Orientia tsutsugamushi, a gram-negative bacterium, causes severe acute febrile illness in humans. Despite this danger, the route of infection, infectivity, and protective mechanisms of the host's immune response to O. tsutsugamushi are unclear. Dendritic cells (DCs) are one of the most important cell types in bridging the innate and adaptive immune responses. In this study, we observed that O. tsutsugamushi infects and replicates in monocyte-derived DCs (MODCs). During infection and replication, the expressions of the cytokines IL-12 and TNF-α, as well as the co-stimulatory molecules CD80, CD83, CD86, and CD40, were increased in MODCs. When O. tsutsugamushi-treated MODCs were co-cultured with autologous CD4(+) T cells, they enhanced production of IFN-γ, a major Th1 cytokine. Collectively, our results show that O. tsutsugamushi can replicate in MODCs and can simultaneously induce MODC maturation and increase proinflammatory cytokine levels in MODCs that subsequently activate CD4(+) T cells.

Some lactic acid bacteria (LAB) and their cellular components have antiobesity effects. In this study, we evaluated the antiadipogenic effects of a mixture of two LAB-Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032-using 3T3-L1 preadipocytes and HepG2 hepatocarcinoma cells. 3T3-L1 cells treated with a 1:1 ratio of HY7601 and KY1032 during differentiation showed reduced lipid accumulation by Oil Red O staining, as well as decreased leptin secretion and mRNA expression of peroxisome proliferator-activated receptor-γ and CCAAT/enhancer binding protein-α. HY7601 and KY1032 treatment also suppressed mitochondrial biogenesis and inhibited the expression of genes encoding mitochondrial transcription factors, as well as those related to fatty acid synthesis in HepG2 cells. The antiadipogenic effects of LAB were associated with the cell membrane fraction. These results demonstrate that a mixture of two LAB (HY7601 and KY1032) inhibits adipogenesis in preadipocytes and liver cells and is a potential therapeutic strategy for the treatment of obesity.

Obesity is a major health issue worldwide, and is associated with many diseases including type 2 diabetes. In this study, we evaluated the anti-obesity effects of combinations of two lactic acid bacteria (LAB), Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032, and Cinnamomi Ramulus (CR) extract, and explored the mechanism through which they modulate gut microbiota using diet-induced obese mice. Male C57BL/6J mice were randomly divided into five groups that received a high-fat diet (HFD), HFD and LAB (HFD+LAB), HFD and CR extract (HFD+CR), HFD with LAB and CR extract (HFD+LAB+CR), or normal diet for 10 weeks. The mice in the HFD+LAB+CR group showed significant reductions in body weight gain, in particular epididymal fat and liver, blood leptin levels, and an increase in the levels of blood adiponectin. In addition, the LAB and CR extract altered the gut microbiota, mainly increasing the alpha diversity. These results demonstrate that a mixture of two LAB (Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032) and CR extracts alleviate HFD-induced obesity, and has potential of being used as a strategy for the treatment of obesity.

In addition to intestinal balance, probiotics are known to have beneficial effects on skin inflammation, metabolic diseases, and emotions. Previously, we have reported the skin anti-aging effects of Lactobacillus plantarum HY7714 (HY7714) in a clinical trial. To prove the protective skin effects of HY7714 through the intestinal tight junction (TJ), we investigated the effects of HY7714 on the intestines through tumor necrosis factor (TNF)-α induced TJ defects in Caco-2 cells. Specifically, 24 h treatment with HY7714 restored the decreased expression of zonula occludens-1, occludin, and claudin-1 compared to the TNF-α-treated groups (P<0.05). It also attenuated the level of pro-inflammatory cytokines interleukin-6, 8, and 1β. Further, increases in the mRNA levels of Elk-1, nuclear factor-κB, and myosin light chain kinase expression induced by TNF-α were recovered by HY7714. These findings imply that HY7714 improves intestinal barrier integrity and is a potential therapeutic agent for dysfunctions derived from TJ defects.