Relationship between antioxidant defense in Acanthamoeba spp. infected lungs and host immunological status

The role of oxidative stress in the pathogenicity of acanthamoebiasis is an important aspect of the intricate and complex host-parasite relationship. The aim of this experimental study was to determine oxidative stress through the assessment of lipid peroxidation product (LPO) levels and antioxidant defense mechanism in Acanthamoeba spp. lung infections in immunocompetent and immunosuppressed hosts. In Acanthamoeba spp. infected immunocompetent mice we noted a significant increase in lung lipid peroxidation products (LPO) at 8 days and 16 days post infection (dpi). There was a significant upregulation in lung LPO in immunocompetent and immunosuppressed mice infected by Acanthamoeba spp. at 16 dpi. The superoxide dismutase activity decreased significantly in lungs in immunosuppressed mice at 8 dpi. The catalase activity was significantly upregulated in lungs in immunocompetent vs. immunosuppressed group and in immunocompetent vs. control mice at 16 dpi. The glutathione reductase activity was significantly lower in immunosuppressed group vs. immunosuppressed control at 24 dpi. We found significant glutathione peroxidase downregulation in immunocompetent and immunosuppressed groups vs. controls at 8 dpi, and in immunosuppressed vs. immunosuppressed control at 16 dpi. The consequence of the inflammatory response in immunocompetent and immunosuppressed hosts in the course of experimental Acanthamoeba spp. infection was the reduction of the antioxidant capacity of the lungs resulting from changes in the activity of antioxidant enzymes. Therefore, the imbalance between oxidant and antioxidant processes may play a major role in pathology associated with Acanthamoeba pneumonia.