**3.4 Toxoplasmosis**

*Toxoplasma gondii* is an obligate intracellular protozoan pathogen that infects nearly all warm-blooded animals. Toxoplasmosis is one of the most prevalent parasitic diseases, an estimated one-third of the global population are at risk. Still, it is considered a neglected parasitic disease [88]. *T. gondii* causes life-threatening illnesses in developing fetuses and in persons with immunocompromised [89]. In chronic infection, *T. gondii* spreads in various organs such as the heart and brain through the circulatory system [90]. *T. gondii* RH tachyzoites treated with resveratrol and pyrimethamine significantly increased SOD activity to restrain ROS action for their survival [44]. Interestingly, human macrophages failed to produced ROS during *T. gondii*-infection [91], possibly due to an immune evasion mechanism of parasites. *T. gondii* targets the host NADPH oxidase enzyme by reducing the expression of Nox4 transcript and protein, resulting in diminished the release of intracellular ROS. In infected cells, Nox4 gene expression was associated with activation of PI3K/AKT signaling [92]. However, superoxide dismutase and catalase enzymes might be playing a role in intracellular survival but, it does not have a basis for differences in virulence to mice [93]. *In T. gondii,* SODs are found in nearly all developmental stages of parasites, suggesting their importance in detoxifying superoxide radicals to protect the parasite. *T. gondii* contains three types of SOD; SOD-B1 (Fe-SOD), different from the Mn-binding SOD of humans. SOD-B1 is a cytoplasmic and essential enzyme, and SOD-B1 gene knock-outs lead to be lethal for parasites [94, 95]. SOD2 and SOD3 are found in the mitochondria of parasites and have conserved residues to bind iron. However, they are very similar in the primary sequence to SODs from *P. falciparum* [45] *T. gondii* superoxide dismutase (*Tg*SOD) also affects the intracellular multiplication of both bradyzoite and tachyzoite forms of parasites. A recombinant DNA vaccine containing the antigen gene of *T. gondii* were elicited high levels of antibodies, a Th1 type of immune response with significant production of IFN-γ, and low levels of IL-4 or IL-10 in BALB/c mice [96]. Moreover, a DNA vaccine containing the TgSOD gene triggered potent humoral and cellular immune responses, and it stimulates biased protective immunity against acute *T. gondii* infection in BALB/c mice [46]. SOD-DNA vaccines of L. amazonensis immunized mice were partially protected from parasites once challenged. Mice showed a mixed immune response, including the production of IFN-γ and IL-4 from CD4+ and CD8+ T lymphocytes [69]. In addition, the SOD vaccine of *Brugia malayi* was also shown to trigger a typical Th1 response against infective larvae and microfilariae in jirds with filarial infection [97]. The above finding reveals that SOD-dependent vaccines have potential vaccine efficacy, either by protein or DNA-based vaccines, to control intracellular pathogen by activating the protective Th1 type of immune responses in animals.

*Superoxide Dismutase: A Key Enzyme for the Survival of Intracellular Pathogens in Host DOI: http://dx.doi.org/10.5772/intechopen.100322*
