Toxoplasmosis : Role of Cytokines in Disease Modulation & Tissue Pathology
- 1. Department of Microbiology, Kuwait University, Kuwait
Abstract
Toxoplasmosis caused by Toxoplasma gondii parasite has a world - wide distribution effecting one third of the world population. A number of parasite and host factors determine the outcome of prevalence, disease severity and tissue damage ranging from asymptomatic self - limiting infection in health adults to serious destructive inflammatory consequences in congenitally infected infants and in individuals with a weakened immune system. There is strong experimental evidence that the cytokines play a major role in the pathogenesis of Toxoplasma gondii and manipulation of these cytokines can put forth a beneficial or damaging effect on the host and thus modulate the disease pathology. The importance of interferon gamma (IFN-γ) was clearly demonstrated when the neutralization of interleukin (IL) IL-12 and of IFN-γ using anti-IFN-γ & anti-IL-12 monoclonal antibodies (MAb) resulted in reactivation and loss of control on the parasite’s multiplication leading to disease. Cytokine IL-27 was deemed as an endogenous suppresser on IL-17, the inflammatory cytokine that is capable of enhancing the inflammatory response in the brain. Although Toxoplasma is an intracellular pathogen thereby requiring a cell mediated immune response from the host, the cytokine IL-10 protects the infected mice from an exaggerated cellular immune response by inhibiting the production of pro - inflammatory cytokines: IL12, IFN-γ, and TNF-β. Following Toxoplasma infection the host triggers a sequential balanced cytokine response to limit the infection and the disease pathology. However, cytokines can sometimes exert a negative effect on the host and augment the disease leading to severe irreversible tissue damage.