Aims:  Atopic dermatitis (AD) is marked by elevated levels of immunoglobulin E and skin lesions such as oedema and haemorrhage. Kimchi is a Korean fermented food that contains beneficial bacteria for human health. In this study, Lactobacillus plantarum CJLP55, CJLP56, CJLP133 and CJLP136 isolated from Kimchi were investigated for their capacity to inhibit AD. Methods and Results:  The three strains, CJLP55, CJLP133 and CJLP136, suppressed AD‐like skin lesions, high serum IgE levels and epidermal thickening. The three strains diminished the accumulation of eosinophils and mast cells into topical inflammatory sites and the enlargement of axillary lymph nodes, which are responsible for the dorsal dermatitis. CJLP55, CJLP133 and CJLP136 decreased production of type 2 cytokines such as IL‐4 and IL‐5 in lymph node cell culture. CJLP133 and CJLP136 increased IFN‐γ secretion, while CJLP55 enhanced IL‐10 production. Conclusions:  The three strains isolated from Kimchi suppress house‐dust mite‐induced dermatitis in NC/Nga mouse, a representative animal model of human AD. Significance and Impact of the Study:  These findings suggest that lactobacilli isolated from Kimchi inhibit AD, probably by altering the balance of Th1/Th2 ratio or inducing IL‐10 production.

Allergic reactions including asthma and atopy are caused by predominance of Th2 response over Th1 response. Lactobacilli isolated from fermented foods such as yogurt, cheese, and Kimchi showed health-promoting activities. The present study indicated that several lactobacilli strains from Kimchi may reduce allergic reactions through macrophage-mediated induction of Th1 response.

Peroxiredoxin is a well-studied antioxidant enzyme. Enzymes in this category eliminate ROS in order to protect cells from oxidative stresses. PRX-1 exerts a protective antioxidant role in cells through its peroxidase activity, reCorrespondence Kwang Woo Hwang, Laboratory of Host Defense Modulation, College of Pharmacy, Chung-Ang University, 221 Heukseok-dong, Dongjakgu, Seoul, Korea. Tel: +82 2 820 5597; Fax: +82 2 823 5597; e-mail: khwang@cau.ac.kr List of Abbreviations: DMEM, Dulbecco's modified Eagle's medium; dNTP, deoxyribonucleotide triphosphate; FACS, fluorescence-activated cell sorting; GFP, green fluorescent protein; IL, interleukin; IκBα, nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha; iNOS, inducible nitric acid synthase; LPS, lipopolysaccharide; NF-κB , nuclear factor kappa-light-chain-enhancer of activated B cells; NK, natural killer; PMA, phorbol 12-myristate 13-acetate; PRX, peroxiredoxin; ROS, reactive oxygen species; shPRX-1, shRNA lentiviral vector targeting peroxiredoxin-1; STAT, signal transducers and activators of transcription; TNF, tumor necrosis factor. ducing H 2 O 2 , peroxynitrite, and a wide range of organic hydroperoxides for detoxification (1).The mammalian PRX family can be classified into six distinct groups (types I through VI). Other,

-T-cell activation depends on signals received by the T-cell receptor and CD28 co-stimulatory receptor. Since B7.1 and B7.2 molecules expressed on the surface of antigen presenting cells provide co-stimulatory signals through CD28 to T-cells, an inhibitor of CD28-B7.1/B7.2 binding has been proposed as a therapeutic agent for suppression of excessive T-cell activity. Although anti-B7.1/B7.2 antibodies are known to block B7.1 and B7.2 molecules, their effects on intracellular events in antigen presenting cells remain unclear. In this study, anti-B7.1/B7.2 antibodies decreased secretion of nitric oxide and pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-12 in LPS-activated RAW264.7 macrophage-like cells and peritoneal macrophages. Moreover, anti-B7.1/B7.2 antibodies inhibited IκBα phosphorylation and down-regulated expression of co-stimulatory molecules including B7.1, B7.2, and PD-L1 in LPS-stimulated peritoneal macrophages. These findings suggest that CTLA4-Ig and anti-B7.1/B7.2 antibodies may be candidates to treat chronic inflammatory diseases and autoimmune responses caused by excessive activation of both T-cells and macrophages.

Pancreatic β-cells play a crucial role in glucose homeostasis, and the failure of these cells to function results in the development of type 1 diabetes (T1D). The MIN6 cell line, which closely resembles pancreatic β-cells, was used to unravel the relationship between pancreatic β-cell function and the antioxidant enzyme PRX-1. PRX-1 was knocked down in MIN6 cells using a shPRX-1 lentiviral construct, and a mixture of inflammatory cytokines was administered to challenge the MIN6 cells. Nitric oxide (NO) production and inducible NO synthase (iNOS) expression were elevated in shPRX-1 compared with the control. Also, shPRX-1 transduced cells showed higher levels of NF-κB nuclear translocation, suggesting that PRX-1 has a regulatory role in NF-κB nuclear translocation and iNOS expression. In correlation with NO levels, decreased anti-apoptotic gene Bcl-xl level and elevated pro-apoptotic gene Bim levels were observed in shPRX-1 cells compared with scramble, and cell viability decreased accordingly. A rescue experiment was performed subsequently using an iNOS inhibitor to confirm NO as the cause of cell death. Overall, the results of this study suggest possible protective roles of the antioxidant enzyme PRX-1 in the insulinoma cell line MIN6 and possibly in pancreatic β-cells under T1D conditions.