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Bee Venom Decreases LPS-Induced Inflammatory Responses in Bovine Mammary Epithelial Cells

  • Jeong, Chang Hee;Cheng, Wei Nee;Bae, Hyojin;Lee, Kyung Woo;Han, Sang Mi;Petriello, Michael C.;Lee, Hong Gu;Seo, Han Geuk;Han, Sung Gu
    • Journal of Microbiology and Biotechnology
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    • v.27 no.10
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    • pp.1827-1836
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    • 2017
  • The world dairy industry has long been challenged by bovine mastitis, an inflammatory disease, which causes economic loss due to decreased milk production and quality. Attempts have been made to prevent or treat this disease with multiple approaches, primarily through increased abuse of antibiotics, but effective natural solutions remain elusive. Bee venom (BV) contains a variety of peptides (e.g., melittin) and shows multiple bioactivities, including prevention of inflammation. Thus, in the current study, it was hypothesized that BV can reduce inflammation in bovine mammary epithelial cells (MAC-T). To examine the hypothesis, cells were treated with LPS ($1{\mu}g/ml$) to induce an inflammatory response and the anti-inflammatory effects of BV (2.5 and $5{\mu}g/ml$) were investigated. The cellular mechanisms of BV against LPS-induced inflammation were also investigated. Results showed that BV can attenuate expression of an inflammatory protein, COX2, and pro-inflammatory cytokines such as IL-6 and TNF-${\alpha}$. Activation of NF-${\kappa}B$, an inflammatory transcription factor, was significantly downregulated by BV in cells treated with LPS, through dephosphorylation of ERK1/2. Moreover, pretreatment of cells with BV attenuated LPS-induced production of intracellular reactive oxygen species (e.g., superoxide anion). These results support our hypothesis that BV can decrease LPS-induced inflammatory responses in bovine mammary epithelial cells through inhibition of oxidative stress, NF-${\kappa}B$, ERK1/2, and COX-2 signaling.

Immunostimulatory effects of BCG-CWS on the proliferation and viability of mouse spleen cells (마우스 비장세포의 증식과 생존율에 대한 BCG-CWS의 면역자극 효과)

  • Lee, Che-Wook;Ko, Eun-Ju;Joo, Hong-Gu
    • Korean Journal of Veterinary Research
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    • v.52 no.2
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    • pp.89-97
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    • 2012
  • Mycobacterial cell-wall skeleton (CWS) is an immunoactive and biodegradable particulate adjuvant and has been tried to use for immunotherapy. The CWS of Mycobacterium bovis bacillus Calmette-Guerin (BCG-CWS) was studied as an universal vaccine vehicle for antigen conjugation, to develop potentially effective and safe vaccine. Although a variety of biological activities of BCG-CWS have been studied, the effects of BCG-CWS on spleen cells are not fully elucidated. Using MTT assay and trypan blue exclusion test, we found that BCG-CWS significantly enhanced the viability and proliferation of cells. Multiple clusters, indicating proliferation, were observed in BCG-CWS-treated spleen cells and surface marker staining assay revealed that BCG-CWS promoted the proliferation of $CD19^+$ B lymphocyte rather than $CD4^+$ or $CD8^+$ T lymphocyte. In addition, BCG-CWS up-regulated the expression of anti-apoptotic molecules such as bcl-2, bcl-xL. BCG-CWS increased the surface expression of CD25 and CD69 as well as IL-2 production of spleen cells, suggesting increased activation. Furthermore, BCG-CWS enhanced the antigen-specific cell proliferation and interferon-gamma production of spleen cells. Taken together, these results demonstrate the immunostimulatory effects of BCG-CWS on spleen cells via multiple mechanisms, providing valuable information to broaden the use of BCG-CWS in clinical and research settings.

