Objective: We evaluated the effect of maternal administration of betam
ethasone (0.2 mg/kg per day) on mitogen-induced lymphocyte proliferati
on and interleukin-2 (IL-2) production by maternal, fetal, and neonata
l rat splenic lymphocytes. Study Design: Betamethasone was injected in
tramuscularly on days 19 and 20 of gestation to timed-pregnant rats (S
prague-Dawley). Fetuses were delivered on day 21 of gestation, or allo
wed to deliver spontaneously at term (22 days), followed by sacrifice
at various intervals after birth. Lymphocyte proliferation was determi
ned by H-3-thymidine incorporation with and without phytohemagglutinin
(PHA), and IL-2 by proliferation of IL-2 dependent CTLL-2 cells. Resu
lts: Maternal lymphocytes had higher spontaneous proliferation than ly
mphocytes 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 aft
er 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. Conclusio
n: These findings suggest that, in the rat, exposure to betamethasone
during late pregnancy results in marked, but transient decreases in PH
A-induced lymphocyte proliferation and IL-2 production in both the mot
hers and their offspring.