Nitric oxide inhibition after Toxoplasma gondii infection of chicken macrophage cell lines

Abstract

Toxoplasma gondii infects many warm-blooded animals, including chickens. However, little is known about how this protozoan behaves within chicken macrophages. Thus, the microbicidal biology of HD11 and MQ-NCSU (available chicken macrophage cell lines) and the escaping mechanism of T. gondii were investigated. After infection, both cell lines were activated with lipopolysaccharide (LPS) and nitric oxide (NO), and reactive oxygen intermediates (ROI) were evaluated. T. gondii infected both cell lines, and 30 and 60% inhibition of NO production was detected in MQ-NCSU and HD11, respectively. In HD11, NO inhibition was not dependent on cyclooxygenase products. Although NO was partially inhibited, it did control T. gondii multiplication, showing the importance of this microbicidal molecule. Production of ROI was not detected in either cell line after T. gondii or yeast interaction. NADPH diaphorase (NADPH-d) activity, a histochemical marker of inducible NO synthase (iNOS), was detected at various levels in the HD11 population activated with LPS. The HD11 population infected with T. gondii showed a decrease in NADPH-d, indicating that NO production inhibition was related to iNOS disappearance in infected macrophages. These results demonstrate that in chicken macrophages T. gondii can also inhibit NO production, which suggests that an iNOS suppression mechanism might be used for better survival in macrophages.