Transforming growth factor-beta (TGF-β) plays a role in enterocyte proliferation control, cell differentiation, and immune regulation via binding to specific TGF-β receptors (TGF-β R) in the intestinal epithelium. Endogenous TGF-β production is low in the intestine during the perinatal period, but some exogenous TGF-β ligands are supplied by amniotic fluid intake in the fetus and by colostrum ingestion in the neonate. It is not clear, however, whether luminal TGF-β receptors are present and functional at this critical time. We studied intestinal TGF-β receptors by immunohistochemistry during the last 20% of gestation in pigs and in chronically catheterized fetuses following exposure to colostrum, milk, and amniotic fluid (control). In fetal pigs, the TGF-β Rs were predominantly localized to the crypt epithelium, but staining intensity increased markedly just before term and shifted to the villous epithelium in newborn pigs, concurrently with marked increases in villous heights and crypt depths (+100–200%, P < 0.05). In contrast to previous observations in term newborn pigs, fetal pigs did not show any milk-induced change in TGF-β receptor densities or localization, although a moderate increase in villous height was observed, relative to control (+25–50%, P < 0.05). We conclude that intestinal TGF-β receptor density and localization are immature and unresponsive to TGF-β containing milk diets in prenatal pigs. Immaturity of TGF-β-mediated immune regulation may play a role in the increased sensitivity of preterm neonates to diet-induced intestinal inflammatory disorders.
Euphol from Euphorbia tirucalli negatively modulates transforming growth factor‐beta (TGF‐β) responsiveness correlate with TGF‐β receptor segregation inside membrane rafts.