Bacillus Licheniformis Reverses the Environmental Ceftriaxone Sodium-Induced Gut Microbial Dysbiosis and Intestinal Inflammation in Mice.

Antibiotics used as a common clinical treatment have saved many lives. Widespread use of antibiotic therapy has been known to disrupt the balance of pathogenic bacteria, host-associated microorganisms and environment. However, our understanding of Bacillus licheniformis for health benefits and ability to restore the ceftriaxone sodium-induced gut microbial dysbiosis is severely limited. We used Caco-2 cell, H&E (hematoxylin-eosin staining), RT-PCR and 16S rRNA sequencing techniques to investigate the influence of Bacillus licheniformis on gut microbial dysbiosis and inflammation following ceftriaxone sodium treatment. The results showed that treatment of ceftriaxone sodium in 7 days suppressed the expression of Nf-κB pathway mRNA levels, which caused cytoplasmic vacuolization in intestinal tissues, afterward, the administration of Bacillus licheniformis could effectively restore intestinal morphology and inflammation levels. Moreover, the ceftriaxone sodium treatment entirely affected the intestinal microbial ecology, leading to a decrease in microbial abundance. Firmicutes, Proteobacteria, and Epsilonbacteraeota were the most predominant phyla in each of the four groups. Specifically, the MA group (ceftriaxone sodium treatment) resulted in a significant decrease in the relative abundance of 2 bacterial phyla and 20 bacterial genera compared to the administration of Bacillus licheniformis after ceftriaxone sodium treatment. The supplementation of Bacillus licheniformis could increase the growth of Firmicutes and Lactobacillus and encourage the construction of a more mature and stable microbiome. Furthermore, Bacillus licheniformis could restore the intestinal microbiome disorders and inflammation levels following ceftriaxone sodium treatment.