Effect of betamethasone on maternal, fetal and neonatal rat cellular immunity

We evaluated the effect of maternal administration of betamethasone (0.2 mg/kg per day) on mitogen-induced lymphocyte proliferation and interleukin-2 (IL-2) production by maternal, fetal, and neonatal rat splenic lymphocytes.

Betamethasone was injected intramuscularly on days 19 and 20 of gestation to timed-pregnant rats (Sprague-Dawley). Fetuses were delivered on day 21 of gestation, or allowed to deliver spontaneously at term (22 days), followed by sacrifice at various intervals after birth. Lymphocyte proliferation was determined by 3H-thymidine incorporation with and without phytohemagglutinin (PHA), and IL-2 by proliferation of IL-2 dependent CTLL-2 cells.

Maternal lymphocytes had higher spontaneous proliferation than lymphocytes from nonpregnant female rats. Betamethasone use resulted in a decrease in PHA-induced lymphocyte proliferation and IL-2 production by maternal lymphocytes. These effects were observed until 4 days after delivery. Significant decreases in these parameters were also seen in 21-day fetuses of betamethasone-treated mothers. These effects were still present 6 days after birth but not at 12 days of age.

These findings suggest that, in the rat, exposure to betamethasone during late pregnancy results in marked, but transient decreases in PHA-induced lymphocyte proliferation and IL-2 production in both the mothers and their offspring.