Evaluation of the heat-killed and dried cell preparation of Enterococcus faecalis against villous atrophy in early-weaned mice and pigs.

Early weaning induces villous atrophy in the small intestine (SI) of piglets. Oral administration of live lactic acid bacteria (LAB) can improve villous shortening. In this study, we evaluated the oral administration of a heat-killed and dried cell preparation of Enterococcus faecalis (a LAB) strain EC-12 against villous atrophy in early-weaned mice (Experiment 1) and pigs (Experiments 2 and 3). Twelve 16-days-old mice were divided into two groups in Experiment 1: gavage of EC-12 (10 mg/kg body weight (BW)/day), or control. On day 21, SI was collected. Eighteen 21-day-old pigs were divided into two groups in Experiment 2: gavage of EC-12 (10 mg/kg BW/day), or control. After 10 days, the villous height of jejunum was measured. Six 21-day-old pigs were divided into two groups in Experiment 3: the basal diet supplemented with EC-12 at 0.05%-fed group, or the basal diet-fed group. After 10 days, the villous height of jejunum was measured. The villous heights in SI were significantly higher by EC-12 administration in all experiments. EC-12 successfully improved the villous atrophy in the early-weaned mice and pigs when EC-12 was administered orally.

A cell preparation of Enterococcus faecalis strain EC-12 stimulates the luminal immunoglobulin A secretion in juvenile calves.

The immune system in juvenile calves is immature, so calves are susceptible to several diarrheal and respiratory diseases. Oral administration of lactic acid bacteria (LAB) is known to improve the growth performance and prevent diarrheal and respiratory diseases by stimulating the immune system in juvenile calves. Most of the immunostimulation by LAB is achieved by their cell wall components, and therefore we evaluated the immunostimulation of the cell preparation of Enterococcus faecalis strain EC-12 (EC-12) in juvenile calves in a clinical field. Twenty-nine 1-week old calves were used. Fourteen calves were administered 0.2% (w/w) of an EC-12 preparation that supplemented a milk replacer, and other calves were not supplemented. Feces and serum was collected at day 0, 7 and 49 after the administration to measure the IgA and IgG concentration. The fecal IgA concentration was increased by EC-12 administration at day 49, and the serum IgA concentration was also increased at day 7. These results suggested that oral administration of EC-12 in juvenile calves might have an immunostimulatory effect and provide earlier recovery of IgA levels in mucosal immunity.

Voluntary running exercise alters microbiota composition and increases n-butyrate concentration in the rat cecum.

The effects of voluntary wheel-running exercise on cecal microbiota and short-chain fatty acid production were investigated in rats. The microbiota composition was notably different between the exercised and sedentary rats. Furthermore, the exercised rats showed a significantly higher n-butyrate concentration than the sedentary rats. This alteration of the cecal microbial environment may contribute to the beneficial effect of exercise on gastrointestinal disorders.

Oral administration of a heat-killed cell preparation of Enterococcus faecalis strain EC-12 stimulates the gene expression of Na(+)-K(+)-2Cl- co-transporter 1 in rat ileal epithelial cells.

The effect of a heat-killed cell preparation of Enterococcus faecalis strain EC-12 (EC-12) on the gene expression of Na(+)-K(+)-2Cl(-) co-transporter 1 (NKCC1) in intestinal epithelial cells was evaluated by using rats. The NKCC1 gene in ileal epithelial cells was significantly up-regulated by the oral administration of EC-12. The results of this study suggest in vivo that EC-12 had the potential to stimulate intestinal NKCC1 expression.

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.

Porcine edema disease (ED) is caused by Shiga toxin 2e-producing Escherichia coli (STEC). ED has become frequent in pig farms, and the use of antimicrobials has resulted in the development of antimicrobial-resistant STEC. Accordingly, the use of materials other than antimicrobials is requested for the prevention of ED. Oral administration of a heat-killed and dried cell preparation of Enterococcus faecalis strain EC-12 (EC-12) to weaning pigs was previously demonstrated to decrease animal mortality in a STEC-contaminated farm at 0.05% (w/w) dose level. In this study, pigs experimentally infected with STEC were used as a model for ED to evaluate the low dose level of EC-12 to prevent ED. Fifteen 21-day-old pigs were divided into 5 groups: STEC challenge with the basal diet, STEC challenge with EC-12 supplemented at 0.005, 0.01, or 0.05% (w/w) to the basal diet, and no STEC challenge with the basal diet. The challenge was carried out when the animals were 25, 26, and 27 days old using STEC contained in capsules resistant against gastric digestion. All pigs were euthanized at 32 days of age. The daily weight gain, feed conversion ratio, and palpebral edema were improved by supplementation with 0.05% EC-12, but not by the low dose levels. Accordingly, 0.05% level of supplementation was needed for EC-12 to improve clinical symptoms in weaning piglets infected by STEC.

Experimental infection of enterotoxemic Escherichia coli associated with porcine edema disease and its pathologic characteristics in the intestine.

Edema disease (ED) has become frequent in Japan, but no effective method for experimental infection has been developed. We report here the use of a capsule that resistant against gastric digestion to induce the ED in piglets. Four 21-day-old piglets were used. Shiga toxin 2e-producing Escherichia coli (STEC) cell pellet was encapsulated and administered orally. Two pigs received 1.0x10(10) CFU for two days, and the others received 3.9x10(8) CFU for three days. The high-dose group caused the typical clinical ED signs (palpebral edema or neurologic impairment). Eosinophil infiltration, swollen lymphoid follicles, and edema were observed in the ileum. The kidney had the thrombus in the glomerulus.