Heat stress (HT) in utero not only induces fetal growth retardation but also influences postnatal performance of the offspring, such as immune function and metabolic adaptation. The objective was to examine the cellular mechanism of altered passive immunity in neonatal bull calves after in utero heat stress during late gestation. Specifically, by examination of the rate of apoptosis of intestinal cells early in life, as that has been shown to influence gut closure. Cows were dried off 60 d before expected calving and randomly assigned to one of 2 treatments: HT or cooling (CL). During the dry period, all cows were housed in a freestall barn, the pen for CL cows was equipped with active cooling including water soakers and fans whereas the pen for HT cows had no soakers. Heat stress was moderate compared with other studies, as HT cows had only 0.1°C increase in rectal temperature and 8 breath/min increase in respiration rate compared with CL cows. After birth all bull calves were immediately separated from their dams and weighed. Bull calves (n = 30) were killed at birth without colostrum feeding (5/trt) and 1 and 2 d of age (DOA, following colostrum feeding, 5/trt). Colostrum (3.8 L) was fed within 2 h after birth to bulls slaughtered on 1 and 2 DOA. After slaughter, the intestine was removed, weighed, and dissected into duodenal, jejunal and ileal segments, and tissue samples from each section were fixed in 4% neutral formalin and then transferred to 70% ethanol for immunohistochemistry. Apoptosis was measured in the jejunum using TUNEL labeling, counting 6 different sections per slide per calf. Small intestine weights did not differ (HT: 1376 ± 45; CL: 1309 ± 45 g; P = 0.30). In both groups, apoptosis reactive cell counts decreased with time after birth (HT: 0DOA: 58.8; 1DOA: 21.6; 2DOA: 41.4; CL: 0DOA: 88.6; 1DOA: 58.0; 2DOA: 53.8; SEM = 16.7; P = 0.05). However, apoptotic counts in CL bulls were higher than HT bulls (66.8 ± 9.6 vs. 40.6 ± 9.6, respectively; P = 0.10). The results indicate that jejunal cell apoptosis progresses with time after birth, but in utero HT reduces the apoptotic rate.