The Two Faces of IL-18 in Tumor Immunology

  • Cho, Dae-Ho
    • Proceedings of the PSK Conference
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    • 2003.04a
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    • pp.80-81
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    • 2003
  • IL-18 has been found to have multiple effects upon various cells involved in tumor immunology. Here, we discuss opposite effects of IL-18 in tumor immunology. IL-18 has been shown that it has significant anti-tumor effects, which are mediated by T cells and NK cells, in a manner similar to IL-12. First, we investigated the evaluation of the effects of the systemic administration of IL-18 in combination with B7-1 (CD80) against murine B16 melanoma in vivo. (omitted)

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Soybean Peptides Induce Apoptosis in HeLa Cells by Increasing Oxidative Stress

  • Sung, Ho Joong;Jeong, Yu Jin;Kim, Jihyun;Jung, Eunsun;Jun, Jin Hyun
    • Biomedical Science Letters
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    • v.21 no.2
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    • pp.77-83
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    • 2015
  • Soy proteins have been extensively studied because of its multiple health benefits. However, the effects of soy proteins on human cervical cancer cells are still unclear. Therefore, this study investigated the effects of soy proteins on HeLa cells and human fibroblasts by using soybean peptides (SPs). SPs selectively increased the generation of reactive oxygen species and apoptosis in HeLa cells but not in fibroblasts. In addition, SPs suppressed the migration of HeLa cells. Although the molecular mechanisms underlying the effects of SPs on human cervical cancer cells need to be investigated further, our findings provide insights on the therapeutic effects of soy protein on cervical cancer.

Polyamines in Multi-drug Resistant Cancer Cells (다제 내성 암세포에서의 Polyamine 특성)

  • 권혁영;이종호;이동권
    • Biomolecules & Therapeutics
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    • v.5 no.3
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    • pp.265-271
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    • 1997
  • Since the advent of chemotherapy, certain types of cancer have been particularly resistant to chemotherapeutic treatment. One of the most well-studied types of resistance is resistance to multiple struc-turally dissimialr hydrophobic chemotherapeutic agents, or multidrug resistance (MDR). We found that MDR cells (KBV20C, KB7D) being highly resistant to colchicine, etoposide, and vincristine were found to have very low level of putrescine and low level of spermidine than the drug sensitive parental cells (KB) but they had almost same level of spermine as the drug sensitive cells. Although both MDR and drug sensitive cells had almost same rate of polyamine uptake, MDR cells were much more sensitive to an inhibitor of polyamine synthesis, methylglyoxal-bis guanylhydrazone (MGBG), suggesting that MDR cells might be defective in polyamine synthesis. These results also suggest that HGBG can be used for treatment of MDR in vivo.

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Heteroface AlGaAs/GaAs Solar Cells grown by MBE (MBE에 의해 성장된 Heteroface AlGaAs/GaAs 태양전지)

  • 장호성;임성규
    • Journal of the Korean Institute of Telematics and Electronics
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    • v.27 no.1
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    • pp.46-50
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    • 1990
  • Heteroface AlGaAs/GaAs drift solar cells with an active area conversion efficiency of 15.9% under one sun and AM 1.5 condition have been grown by molecular beam epitaxy(MBE). These drift solar cells have graded doping profiles in the base and emitter regions. The cells have a short circuit current density (Jsc) of 19.00 mA/cm\ulcorner an open circuit voltage(Voc) of 0.93 V, and f fill factor(FF) of 0.78, respectively. Conventional solar cells with fixed doping profiles were also grown by MBE for comparison with the drift solar cells. Even though the fabrication cost of MBE grown solar cell is higher, the expected highest conversion efficiency of the single or multiple cells could compensate for the increased cost, particularly in case of space applications.

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Regulation of Intestinal Immune System by Dendritic Cells

  • Ko, Hyun-Jeong;Chang, Sun-Young
    • IMMUNE NETWORK
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    • v.15 no.1
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    • pp.1-8
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    • 2015
  • Innate immune cells survey antigenic materials beneath our body surfaces and provide a front-line response to internal and external danger signals. Dendritic cells (DCs), a subset of innate immune cells, are critical sentinels that perform multiple roles in immune responses, from acting as principal modulators to priming an adaptive immune response through antigen-specific signaling. In the gut, DCs meet exogenous, non-harmful food antigens as well as vast commensal microbes under steady-state conditions. In other instances, they must combat pathogenic microbes to prevent infections. In this review, we focus on the function of intestinal DCs in maintaining intestinal immune homeostasis. Specifically, we describe how intestinal DCs affect IgA production from B cells and influence the generation of unique subsets of T cell.

