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Absence of involvement of nitric oxide in LP-BM5-induced immunodeficiency syndrome
Abstract:
To examine the role of nitric oxide (NO) in murine AIDS (MAIDS) pathogenesis, we determined NO production and inducible NOS (iNOS) mRNA expression in the macrophages of LP-BM5-infected mice, together with the in vivo effects of L-NAME, a competitive inhibitor of NO synthase. LP-BM5 infection induced neither spontaneous nitrite production nor iNOS mRNA expression. No differences in IFN gamma + LPS-induced nitrite production or iNOS mRNA expression were observed in macrophages, from non-infected or infected mice. Spleen weight, ecotropic MuLV replication, the blood lymphocyte phenotype and proliferative response of splenocytes were not modified by L-NAME. LP-BM5 infection did not increase macrophage NO production and NO production did not appear to protect against LP-BM5-induced immunodeficiency.
Insights
Nitric oxide (NO) production does not increase in macrophages during murine AIDS (MAIDS). Inhibiting NO synthesis with L-NAME did not alter MAIDS progression, suggesting NO is not protective against this immunodeficiency.
Area of Science:
- Immunology
- Virology
- Pathogenesis
Background:
- Murine AIDS (MAIDS) is an immunodeficiency syndrome induced by the LP-BM5 retrovirus.
- Nitric oxide (NO) plays complex roles in immune responses and inflammation.
- The involvement of NO in MAIDS pathogenesis remains unclear.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in the pathogenesis of murine AIDS (MAIDS).
- To determine NO production and inducible nitric oxide synthase (iNOS) mRNA expression in macrophages from LP-BM5-infected mice.
- To assess the in vivo effects of L-NAME, a nitric oxide synthase inhibitor, on MAIDS progression.
Main Methods:
- LP-BM5 retrovirus infection in mice.
- Measurement of NO production (nitrite levels) in macrophages.
- Quantification of iNOS mRNA expression in macrophages.
- Administration of L-NAME (a competitive inhibitor of NO synthase) in vivo.
- Assessment of spleen weight, MuLV replication, lymphocyte phenotype, and splenocyte proliferation.
Main Results:
- LP-BM5 infection did not induce spontaneous nitrite production or iNOS mRNA expression in macrophages.
- IFN-gamma + LPS-induced nitrite production and iNOS mRNA expression were similar in macrophages from infected and non-infected mice.
- L-NAME treatment did not affect spleen weight, MuLV replication, lymphocyte phenotype, or splenocyte proliferative responses.
- Macrophage NO production was not increased by LP-BM5 infection.
Conclusions:
- Nitric oxide production is not upregulated during LP-BM5-induced murine AIDS.
- Inhibition of NO synthesis does not exacerbate or ameliorate MAIDS.
- NO does not appear to play a protective role in LP-BM5-induced immunodeficiency.