In this study, Lactobacillus paracasei subsp. paracasei NTU101 and Lactobacillus plantarum NTU 102 were used as starter to ferment soy-skim milk, and the optimal mixing ratio was evaluated. The influence of lactic acid bacteria (LAB)-fermented soy-skim milk on mucosal integrity in a gastric mucosal lesion rat model was also investigated. After 24 h, cell densities of L. paracasei subsp. paracasei NTU 101 and L. plantarum NTU 102 fermented in 75% soy milk and 25% milk (optimal condition) were 1.2 × 10(9) and 2.5 × 10(9) CFU/mL. After 180 days at 4 °C, the cell densities of the freeze-dried powders of the fermented soy-skim milks were 1 × 10(9) CFU/g; slight variations in pH and acidity were observed. Pylorus ligation with acidified ethanol treatment was used as the gastric lesion animal model. LAB-fermented soy-skim milk reduced the gastric lesion index and the lipid peroxides (LPO) of gastric mucosa and serum. Administration of the fermented soy-skim milk enhanced superoxide dismutase (SOD) activity and prostaglandin E(2) (PGE(2)) synthesis. Therefore, LAB-fermented soy-skim milk at 10(9) CFU/day protects against gastric injury.
To elucidate the immunomodulation effects of dead lactobacilli, whole cells and gastrointestinal enzymatic hydrolysates of supernatants and precipitates from Lactobacillus paracasei subsp. paracasei NTU 101 and L. plantarum NTU 102 on RAW264.7 macrophages and splenocytes were investigated. Increased NO, COX-2 expression, IL-10 and IL-12 were observed in high-dose precipitates and whole cells of both strains after 24-h stimulation. All of the hydrolysates and whole cells from both strains induced lower pro-inflammatory cytokines (IL-1b and IL-6) than LPS. The supernatants activated cell division to the S phase or promoted advance to the G2/M phase. Regardless of the Lactobacillus strains, higher levels of TNF-a, IL-6, IL-10 and IL-12 in splenocytes were induced by the precipitates. Supernatant of NTU 101 increased the amounts of IFN-g than precipitate in splenocytes. It shows that hydrolysates of NTU 101 induce the proliferations of macrophage and splenocyte and the release of IL-10 and IL-12 cytokines to modulate the innate and adaptive immune systems and inflammatory response.
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