Vancomycin and ceftriaxone can damage intestinal microbiota and affect the development of the intestinal tract and immune system to different degrees in neonatal mice.

Abstract

This study aimed to determine how antibiotic-driven intestinal dysbiosis impairs the development and differentiation of the digestive tract and immune organs of host animals. BALB/C neonatal mice were orally administered ceftriaxone or vancomycin from postnatal day 1 to day 21 and sacrificed on day 21. The diversity and abundance of the intestinal bacteria, morphological changes and barrier function of intestinal tract, and the splenic CD4+CD25+Foxp3+ T cells were investigated. The gut microbiota and intestinal tissue were damaged, and the numbers of Ki67-, Muc2- and ZO-1-positive cells were significantly decreased in the antibiotic treatment groups. Furthermore, the administration of ceftriaxone, but not vancomycin, led to a significant reduction in the abundance of splenic CD4+CD25+Foxp3+ T cells. Each antibiotic caused intestinal dysbiosis and characteristically influenced the regeneration of intestinal epithelial cells, formation of the intestinal mucus layer and tight junctions, and differentiation of splenic Foxp3+ Treg cells of the neonatal mice before any clinical side effects were observed. The potent ability of each antibiotic to affect the makeup of intestinal commensal microbiota may be a key determinant of the spectrum of antibiotics and influence the health of the host animal, at leastpartly.