Previously, we isolated and examined a bacterial strain designated as TM-I-3, belonging to the genus Bacillus, from soil in Nagasaki, Japan. This bacterium was able to inhibit the growth of molds, without coming into direct contact with them. Non-contact antifungals are capable of providing multidirectional inhibition and may contribute to disease prevention. In this study, we revealed the bacteriological properties of TM-I-3 and evaluated the antifungal activity of the compounds emitted from this bacterium. In addition, we analyzed the antimicrobial substances released from TM-I-3 using GC/MS to elucidate the mechanism of its action. Antimicrobial compounds from strain TM-I-3 were identified as acetic acid, propanoic acid, isovaleric acid, 2-methylbutanoic acid, and benzaldehyde, which are all reported to have antimicrobial activity. TM-I-3 demonstrated possible efficacy in inhibiting the growth of Aspergillus fumigatus, Cladosporium cladosporioides and Penicillium expansum, which may lead to inhibition of common fungal contaminants of household products and prevention of some pulmonary diseases.

PS-B1 is a fermented product prepared from soybean milk using indigenous lactic acid bacteria of human origin. It has been demonstrated to possess liver-protective activities because of its antioxidant, anti-inflammatory, and antifibrotic properties in vitro, and improvement of dyslipidemia in vivo. This study evaluated the effects of PS-B1 on high-fat diet induced nonalcoholic steatohepatitis in a validated Stelic Animal Model (STAM™) for this condition. Mice were treated orally once daily for 4 weeks vehicle (control), PS-B1 (30g/kg), or PS-B1 (50g/kg). The results show that compared to the control group, liver weights and plasma triglyceride values tended to decrease in the high-dose PS-B1 group. Histopathological analysis performed by hematoxylin and eosin staining displayed a milder deposition of lipid droplets in the livers of mice in the high-dose PS-B1 group than in livers of the control group. These results suggest that compared with the control group, the PS-B1 administration induced a decreasing trend in nonalcoholic fatty liver disease activity score in the treated groups, accompanied by a decrease in liver weights and liver/plasma triglyceride levels, implying a potential anti-steatosis effect of PS-B1.

PS-B1 is a fermented product prepared from soy flour using lactic acid bacteria. Over a 10-week period, C57BL/6J mice were reared under laboratory conditions on a normal diet (control, n=5), high-fat diet (HF, n=5), or high-fat diet supplemented with 4% PS-B1 (HF-P, n=6). After 10 weeks, the change in weight gain, intestinal and epididymal fat accumulation, serum and liver biochemical parameters, and gene expression in the mice was investigated. HF diet-induced weight gain and increase in intestinal and epididymal fat accumulation were lower in mice fed with HF-P diet than in mice fed with HF diet, suggesting that PS-B1 prevented HF diet-induced obesity in HF-P mice. Furthermore, the levels of liver lipids (triglycerides, TG; non-esterified fatty acid, NEFA; total cholesterol, TC), serum TC, serum glucose, and serum insulin were significantly increased in the HF group than those in control mice. In HF-P mice, neither serum TC nor serum glucose levels were reduced. In contrast, the levels of liver lipids and serum insulin were lower in HF-P mice than in HF mice, suggesting that PS-B1 reduced these parameters in HF-P mice. The homeostatic model assessment of insulin resistance (HOMA-IR) value, which was calculated from the serum glucose and insulin levels, was 21.5 ± 4.2 in the HF mice. However, the HOMA-IR (8.2 ± 0.2) values were significantly decreased in the HF-P mice, suggesting that PS-B1 improves insulin resistance. Additionally, we compared the expression levels of stearoyl-CoA desaturase-1 (Scd1) in the liver. Quantitative RT-PCR showed increased expression of Scd1 in HF mice compared to that in control mice. Furthermore, ingestion of PS-B1 led to reduced expression of Scd1 mRNA in HF-P mice, implying that PS-B1 is effective in reducing the expression of the gene encoding SCD1. These results suggest that the anti-obesity effect of PS-B1 and improvement in fat accumulation upon PS-B1 uptake may be due to improvement in insulin resistance and reduction in the expression level of Scd1.