Effect of a cell preparation ofEnterococcus faecalisstrain EC-12 on digesta flow and recovery from constipation in a pig model and human subjects

Abstract

The effects of a cell preparation of Enterococcus faecalis strain EC-12 (EC-12) on the digesta flow in a pig model and its oral administration to humans were examined for its effect on frequency of defecation and faecal consistency. Latin square model was used in the pig study. Three sows fistulated at the caecum were fed a diet supplemented with either EC-12 or yeast cell wall (10 mg/kg body weight per day) for 9 days. An untreated control (C) was also obtained. Four markers (two were liquid and others solid markers) were used to determine the transit time of the liquid and solid phases of digesta in the gastrointestinal tract. The use of a dual marker system was for the better understanding of the digesta kinetics. YbCl 3 and Co-EDTA were given with a morning meal, and CeCl 3 and Eu-EDTA were given with a night meal on day 8. Caecal digesta were sampled every 2 h for 48 h after morning dosing. The total bioavailabilities of the liquid markers were lower in the EC-12 group than in the C group (Co-EDTA, 72%; Eu-EDTA, 63%). The relative concentrations of chloride to the liquid markers were higher in the EC-12 group than in other groups. Eleven volunteers ingested EC-12 (600 mg/day) for 30 days. EC-12 administration increased the frequency of defecation on day 30 in comparison with day 0. EC-12 stimulates the inflammatory reactions that relate ion and water secretion from the intestine. Accordingly, EC-12 may aid in the recovery from constipation through an acceleration of the liquid digesta flow in the large intestine.

Stimulation of Indigenous Lactobacilli by Fermented Milk Prepared with Probiotic Bacterium, Lactobacillus delbrueckii subsp. bulgaricus Strain 2038, in the Pigs

“…However, the relationship between probiotic lactobacilli and intestinal indigenous lactobacilli is very complex; we must consider not only bacterial ecology but also physiological responses of the intestine, such as absorption and secretion, digesta kinetics and retention time. Digesta kinetics is modified by fermented milk (23) and the cell component of LAB (27). The modification of digesta retention time should affect the bacterial composition, then the fermentation pattern (28).…”

Evaluation of the Low Dose Level of a Heat-Killed and Dried Cell Preparation of Enterococcus faecalis to Prevent Porcine Edema Disease Using Experimental Infection Model with Enterotoxcemic Escherichia coli in Weaning Pigs

“…In this study, the lower dose levels (0.005% and 0.01%) of EC-12 did not prevent ED. Presently used EC-12 had a high cell pellet density of at least 5 trillion cells/g [15]. Therefore, the diet offered to pigs of E-0.05 group contained 2.5 × 10 9 E. faecalis EC-12 cells/g diet.…”

Oral Administration of a Heat-Killed Cell Preparation ofEnterococcus faecalisStrain EC-12 Stimulates the Gene Expression of Na+–K+–2Cl−Co-Transporter 1 in Rat Ileal Epithelial Cells

“…Stimulation of the NKCC1 gene was only achieved by a high dose of EC-12 which was 10-fold more concentrated than the normal dose. 5) Thus, the ability of EC-12 to induce inflammation or chloride secretion from IEC should be quite moderate compared to that of pathogens. This non-excess effect of EC-12 on chloride secretion from IEC could be beneficial for treating constipation because decreased chloride secretion activity is considered to be a cause of constipation.…”

“…This non-excess effect of EC-12 on chloride secretion from IEC could be beneficial for treating constipation because decreased chloride secretion activity is considered to be a cause of constipation. 17) In fact, Tsukahara et al 5) have demonstrated in human subjects that the administration of EC-12 was effective for improving constipation. Considering that the human subjects took a normal dose of EC-12 for 30 days by Tsukahara et al, it is implied that long-term administration of EC-12 may stimulate NKCC1 expression even with a normal dose.…”

“…5) Secondly, EC-12 interacted with immune cells and stimulated the production of inflammatory cytokines in the mouse intestine. 6) Thirdly, non-pathogenic Enterococcus faecalis stimulated RelA phosphorylation and thus NF-B activation in mouse IEC both in vivo and in vitro.…”