The small intestine of an infant differs from the adult small intestine. It takes several months of morphological and functional maturation for the infant intestinal cells to acquire all the adult characteristics. In some cases, this developmental process of intestinal maturation is affected, which can leave long-lasting consequences for health. One of the factors known to affect intestinal postnatal development is antibiotics. Antibiotics are the most common drug prescribed to infants and children. However, the use of antibiotics has been associated with an increased incidence of later-life diseases. This thesis demonstrates that mouse intestinal fetal organoids can be used as an in vitro model to study the influence of external factors on intestinal epithelial maturation. Further, it reveals that antibiotic treatment in early life accelerates the maturation of the mouse intestinal epithelium, induces the differentiation of enteroendocrine cells, and reduces the metabolic capacity of mouse fetal intestinal organoids. Besides, this work demonstrates that some of the effects result from the direct action of antibiotics on the immature intestinal epithelial cells, independently of the antibiotics-induced effects on the gut microbiome or other intestinal cell types. Additionally, this thesis shows that antibiotic treatment in early life has long-term effects on gut functioning and may even contribute to the onset of diseases later in life. The next steps should determine the mechanism behind these effects and study whether human milk oligosaccharides, pre-, pro-, or synbiotics are able to limit or even prevent the detrimental short- and long-term effects of antibiotics.