Late Gestation Glucocorticoids and Programming of Immune Function

Function of the immune system is influenced by basal glucocorticoid levels and by HPA axis responsiveness,48 raising the possibility that alterations in postnatal HPA axis function induced by exposure to excess glucocorticoids in late gestation might alter susceptibility to postnatal inflammatory/immune disease.

Investigations in rats and pigs have demonstrated that prenatal stress results in postnatal immunosuppression.49"51 These effects are likely mediated by prenatal exposure to glucocorticoids but alterations in postnatal HPA axis function do not necessarily account for altered postnatal immune function in these studies,50'51 suggesting that prenatal stress has direct programming effects on development of the immune system.

Only a few experimental studies have examined effects on postnatal immune function, beyond the immediate neonatal period, of glucocorticoid exposure in late gestation. Mice aged 5 months, born after prolonged maternal dexamethasone treatment during the final half of gestation, had impaired immunological function, associated with low thyroxine levels and anatomically abnormal thymus, adrenal and thyroid glands.52 Immunosuppression was also observed in juvenile monkeys born at term, 1 month after 2 days of maternal dexamethasone administration.53

A few studies of human neonates, born after antenatal corticosteroid therapy, indicate that immediate postnatal immune function is impaired. Total numbers of circulating white cells are decreased by antenatal corticosteroids, with particular effects on T cells.54 T cell proliferation is impaired in infants born after antenatal corticosteroids but natural killer cell activity is increased.55 These effects do not result in an increased (or decreased) incidence of infection in neonates born after a single course of antenatal corticosteroids12 but data suggest that the incidence of infection in childhood may be increased by the therapy.56 Multiple courses of antenatal corticosteroids increase the risk of early onset sepsis and sepsis-related neonatal death.57 The long term effects in humans of single or repeated courses of antenatal corticosteroids remain to be determined.

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