• The Korean Journal of Physiology and Pharmacology
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• v.19 no.2
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• pp.183-189
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• 2015

Foeniculum vulgare Mill. (fennel) is used to flavor food, in cosmetics, as an antioxidant, and to treat microbial, diabetic and common inflammation. No study to date, however, has assessed the anti-inflammatory effects of fennel in experimental models of inflammation. The aims of this study were to investigate the anti-inflammatory effects of fennel in model of lipopolysaccharide (LPS)-induced acute lung injury. Mice were randomly assigned to seven groups (n=7~10). In five groups, the mice were intraperitoneally injected with 1% Tween 80-saline (vehicle), fennel (125, 250, $500{\mu}l/kg$), or dexamethasone (1 mg/kg), followed 1 h later by intratracheal instillation of LPS (1.5 mg/kg). In two groups, the mice were intraperitoneally injected with vehicle or fennel ($250{\mu}l/kg$), followed 1 h later by intratracheal instillation of sterile saline. Mice were sacrificed 4 h later, and bronchoalveolar lavage fluid (BALF) and lung tissues were obtained. Fennel significantly and dose-dependently reduced LDH activity and immune cell numbers in LPS treated mice. In addition fennel effectively suppressed the LPS-induced increases in the production of the inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, with $500{\mu}l/kg$ fennel showing maximal reduction. Fennel also significantly and dose-dependently reduced the activity of the proinflammatory mediator matrix metalloproteinase 9 and the immune modulator nitric oxide (NO). Assessments of the involvement of the MAPK signaling pathway showed that fennel significantly decreased the LPS-induced phosphorylation of ERK. Fennel effectively blocked the inflammatory processes induced by LPS, by regulating pro-inflammatory cytokine production, transcription factors, and NO.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.2
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• pp.83-88
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• 2015

CD4+CD25+ regulatory T cells (CD4+CD25+ Tregs) have been shown to play a regulatory or suppressive role in the immune response and are possibly relevant to the pathogenesis of autoimmune diseases. In the present study, we attempted to investigate the frequency of CD4+CD25+ Tregs in peripheral blood (PB) of collagen-induced arthritis (CIA) rats during the development of arthritis, to determine whether their frequency is involved in the immunoregulation of this disease. The results showed that normal rats had similar frequencies of CD4+CD25+ Tregs in PB during the experiment time, expressed as a percentage of CD4+CD25+Foxp3+ T cells among the CD4+ T lymphocyte population. In contrast, the frequency of CD4+CD25+Foxp3+ T cells in CIA rats was found to change during the development of arthritis. In CIA rats, there is a significant negative correlation between the frequency of CD4+CD25+Foxp3+ T cells and paw swelling (r=-0.786, p< 0.01). The relationship between the frequency of CD4+CD25+Foxp3+ T and immune activation was not found in normal rats. During the time course, the frequency of CD4+CD25+Foxp3+ T was lower in CIA rats than in normal ones. The data suggest that the frequency of PB CD4+CD25+ Tregs may be a promising marker for arthritis activity.

• The Korea Journal of Herbology
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• v.30 no.5
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• pp.67-74
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• 2015

Objectives : TheHaedokgumhwa-sanwater extract (HDKHS) is used in Korea, Japan and China as a traditional therapeutic agent to cure an infectious disease. But its study is not enough. Therefore, the present study focused on the elucidation of HDKHS to investigate the anti-inflammatory effects and to established the possible mechanisms involved in its action on LPS-stimulated immune response in murine macrophages.Methods : Inflammatory status was induced by LPS and measured by increasement of inflammatory mediators. LPS induced secretions of NO and PGE₂in RAW 264.7 cells were measured using griess reagent and enzyme-linked immunosorbent assay (ELISA) kit respectively. production of IL-6 was examined using ELISA kit and expression of IL-6 mRNA was measured by RT-PCR method. To investigate the effects of HDKHS on inflammatory mediators, such as iNOS, COX-2 and MAPKs, western blot and RT-PCR were performed.Results : HDKHS significantly reduced production of NO and PGE2 which were induced by LPS. Also, activation of IL-6 was reduced both protein and mRNA levels. The expressions of inflammatory mediator include iNOS and COX-2 were decreased by pretreatment with HDKHS. futhermore The result showed HDKHS down-regulate the LPS induced phosphorylation of ERK 1/2, one of the MAPK family, which is considered as a main regulator of transmission from pathogens to nucleus of immune cells.Conclusions : Our results suggest that the anti-inflammatory properties of HDKHS may stem from the inhibition of pro-inflammatory mediators via suppression of initiation of inflammatory response by inhibiting MAPKs signaling pathways.

• IMMUNE NETWORK
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• v.13 no.5
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• pp.205-212
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• 2013

Dectin-1, which specifically recognizes ${\beta}$-glucan of fungal cell walls, is a non-Toll-like receptor (TLR) pattern recognition receptor and a representative of C-type lectin receptors (CLRs). The importance of Dectin-1 in innate immune cells, such as dendritic cells and macrophages, has previously been well studied. However, the function of Dectin-1 in B cells is very poorly understood. To determine the role of Dectin-1 in B cell activation, we first investigated whether mouse B cells express Dectin-1 and then assessed the effect of Dectin-1 stimulation on B cell proliferation and antibody production. Mouse B cells express mRNAs encoding CLRs, including Dectin-1, and surface Dectin-1 was expressed in B cells of C57BL/6 rather than BALB/c strain. Dectin-1 agonists, heat-killed Candida albicans (HKCA) and heat-killed Saccharomyces cerevisiae (HKSC), alone induced B cell proliferation but not antibody production. Interestingly, HKSC, HKCA, and depleted zymosan (a selective Dectin-1 agonist) selectively enhanced LPS-driven IgG1 production. Taken together, these results suggest that, during fungal infection, ${\beta}$-glucan-stimulated Dectin-1 may cooperate with TLR4 to specifically enhance IgG1 production by mouse B cells.

