Effect of Lysinibacillus isolated from environment on probiotic properties and gut microbiota in mice.

Soil microorganisms (SM) are primarily involved in organism degradation, plant nitrogen nutrient immobilization, host microorganisms and oxidation. However, research on the effect of soil-derived Lysinibacillus on the intestinal microbiota spatial disparity of mice is lacking. To test the probiotic properties of Lysinibacillus and the spatial disparity on mice intestinal microorganisms, hemolysis test, molecular phylogenetic analysis, antibiotic sensitivity testing, serum biochemical assays and 16S rRNA profiling were applied. The results showed that Lysinibacillus (LZS1 and LZS2) was resistant to two common antibiotics, Tetracyclines and Rifampin, and sensitive to other antibiotics among the 12 antibiotics tested and negative for hemolysis. In addition, the body weight of group L (treatment of Lysinibacillus, 1.0 × 108 CFU/d for 21days) mice was significantly greater than that of the control group; serum biochemical tests showed that the TG and UREA were significantly lower in group L. The spatial disparity of intestinal microorganisms in mice was significant, treatment of Lysinibacillus (1.0 × 108 CFU/d for 21days) reduced the intestinal microbial diversity and decreased the richness of Proteobacteria, Cyanobacteria and Bacteroidetes in mice. Furthermore, Lysinibacillus treatment enhanced Lactobacillus and Lachnospiraceae richness and significantly reduced 6 bacterial genera in jejunum community, reduced 8 bacterial genera, but increased bacteria at the 4 genera level in cecum microorganisms. In conclusion, this study demonstrated spatial disparity of intestinal microorganisms in mice and probiotic potential of Lysinibacillus isolated from soil.

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.