Immune Responses of Mice Intraduodenally Infected withToxoplasma gondiiKI-1 Tachyzoites

Abstract

Toxoplasma gondii Korean isolate (KI-1) tachyzoites were inoculated intraduodenally to BALB/c mice using a silicon tube, and the course of infection and immune responses of mice were studied. Whereas control mice, that were infected intraperitoneally, died within day 7 post-infection (PI), the intraduodenally infected mice survived until day 9 PI (infection with 1×105 tachyzoites) or day 11 PI (with 1×106 tachyzoites). Based on histopathologic (Giemsa stain) and PCR (B1 gene) studies, it was suggested that tachyzoites, after entering the small intestine, invaded into endothelial cells, divided there, and propagated to other organs. PCR appeared to be more sensitive than histopathology to detect infected organs and tissues. The organisms spread over multiple organs by day 6 PI. However, proliferative responses of splenocytes and mesenteric lymph node (MLN) cells in response to con A or Toxoplasma lysate antigen decreased significantly, suggesting immunosuppression. Splenic CD4+ and CD8+ T-lymphocytes showed decreases in number until day 9 PI, whereas IFN-γ and IL-10 decreased slightly at day 6 PI and returned to normal levels by day 9 PI. No TNF-α was detected throughout the experimental period. The results showed that intraduodenal infection with KI-1 tachyzoites was successful but did not elicit significant mucosal immunity in mice and allowed dissemination of T. gondii organisms to systemic organs. The immunosuppression of mice included reduced lymphoproliferative responses to splenocytes and MLN cells to mitogen and low production of cytokines, such as IFN-γ, TNF-α, and IL-10, in response to T. gondii infection.

The merits of designed ELISA avidity kit in detection of Toxoplasma gondii IgG antibody in laboratory conditions

“…[131415] Thus, in principle, ESA could play a role in the persistent stimulation of cell–mediated immunity in chronically infected healthy subjects. Excretory/secretory antigens may be the best form of antigens for stimulation of the cell-mediated immune response and a good candidate as a vaccine for toxoplasmosis prevention.…”

“…The upper level of this centrifuged fluid could be used for extracting excretory – secretory antigens to design ELISA avidity kit. [101112]…”

Increase in the nuclear localization of PTEN by the Toxoplasma GRA16 protein and subsequent induction of p53‐dependent apoptosis and anticancer effect

“…[1][2][3][6][7][8] Conversely, the negative regulation of HAUSP exhibits a crucial clinical significance for estimating the prognosis of tumour suppression. Based on the findings of a recent study, 9 the authors probed whether the properties of GRA16 recognized as a new HAUSP inhibitor could be available for anticancer intervention because the precise mechanism of GRA16 in inducing an anticancer effect remains unclear to date. Based on the findings of a recent study, 9 the authors probed whether the properties of GRA16 recognized as a new HAUSP inhibitor could be available for anticancer intervention because the precise mechanism of GRA16 in inducing an anticancer effect remains unclear to date.…”

“…5,7 Thus, identification of HAUSP inhibitors is imperative for the therapeutic intervention of cancer. Based on the findings of a recent study, 9 the authors probed whether the properties of GRA16 recognized as a new HAUSP inhibitor could be available for anticancer intervention because the precise mechanism of GRA16 in inducing an anticancer effect remains unclear to date.…”

“…10,11 Briefly, the immunomodulatory activities of T gondii are mediated by infection as well as several T gondii-specific molecules such as rhoptry proteins (ROP), dense granule proteins (GRA), T gondii profilin-like protein (TgPLP) and the lysate antigenic proteins. 9,10 Thus, our objective was to determine the intermediate events between HAUSP inhibition and p53 stabilization and also the anticancer effect. In particular, p53 transcriptional activity is often disrupted in HCC by highly expressed HAUSP; moreover, the expression of nuclear PTEN decreases in patients with advancedstage HCC.…”