Anti-inflammatory effects of the genus Bifidobacterium on macrophages by modification of phospho-I kappaB and SOCS gene expression.

Although beneficial roles of probiotics for inflammatory bowel diseases have been reported, their direct action on immune cells has not been elucidated. In this study, we investigated how three species of Bifidobacterium and Enterococcus faecalis differentially modulate production of cytokines from lipopolysaccharide (LPS)-stimulated macrophages in vitro using RAW264.7 cells. The mRNA levels of proinflammatory cytokines were remarkably increased after exposure to LPS, E. faecalis alone and LPS combined with E. faecalis. In contrast, IL-10 mRNA levels were significantly decreased after exposure to E. faecalis compared with exposure to Bifidobacterium species. When cells were exposed to Bifidobacterium species combined with LPS, mRNA levels of IL12p40 were decreased by co-culture with B. breve and B. longum, IL-1 beta mRNA levels were decreased by B. breve and B. adorescentis and TNF-alpha mRNA levels were decreased by B. adolescentis compared with LPS alone. The three species of Bifidobacterium significantly inhibited phosphorylation of I kappaB-alpha induced by LPS. The mRNA levels of SOCS1 and SOCS3 were increased by exposure to LPS alone; however, the mRNA levels of SOCS1 or SOCS3 were increased more by exposure to Bifidobacterium species combined with LPS. Conversely, E. faecalis combined with LPS induced significantly lower levels of SOCS mRNA than those induced by Bifidobacterium species combined with LPS. These results indicated that certain species of genus Bifidobacterium could negatively modulate mRNA levels of proinflammatory cytokines produced from LPS-stimulated RAW264.7 cells, which is possibly related to inhibition of I kappaB-alpha phosphorylation and stimulation of SOCS signalling.