ABSTRACT
In vitro activation of murine peritoneal macrophages by TNF and IL-I cytokines resulted in significant elevation of respiratory burst (toxic oxygen metabolites) in comparison to inactivated cells when challenged with Toxoplasma gondii. These oxygen metabolites have been known to have microbicidal activity and so, they may be the direct cause of intracellular killing of T. gondii tachyzoites. The level of these oxygen metabolites was measured by chemiluminescence index. A possible biotherapeutic role for TNF and IL-1, through this mechanism, was also emphasized.
Subject(s)
Interleukin-1/pharmacology , Macrophage Activation , Macrophages, Peritoneal/physiology , Macrophages, Peritoneal/parasitology , Respiratory Burst/drug effects , Toxoplasma/physiology , Tumor Necrosis Factor-alpha/pharmacology , Animals , Cells, Cultured , Female , Macrophages, Peritoneal/drug effects , Toxoplasma/pathogenicity , VirulenceABSTRACT
Macrophages and monocytes have been shown to have an important role in the defence mechanism against Taxoplasma gondii infection. Antibodies in the presence of complement have been found capable of killing extracellular T. gondii. This study demonstrated that tachyzoites in the presence of antitoxoplasma antibodies with complement were detected in 39-58% of monocytes that had phagocytosed them and the mean number of Toxoplasma tachyzoites in this group was significantly low one hour post infection, while only 10-25% of monocytes phagocytosed Toxoplasma tachyzoites in absence of antibodies and complement with significant high number of replicated tachyzoites. This indicated that specific antibodies had a strong opsonizing action. Complement alone was weak in increasing the phagocytic activity.
