Humoral responses and immune protection in mice immunized with irradiated T. gondii tachyzoites and challenged with three genetically distinct strains of T. gondii

Abstract

Toxoplasma gondii is an obligate intracellular parasite that infects a variety of mammals and birds. T. gondii also causes human toxoplasmosis; although toxoplasmosis is generally a benign disease, ocular, congenital or reactivated disease is associated with high numbers of disabled people. Infection occurs orally through the ingestion of meat containing cysts or by the intake of food or water contaminated with oocysts. Although the immune system responds to acute infection and mediates the clearance of tachyzoites, parasite cysts persist for the lifetime of the host in tissues such as the eye, muscle, and CNS. However, T. gondii RH strain tachyzoites irradiated with 255Gy do not cause residual infection and induce the same immunity as a natural infection. To assess the humoral response in BALB/c and C57BL/6J mice immunized with irradiated tachyzoites either by oral gavage (p.o.) or intraperitoneal (i.p.) injection, we analyzed total and high-affinity IgG and IgA antibodies in the serum. High levels of antigen-specific IgG were detected in the serum of parenterally immunized mice, with lower levels in mice immunized via the oral route. However, most serum antibodies exhibited low affinity for antigen in both mice strain. We also found antigen specific IgA antibodies in the stools of the mice, especially in orally immunized BALB/c mice. Examination of bone marrow and spleen cells demonstrated that both groups of immunized mice clearly produced specific IgG, at levels comparable to chronic infection, suggesting the generation of IgG specific memory. Next, we challenged i.p. or p.o. immunized mice with cysts from ME49, VEG or P strains of T. gondii. Oral immunization resulted in partial protection as compared to challenged naive mice; these findings were more evident in highly pathogenic ME49 strain challenge. Additionally, we found that while mucosal IgA was important for protection against infection, antigen-specific IgG antibodies were involved with protection against disease and disease pathogenesis. Most antigen responsive cells in culture produced specific high-affinity IgG after immunization, diverse of the findings in serum IgG or from cells after infection, which produced low proportion of high-avidity IgG.

Immunization of Lambs Against Coccidiosis by Using Ultraviolet Irradiated Eimeria Oocysts for the First Time

“…This indicated that immunization of lambs by UV attenuated Eimeria species succeeded in rising IgA which usually secreted in mucous that secreted by goblet cell in intestine and attack Eimeria sporozoites and merozoites. This result agreed with Zorgi et al, (2011) who showed that high levels of IgA antibodies in the immunized mice serum with irradiated Toxoplasma gondii.…”

Protective effect of intranasal immunization with Neospora caninum membrane antigens against murine neosporosis established through the gastrointestinal tract

“…As N. caninum is an obligate intracellular pathogen a cell-mediated rather than a humoral immune response could be expected to be protective. Nevertheless, previous studies have reported a host protective role of intestinal IgA in cats 42 and mice 43 infected with the closely related protozoan Toxoplasma gondii, in agreement with the evidence presented here indicating that such a protective role may also be played by IgA in the course of N. caninum infection. Interestingly, non-infected mice immunized with NcMP plus CpG still presented antigen-specific intestinal IgA antibodies by 4 months after the last i.n.…”

CD103+ CD8 T Cells in the Toxoplasma-Infected Brain Exhibit a Tissue-Resident Memory Transcriptional Profile

“…Mice chronically infected with T. gondii exhibit protection against challenge with the virulent RH strain of the parasite, which is lethal in naïve mice (10). Persisting antigen is not required for such protection as infection of mice with attenuated strains of T. gondii confers protection upon rechallenge (10, 11). This suggests that the memory populations generated during chronic T. gondii infection are indeed functional, but it is unclear whether there is a distinction in the protection afforded by effector and memory T cell subsets in an environment of persistent antigen.…”