Fig. 1

Schematic representation of perinatal stressors and factors that can impact intestinal development and maturation. Before calving maternal nutrition (e.g., undernutrition) can have a detrimental effect on intestinal growth and functionality, including downregulation of soluble guanylate cyclase 1β3 (gene symbol GUCY1B3) in the jejunum. Prenatal heat stress may lead to lower placental function and reduced gestation length. The latter can considerably affect the newborn’s ability to ingest valuable nutrients, immunoglobulins, cortisol, and bioactive compounds (e.g., growth factors and hormones) in colostrum, consequently, disrupting the natural intestinal maturation after birth. Intestinal maturation refers to the timely replacement of highly vacuolated enterocytes for more matured and highly functional enterocytes as well as increased crypts depth and cell proliferation. Intestinal diseases in neonatal dairy calves have been associated with morphological and functional immaturity. In this context, little is known about how intestinal immaturity can render neonatal calves vulnerable to pathogen recognition of host receptors (or docking sites), allowing the initial attachment of such pathogens to the intestinal epithelium. For instance, glycolipid gangliosides (e.g., NeuGc-GM3) are host receptors located in the cell membrane epithelium that facilitates the attachment of enterotoxigenic Escherichia coli (ETEC). Intestinal development figure adapted from Walton et al. [83]