Lactobacillus brevis OK56 ameliorates high-fat diet-induced obesity in mice by inhibiting NF-κB activation and gut microbial LPS production

• Lactobacillus brevis OK56 inhibited NF-κB activation in LPS-stimulated macrophages.
• OK56 suppressed high-fat diet-induced body and epididymal fat weight gains in mice.
• OK56 inhibited the expression of macrophage infiltration markers in adipose tissues.
• OK56 suppressed HFD-induced bifidobacteria reduction and LPS production.
• OK56 ameliorated HFD-induced NF-κB activation in the colon.

The anti-obesity effects of anti-inflammatory probiotics, isolated Lactobacillus brevis OK56 from the kimchi lactic acid bacteria collection, were examined and its effects on high-fat diet (HFD)-induced obesity (DIO) mice were evaluated. OK56 strongly inhibited NF-κB activation and TNF-α, IL-1β, and IL-6 expression in lipopolysaccharide (LPS)-stimulated macrophages. Oral administration of OK56 (1 × 109 CFU/mouse) suppressed the HFD-induced increase in body and epididymal fat weight gains (by 28 and 31%, respectively), as well as plasmatic atherogenic index, and LPS level. Real-time PCR analysis revealed that OK56 also inhibited HFD-induced expression of F4/80, CD68, CD204, TNF-α, and IL-1β in the adipose tissue of DIO mice. OK56 abrogated the HFD-induced disturbance to gut microbiota, such as the reduction in the number of bifidobacteria, the increase in the colonic fluid LPS, and the increase in the breath H2 levels. OK56 also inhibited HFD-induced expression of inducible NO synthetase (iNOS) and cyclooxygenase (COX)-2 and the activation of nuclear factor (NF)-κB in the colon. Furthermore, OK56 inhibited HFD-reduced expression of tight junction proteins ZO-1, occludin and claudin-1. These results suggest that OK56 has anti-obesity, which exerts through the inhibition of gut microbiota LPS production, colonic NF-κB signaling pathway, and macrophage infiltration into the adipose tissue.