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This study evaluated the effects of surrogate fostering as a procedure to control for postnatal effects of ethanol on the maternal female that may indirectly affect the offspring. Effects of fostering on the development of splenic lymphocytes, as well as possible differential effects of fostering on female and male offspring were examined. Litters from prenatal ethanol exposed (E), pair‐fed (PF), and ad libitum‐fed control (C) condRions were fostered at birth to surrogate untreated dams who had given birth within the same 12‐hr period, or were reared by their biological mothers. At 15 and 60 days of age, offspring from each of the conditions were sacrificed and splenic leukocytes were enumerated and analyzed for expression of differentiation antigens, using flow cytometry. At 15 days of age, fostering reduced the percentages of CD45RA+and CD5+cells in E compared with PF and in PF compared with C offspring, and reduced the percentage of CD4+cells in E compared with C offspring. Fostering also had differential effects on E and C offspring, resulting in reduced percentages of CD45RA+and CD5+cells in fostered E compared with nonfostered E offspring, but increased percentages of CD45RA+, CD5+, and CD8+cells in fostered C compared with non‐fostered C offspring. Fostering also down‐regulated CD5 antigen expression in E compared with C offspring and up‐regulated CD4 antigen expression in C offspring compared with their nonfostered counterparts. At 60 days of age, E females overall had higher percentages of CD45RA+cells compared with C females and higher percentages of CD4+cells compared with PF and C females. Nonfostered E females had higher percentages of CD5+cells than nonfostered C females. In contrast, E males overall had greater percentages of CD4+cells compared with PF and C males. Among males, the percentage of CD5+cells was increased in nonfostered E compared with nonfostered C, whereas the percentages of CD45RA+and CD5+cells were decreased in fostered E males compared with nonfostered E. For both females and males in the nonfostered condition there were no effects of prenatal ethanol treatment on differentiation antigen expression. However, after fostering, E females had higher CD45RA and CD5 antigen expression compared with PF and C females, whereas E males had increased CD4 antigen expression and C males had decreased CD5 antigen expression compared with their nonfostwed Counterparts. These data demonstrate that fostering at birth has differential effects on splenic lymphocyte populations in E, PF, and C offspring. Moreover, the effect of fostering varies with age and has differential long‐term effects on female and male offspring. Thus, rather than serving as a control for indirect maternal effects of ethanol on offspring, fostering appears to be a treatment in itself and may actually confound the effects of prenatal ethanol exposure by differentially affecting E, PF, and C females and males.

Prenatal ethanol exposure and stress have each been shown to have significant effects on the immune system. This study examined the possible interactive effects of prenatal ethanol exposure and exposure to stress later in life on the immune system. Differential vulnerability to these challenges in female and male offspring was assessed. At 5 to 6 months of age, female and male offspring from prenatal ethanol‐exposed (E), pair‐fed (PF), and ad libitum‐fed control (C) conditions were exposed to 0, 1, or 3 days of cold (4°C). At the end of the cold period, the proliferative response of splenic lymphocytes to the mitogens concanavalin A (Con A) and pokeweed mitogen (PWM) was assessed. The data demonstrate a significant interactive effect between prenatal ethanol exposure and cold stress in female offspring. After 1 day of cold stress, E females had significantly increased PWM‐induced lymphocyte proliferation compared with PF and C females, and significantly increased Con A‐induced lymphocyte proliferation compared with PF females. There were no differences in PWM or Con A‐induced lymphocyte proliferation among E, PF, and C females after 0 or 3 days of cold stress, nor among E, PF, and C males on any test day. Regardless of prenatal treatment, females exposed to 1 or 3 days of cold had significantly greater basal plasma corticosterone levels than females not exposed to cold. In contrast, only E males exposed to 1 or 3 days of cold had significantly increased basal plasma corticosterone levels, compared with E males not exposed to cold; PF and C males showed no significant change in basal corticosterone after cold stress. These data demonstrate that, in response to the challenge of cold stress, changes in lymphocyte proliferation to PWM and Con A may occur selectively in E females. Moreover, the interactive effects of prenatal ethanol and cold stress may result in enhanced rather than suppressed immune responsiveness.