Abstract
Late-gestation heat stress of dairy cows reduces fetal growth and influences postnatal performance and immune status of the offspring. Our first objective was to evaluate the effect of in utero heat stress on overall fetal and organ growth, particularly organs associated with immune function. The second objective was to examine the cellular mechanism of altered passive immunity in neonatal bull calves after in utero heat stress. Specifically, we examined the rate of apoptosis of intestinal cells early in life, as it is associated with gut closure. Dams were dried off approximately 45 d before expected calving and randomly assigned to 1 of 2 treatments: heat stress (HT) or cooling (CL). During the dry period all cows were housed under shade in a freestall barn, where the pen for CL cows was equipped with active cooling, including water soakers and fans, whereas the pen for HT cows had no soakers or fans. Using rectal temperature and respiration rate as indicators, heat stress was severe. Average rectal temperature in HT cows was 39.3°C compared with 39.0°C in CL cows, and HT cows had a respiration rate of 66.7 breaths/min compared with 43.2 breaths/min for CL cows. Bull calves (n = 30) were immediately separated from their dams at birth, weighed, and then killed before colostrum feeding (n = 5/treatment; d 0) or at 1 or 2 d of age following colostrum feeding (n = 5/treatment per day). After slaughter, the small intestine was removed and weighed, and samples from the jejunum were fixed for immunohistochemistry. Birth weight of bulls from HT dams was 1.1 kg lower than that of bulls from CL dams. Thymus, spleen, and heart weights of HT bulls were lower relative to those of CL bulls, whereas liver weight of HT bulls tended to be lower relative to that of CL bulls. Jejunal cell apoptosis decreased with age in both HT and CL calves after birth, mirroring gut closure. However, in utero heat stress increased the apoptotic rate in the jejunum, particularly at birth. We conclude that the chronic exposure to heat strain of HT compared with CL dams in late gestation significantly affected fetal growth and immune tissue development, which may be associated with reduced immune function in early life. Also, late-gestation heat stress increased calves' intestinal apoptosis in the first 2 d of life, which might explain the decreased IgG uptake and limited passive immune competence observed in previous studies.
Highlights
Late-gestation heat stress increased calves’ intestinal apoptosis in the first 2 d of life, which might explain the decreased IgG uptake and limited passive immune competence observed in previous studies
Studies indicate that calves born to and fed with colostrum from cows exposed to heat stress during late gestation have compromised passive immunity, as measured by apparent efficiency of IgG absorption (AEA) and cell-mediated immune function, compared with calves born to cows that were cooled when dry (Tao et al, 2012)
The second objective was to examine the cellular mechanisms of altered passive immunity in neonatal bull calves after in utero heat stress during late gestation, by examining the rate of apoptosis of intestinal cells early in life
Summary
Late-gestation heat stress increased calves’ intestinal apoptosis in the first 2 d of life, which might explain the decreased IgG uptake and limited passive immune competence observed in previous studies. Dams exposed to heat stress in late gestation have calves with lower birth weights, which reflects compromised fetal development (Tao et al, 2011, 2012; Tao and Dahl, 2013).
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