Lactocrine deficiency alters postnatal porcine uterine development

Nursing provides the mammalian neonate with nutrition and passive immunity and serves as a mechanism for delivery of milk-borne bioactive factors (MbFs) such as growth factors and hormones present in colostrum and milk to nursing offspring. The lactocrine hypothesis suggests that MbFs communicated from mother to nursing offspring have both short- and long-term effects on postnatal development of the female reproductive tract. Data for the pig show that experimental imposition of a lactocrine-null condition by milk replacer feeding from birth (postnatal day = PND 0) has negative effects on uterine endometrial development in the neonate. In addition, pigs determined to be lactocrine-deficient from birth, as reflected by a low serum immunoglobulin immunocrit (iCrit) ratio, showed long-term, negative effects on litter size and uterine capacity that persisted into adulthood. Effects of lactocrine deficiency on postnatal porcine uterine development at PND 14 have not been studied extensively. In addition, FOXA2, a marker of uterine gland development, was identified in endometrial glandular epithelium in multiple species including mice, rats, humans, and in both the developing and adult ovine uterus. However, uterine FOXA2 expression and immunolocalization of FOXA2 have not been reported for the pig. Therefore, the goal of this research was to learn more about the effects of lactocrine deficiency, indicated by low serum iCrit at birth, on maternal programming of porcine uterine development. Objectives of research described here were to: 1) identify effects of lactocrine deficiency from birth on endometrial morphology at PND 14; 2) determine if FOXA2 expression is detectable in neonatal porcine uterine tissues and whether neonatal porcine uterine FOXA2 expression is lactocrine-sensitive; and 3) evaluate effects of lactocrine deficiency from birth on patterns of FOXA2 distribution in the uterine endometrium on PND 14. Results showed that the endometrial area occupied by glandular epithelial cells (P < 0.05) and, to a lesser extent, endometrial thickness (P < 0.08) were reduced in low as compared to high iCrit gilts on PND 14. However, uterine gland penetration depth did not differ between the two groups. The FOXA2 protein was immunolocalized consistently and uniquely in nascent glandular epithelium in both low and high iCrit gilts on PND 14. Uterine FOXA2 expression was reduced (P