Corticosterone regulation of the effector function of malarial immunity during pregnancy.

In the experimental Plasmodium berghei mouse model, as in human malaria, reduced maternal responsiveness and even loss of immunity were observed during pregnancy. Loss of immunity in the second half of pregnancy occurred during a period of elevated plasma corticoid levels. Further analysis showed that plasma corticoid levels were significantly higher in immunodepressed mice than in mice that remained immune throughout pregnancy. Plasma corticosterone levels differed increasingly from those in mice with persistent immunity towards recrudescence. In nonimmune infected controls, however, only a slight increase in plasma corticosterone, already present during the subpatent period, was measured. Blocking the maternal corticoid production by adrenalectomy delayed the increase of plasma corticosterone (fetoplacental origin) and reduced the number of mice that lost immunity during pregnancy considerably. The role of various plasma corticoid levels in the regulation of effector function of immunity during pregnancy is discussed.