The role of IL-4 in adult acquired and congenital toxoplasmosis

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Alexander, J. and Jebbari, H. and Bluethmann, H. and Brombacher, F. and Roberts, C.W. (1998) The role of IL-4 in adult acquired and congenital toxoplasmosis. International Journal for Parasitology, 28 (1). pp. 113-120. ISSN 0020-7519 (https://doi.org/10.1016/S0020-7519(97)00168-9)

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Abstract

The course of Toxoplasma gondii infection was studied in IL-4-deficient mice from three genetic backgrounds and their wild-type counterparts following peroral inoculation of tissue cysts. Survival rates were significantly reduced in disease-susceptible C57 BL6 mice and F1 (C57BL6× 129Sv) mice deficient in IL-4 compared with wild-type controls. In contrast, this difference was not observed in T. gondii-resistant BALBc mice. However, brain tissue cyst burdens in IL-4-deficient mice were either equivalent to (C57BL6 and BALBc mice) or significantly less (B6129 mice) than similarly infected wild-type mice. Thus strain-specific differences in the course of T. gondii were demonstrated in the absence of IL-4. The course of T. gondii infection was also compared between B6129 IL-4-deficient mice and their wild-type counterparts following peroral challenge with 20 tissue cysts on day 12 of pregnancy. Age-matched non-pregnant IL-4−/− and IL-4+/+ mice were also infected to assess the role of IL-4 on T. gondii infection during pregnancy. Disease phenotypes, as measured by mortality, were reversed if infections were initiated during pregnancy compared with non-pregnant infection. Thus significant mortality occurred immediately post partum in IL-4+/+ mothers, while all IL-4−/− mothers survived. Cyst burdens 28 days p.i. were significantly lower in IL-4−/− mothers than IL-4+/+ mothers and both IL-4−/− and IL-4+/+ non-pregnant mice. Congenital disease transmission as measured by foetal death or vertical disease transmission was independent of the presence or absence of IL-4. These studies demonstrate a role for IL-4 in pregnancy-induced immunosuppression and the associated increased susceptibility to T. gondii infection.

ORCID iDs

Alexander, J., Jebbari, H., Bluethmann, H., Brombacher, F. and Roberts, C.W. ORCID logoORCID: https://orcid.org/0000-0002-0653-835X;
CORE (COnnecting REpositories)