Choon-Soo Jeong

LIGHT/TNFSF14 enhances adipose tissue inflammatory responses through its interaction with HVEM

Obesity‐induced adipose tissue inflammation is characterized by increased macrophage infiltration and cytokine production, and is associated with metabolic disorders. LIGHT/TNFSF14, a member of the TNF superfamily, plays a role in the development of various inflammatory diseases. The purpose of this study was to examine the involvement of soluble LIGHT (sLIGHT) in obesity‐induced adipose tissue inflammatory responses. LIGHT gene expression on macrophages/adipocytes was upregulated by treatment with obesity‐related factors. sLIGHT displayed chemotactic activity for macrophages and T cells, and enhanced inflammatory cytokine release from macrophages, adipocytes, and adipose tissue‐derived SVF cells. The sLIGHT‐induced inflammatory responses were blunted by neutralizing anti‐HVEM antibody or knockout of HVEM, a receptor for sLIGHT. These findings indicate that sLIGHT enhances adipose tissue inflammatory responses through its interaction with HVEM.

HVEM-deficient mice fed a high-fat diet are protected from adipose tissue inflammation and glucose intolerance.

HVEM is a member of the TNF receptor superfamily that plays a role in the development of various inflammatory diseases. In this study, we show that HVEM deficiency attenuates adipose tissue inflammatory responses and glucose intolerance in diet‐induced obesity. Feeding a high‐fat diet (HFD) to HVEM‐deficient mice elicited a reduction in the number of macrophages and T cells infiltrated into adipose tissue. Proinflammatory cytokine levels in the adipose tissue decreased in HFD‐fed HVEM‐deficient mice, while levels of the anti‐inflammatory cytokine IL‐10 increased. Moreover, glucose intolerance and insulin sensitivity were markedly improved in the HFD‐fed HVEM‐deficient mice. These findings indicate that HVEM may be a useful target for combating obesity‐induced inflammatory responses and insulin resistance.

A lactic acid bacterium isolated from kimchi ameliorates intestinal inflammation in DSS-induced colitis

Some species of lactic acid bacteria have been shown to be beneficial in inflammatory bowel disease (IBD). In the present study, a strain of lactic acid bacterium (Lactobacillus paracasei LS2) was isolated from the Korean food, kimchi, and was shown to inhibit the development of experimental colitis induced by dextran sulfate sodium (DSS). To investigate the role of LS2 in IBD, mice were fed DSS in drinking water for seven days along with LS2 bacteria which were administered intragastrically to some of the mice, while phosphate-buffered saline (PBS) was administered to others (the controls). The administration of LS2 reduced body weight loss and increased survival, and disease activity indexes (DAI) and histological scores indicated that the severity of colitis was significantly reduced. The production of inflammatory cytokines and myeloperoxidase (MPO) activity also decreased. Flow cytometry analysis showed that the number of Th1 (IFN-γ) population cells was significantly reduced in the LS2-administered mice compared with the controls. The administration of LS2 induced the increase of CD4+FOXP3+ Treg cells, which are responsible for IL-10. Numbers of macrophages (CD11b+ F4/80+), and neutrophils (CD11b+ Gr-1+) among lamina propria lymphocytes (LPL) were also reduced. These results indicate that LS2 has an anti-inflammatory effect and ameliorates DSS-induced colitis.

The bactericidal effect of an ionizer under low concentration of ozone

BackgroundSeveral mechanisms have been suggested for the bactericidal action of ionizers including electrical phenomena, effects of negative and positive ions and electrostatic repulsion. Negative and positive ions have indeed been shown to have bactericidal effects. In addition, since ozone is generated along with ions, these may contribute to the bacterial killing. In this study, we used a newly developed ionizer, which generates a relatively low concentration of ozone, to determine whether its effect on bacterial cells were due to ions or ozone, and, if ions, how the ions exerted their effects.ResultsThe effect of ions on bacterial killing was compared with that of the ozone produced using an ion trap to remove the ions. The ionizer had the ability to kill the bacteria, and ion capture dramatically reduced its bactericidal effect, indicating that the ozone generated had little or no bactericidal effect under these conditions, and the ions produced were responsible for almost all the bacterial killing. Operation of the ionizer increased the level of 8-oxo-dG, a marker of oxidative DNA damage, and decreased aconitase activity, which is known to be sensitive to ROS. The ionizer further affected the adenylate energy charge of bacterial cells. Removal of the ions with the ion trap greatly reduced all these effects.ConclusionThese results indicate that negative and positive ions generated by the ionizer are responsible for inducing oxidative stress and so reducing bacterial survival.