Effects of Photobiomodulation on Stem Cells Important for Regenerative Medicine

  • Chang, So-Young;Carpena, Nathaniel T.;Kang, Bong Jin;Lee, Min Young
    • Medical Lasers
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    • v.9 no.2
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    • pp.134-141
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    • 2020
  • The use of stem cell therapy to treat various diseases has become a promising approach. The ability of stem cells to self-renew and differentiate can contribute significantly to the success of regenerative medical treatments. In line with these expectations, there is a great need for an efficient research methodology to differentiate stem cells into their specific targets. Photobiomodulation (PBM), formerly known as low-level laser therapy (LLLT), is a relatively non-invasive technique that has a therapeutic effect on damaged tissue or cells. Recent advances in adapting PBM to stem cell therapy showed that stem cells and progenitor cells respond favorably to light. PBM stimulates different types of stem cells to enhance their migration, proliferation, and differentiation in vitro and in vivo. This review summarizes the effects of PBM on targeted differentiation across multiple stem cell lineages. The analytical expertise gained can help better understand the current state and the latest findings in PBM and stem cell therapy.

The Role of CD4 T Cell Help in CD8 T Cell Differentiation and Function During Chronic Infection and Cancer

  • Paytsar Topchyan;Siying Lin;Weiguo Cui
    • IMMUNE NETWORK
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    • v.23 no.5
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    • pp.41.1-41.21
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    • 2023
  • CD4 and CD8 T cells are key players in the immune response against both pathogenic infections and cancer. CD4 T cells provide help to CD8 T cells via multiple mechanisms, including licensing dendritic cells (DCs), co-stimulation, and cytokine production. During acute infection and vaccination, CD4 T cell help is important for the development of CD8 T cell memory. However, during chronic viral infection and cancer, CD4 helper T cells are critical for the sustained effector CD8 T cell response, through a variety of mechanisms. In this review, we focus on T cell responses in conditions of chronic Ag stimulation, such as chronic viral infection and cancer. In particular, we address the significant role of CD4 T cell help in promoting effector CD8 T cell responses, emerging techniques that can be utilized to further our understanding of how these interactions may take place in the context of tertiary lymphoid structures, and how this key information can be harnessed for therapeutic utility against cancer.

Nerve Growth Factor Activates Brain-derived Neurotrophic Factor Promoter IV via Extracellular Signal-regulated Protein Kinase 1/2 in PC12 Cells

  • Park, So Yun;Lee, Ji Yun;Choi, Jun Young;Park, Mae Ja;Kim, Dong Sun
    • Molecules and Cells
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    • v.21 no.2
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    • pp.237-243
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    • 2006
  • Brain-derived neurotrophic factor (BDNF) is a neuromodulator of nociceptive responses in the dorsal root ganglia (DRG) and spinal cord. BDNF synthesis increases in response to nerve growth factor (NGF) in trkA-expressing small and medium-sized DRG neurons after inflammation. Previously we demonstrated differential activation of multiple BDNF promoters in the DRG following peripheral nerve injury and inflammation. Using reporter constructs containing individual promoter regions, we investigated the effect of NGF on the multiple BDNF promoters, and the signaling pathway by which NGF activates these promoters in PC12 cells. Although all the promoters were activated 2.4-7.1-fold by NGF treatment, promoter IV gave the greatest induction. The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, phosphatidylinositol 3-kinase (PI-3K) inhibitor, LY294003, protein kinase A (PKA) inhibitor, H89, and protein kinase C (PKC) inhibitor, chelerythrine, had no effect on activation of promoter IV by NGF. However, activation was completely abolished by the MAPK kinase (MEK) inhibitors, U0126 and PD98059. In addition, these inhibitors blocked NGF-induced phosphorylation of extracellular signal-regulated protein kinase (ERK) 1/2. Taken together, these results suggest that the ERK1/2 pathway activates BDNF promoter IV in response to NGF independently of NGF-activated signaling pathways involving PKA and PKC.