Nitric oxide production: a mechanism ofChlamydia trachomatisinhibition in interferon-γ-treated RAW264.7 cells
Open Access
- 1 June 1996
- journal article
- Published by Oxford University Press (OUP) in FEMS Immunology & Medical Microbiology
- Vol. 14 (2-3) , 109-120
- https://doi.org/10.1111/j.1574-695x.1996.tb00277.x
Abstract
IFN-γ and/or LPS induced nitrite production and inhibition of Chlamydia trachomatis (CT) replication in the murine macrophage cell line, RAW264.7. Linear regression analysis demonstrated a strong correlation between nitrite production and inhibition of CT replication (correlation coefficients: −0.93, P < 0.001). l-NMMA specifically inhibited nitrite production and restored CT replication (55–71%). Inducible nitric oxide synthase (iNOS) mRNA was analyzed by Northern and dot blot hybridization with an iNOS cDNA probe. A strong correlation between iNOS mRNA expression and inhibition of CT replication also was observed (correlation coefficient: −0.97, P< 0.05). Furthermore, anti-TNF-α antibody, which completely neutralized biological activity of the secreted TNF-α, neither inhibited nitrite production nor restored CT replication in the LPS- and/or IFN-γ-treated RAW264.7 cells. In mouse peritoneal macrophages treated with IFN-γ, both l-NMMA and anti-TNF-α antibody inhibited nitrite production and restored CT replication. However, l-NMMA and the antibody had no effect upon nitrite production and CT inhibition in LPS-treated peritoneal macrophages. These data indicate that NO production is one mechanism for inhibition of CT replication in IFN-γ-activated murine macrophages.Keywords
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