D J and McLeod, R (2000) Inhibition of nitric oxide production exacerbates chronic ocular toxoplasmosis. Parasite Immunology, 22 (1). pp. 1-5. ISSN 0141-9838Full text not available in this repository. (Request a copy from the Strathclyde author)
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.
|Keywords:||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, Pharmacy and materia medica, Immunology, Parasitology|
|Subjects:||Medicine > Pharmacy and materia medica|
|Department:||Faculty of Science > Strathclyde Institute of Pharmacy and Biomedical Sciences|
|Depositing user:||Pure Administrator|
|Date Deposited:||28 Sep 2011 15:26|
|Last modified:||06 Jan 2017 09:59|