Abstract
The gut microbiota is a bacterial bioreactor whose composition is an asset for human health. However, circulating gut microbiota derived endotoxins cause metabolic endotoxemia, promoting metabolic and liver diseases. This study investigates the potential of orally delivered microencapsulated Bifidobacterium infantis ATCC 15697 to modulate the gut microbiota and reduce endotoxemia in F344 rats. The rats were gavaged daily with saline or microencapsulated B. infantis ATCC 15697. Following 38 days of supplementation, the treated rats showed a significant (P < 0.05) increase in fecal Bifidobacteria (4.34 ± 0.46 versus 2.45 ± 0.25% of total) and B. infantis (0.28 ± 0.21 versus 0.52 ± 0.12 % of total) and a significant (P < 0.05) decrease in fecal Enterobacteriaceae (0.80 ± 0.45 versus 2.83 ± 0.63% of total) compared to the saline control. In addition, supplementation with the probiotic formulation reduced fecal (10.52 ± 0.18 versus 11.29 ± 0.16 EU/mg; P = 0.01) and serum (0.33 ± 0.015 versus 0.30 ± 0.015 EU/mL; P = 0.25) endotoxins. Thus, microencapsulated B. infantis ATCC 15697 modulates the gut microbiota and reduces colonic and serum endotoxins. Future preclinical studies should investigate the potential of the novel probiotic formulation in metabolic and liver diseases.
Highlights
The human gut microbiota forms a large ecosystem consisting of approximately 1014 bacterial cells, a number 10 times greater than the number of human body cells [1]
The effect of orally administered APA microencapsulated B. infantis ATCC 15697 on fecal bacteria was investigated after 38 days of daily supplementation (Figure 1)
Results showed that APA microencapsulated B. infantis ATCC 15697 significantly increased the abundance of bacterial populations that do not produce endotoxins
Summary
The human gut microbiota forms a large ecosystem consisting of approximately 1014 bacterial cells, a number 10 times greater than the number of human body cells [1]. Endotoxins are immunogenic molecules derived from the cell wall of Gram-negative bacteria that are produced in large quantities by the human gut microbiota [4]. Metabolic endotoxemia causes a mild and continuous induction of proinflammatory mediators, resulting in low-grade systemic inflammation [5,6,7]. This inflammatory state contributes to the progression of many human diseases, including obesity, type 2 diabetes, and liver, cardiovascular, and inflammatory bowel diseases [5,6,7]. The true incidence and prevalence of metabolic endotoxemia remain unknown, recent data suggests that
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