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.
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