PMID: 9529049Apr 7, 1998Paper

Toxoplasma gondii triggers granulocyte-dependent cytokine-mediated lethal shock in D-galactosamine-sensitized mice

Infection and Immunity
A J Marshall, Eric Y Denkers

Abstract

To investigate the capacity of Toxoplasma gondii to induce cytokine-mediated toxicity, we employed a murine model of lethal shock in which hypersensitivity to microbial toxins is induced by D-galactosamine (D-Gal). Animals injected with D-Gal and tachyzoite lysate died within 12 to 24 h, whereas administration of D-Gal or lysate alone was nonlethal. Analyses of plasma cytokines revealed peaks of tumor necrosis factor (TNF) alpha and interleukin-12 (IL-12) 1 and 3 to 5 h after injection, respectively, and gradually rising levels of gamma interferon (IFN-gamma) continuing until death. Nitric oxide (NO) levels in serum paralleled IFN-gamma production. Transaminase assays revealed elevated levels of liver-associated enzymes in sera of lethally injected mice, indicating severe hepatic damage. Depletion of IL-12, TNF, IFN-gamma, and NO rescued mice from the lethal effect of antigen (Ag) and D-Gal. T-cell-deficient animals remained sensitive to D-Gal and lysate, suggesting that T lymphocytes do not contribute to the response. Nevertheless, monoclonal antibody (MAb)-mediated granulocyte depletion completely abrogated D-Gal- and Ag-induced mortality and accompanying liver pathology. Finally, mice acutely infected with T. gondii displaye...Continue Reading

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