Acute and chronic phases of Toxoplasma gondii infection in mice modulate the host immune responses

Abstract

Murine antibody responses to soluble proteins are generally restricted to the immunoglobulin G1 (IgG1) isotype. When mice were infected with Toxoplasma gondii Beverley and concomitantly immunized with a soluble unrelated protein antigen, a modification in the isotypic distribution of antibodies directed against this nonparasite antigen was observed, with a preferential production of IgG2a. Interestingly, when mice were immunized with a soluble protein antigen during the chronic phase (day 40) of infection with T. gondii Beverley, a similar modification in the isotypic distribution of antiprotein antibodies was observed.

FIG. 1

Detection of IL-12 (p40), IFN-γ, IL-4, and actin mRNAs in spleen cells of BALB/c mice infected with 20 cysts of T. gondii Beverley. Spleen cells were harvested at time zero (control animals) and at 1, 2, 4, 10, and 30 days p.i. as indicated above the lanes and then frozen in TRIzol; mRNA preparations were reverse transcribed, and specific messages were amplified by PCR. Products of PCR amplification were detected by ethidium bromide staining in agarose gels. Lane +, control for cytokine mRNAs.

FIG. 2

Isotypic distribution of antilactoferrin antibodies in uninfected BALB/c mice and in animals infected for 40 days with T. gondii Beverley. Antilactoferrin antibodies in individual sera obtained 3 weeks after lactoferrin immunization were assayed. Results are shown as means ± standard errors for groups of four or five mice. Essentially identical results were obtained in three experiments.

FIG. 3

Isotypic distribution of antilactoferrin antibodies in BALB/c mice immunized on day 0 with 100 μg of lactoferrin per mouse alone or together with 50 ng of rIL-12. Antilactoferrin antibodies in individual sera obtained 3 weeks later were assayed by ELISA. Results are shown as means ± standard errors for groups of four or five mice.