• BMB Reports
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• v.43 no.4
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• pp.225-232
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• 2010

Parkinson's Disease (PD) is a common neurodegenerative disease characterized by the progressive degeneration of nigrostriatal dopaminergic (DA) neurons. Although the causative factors of PD remain elusive, many studies on PD animal models or humans suggest that glial activation along with neuroinflammatory processes contribute to the initiation or progression of PD. Additionally, several groups have proposed that dysfunction of the blood-brain barrier (BBB) combined with infiltration of peripheral immune cells play important roles in the degeneration of DA neurons. However, these neuroinflammatory events have only been investigated separately, and the issue of whether these phenomena are neuroprotective or neurotoxic remains controversial. We here review the current knowledge regarding the functions of these neuroinflammatory processes in the brain. Finally, we describe therapeutic strategies for the regulation of neuroinflammation with the goal of improving the symptoms of PD.

• BMB Reports
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• v.43 no.4
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• pp.250-256
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• 2010

Natural phosphodiester bond CpG-DNA that contains immunomodulatory CpG motifs (PO-DNA) upregulates the expression of proinflammatory cytokines and induces an Ag-driven Th1 response in a CG sequence-dependent manner in mice. In humans, only phosphorothioate backbone-modified CpG-DNA (PS-DNA) and not PO-DNA has immunomodulatory activity. In this study, we found that liposome-encapsulated PO-DNA upregulated the expression of human $\beta$-defensin-2 (hBD-2) and major histocompatibility class II molecules (HLA-DRA) in a CG sequence-dependent and liposome- dependent manner in human B cells. Of the three different liposomes, DOTAP has the unique ability to enhance the immunomodulatory activity of PO-DNA. In contrast, HLA-DRA and hBD-2 promoter activation can be induced by liposome-encapsulated PS-DNA in a CG sequence-independent manner, depending on the CpG-DNA species. Our observations demonstrate that, when encapsulated with a proper liposome in the immune system, natural PO-DNA has the potential to be a useful therapy for the regulation of the innate immune response.

• ALGAE
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• v.22 no.4
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• pp.333-338
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• 2007

A fucoidan, isolated from Korean Undaria pinnatifida spoprophyll (UP-F), was investigated for its immunomodulating activity on murine macrophages and splenocytes, and its activity was compared with that of fucoidan from Fucus vesiculosus (FV-F). Treatment of UP-F resulted in inhibition of the growth of murine macrophage RAW 264.7 cells, but its cytotoxicity was not observed in normal murine splenocytes. FV-F was shown to be highly cytotoxic to both immune cells, and its cytotoxic activity was higher than that of UP-F. Treatment of UP-F induced TNF-α in a dose-dependent manner from two types of macrophages, RAW 264.7 cells and murine peritoneal macrophages. The TNF-α-inducing activity of UP-F was higher than that of FV-F. UP-F also actively induced chemokines (RANTES and MIP-1α) from RAW 264.7 cells. Furthermore, treatment of UP-F gave rise to activation of murine splenocytes to produce cytokine (IL-6) and chemokines (RANTES and MIP-1α), showing significantly higher activity than that of FV-F. These results indicate that UP-F is less cytotoxic to immune cells than FV-F, and possesses immunomodulating activity to produce cytokines and chemokines from macrophages and splenocytes.

• The Journal of the Korean Society for Microbiology
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• v.15 no.1
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• pp.63-69
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• 1980

The effects of intravenous administration of of C. parvum on immune cells in mice were investigated. Significant delayed type hypersensitivity parvum was given intravenously before antigen sensitization. The depressed effect of C. parvum was completely abolished by treatment of cyclophosphamide. However, delayed type hypersensitivity was not depressed when C. parvum given after antigen. This depression is considered to be attributable to the generation of suppressor cells which were either suppressor T cell or C. parvum activated macrophage, because C. parvum inhibited the proliferation of S. typhimurium in vivo and also induced splenomegaly and hepatomegaly, known as manifestation of macrophage activation. Serum antibody titers were not significantly affected by C. parvum regardless of time of C. parvum administration.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.5
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• pp.1397-1403
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• 2004

By recently study, GM (Gamipaemo-tang) treatment have worked well on the allergic asthma. The purpose of this study was effect of GM extract on helper T cell, major regulator of immune system. Splenic cells from 8-week BALB/c mice were cultured in GM containing media without activation for 48 hours. The MTS assay and flow cytometry study revealed that lymphocyte treated with GM were not effective on CD4+ T cells. Subsequently CD4+ T cells were isolated and cultured in GM containing media. Either GM were not effective on CD4+ T cell without APCs. By FACS scan analysis, the expression of INF-γ, IL-4 were down-regulated in the condition skewed Th1 and Th2 cells respectively, Using ELISA analysis, the expression of INF-γ is up-regulated and IL-4 is down-regulated in the condition skewed Th1, Th2 cells respectively. With RT-PCR analysis, the expression of mRNA for INF-γ is down-regulated and IL-4 is down-regulated in the condition skewed Th1 and Th2 cells respectively. The result suggests that GM inhibited the differetiation of Th2 cells significantly and indicates GM could enhance anti-allergic immune system.

• Biomolecules & Therapeutics
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• v.17 no.3
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• pp.293-298
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• 2009

Korean mistletoe lectin (KML) is the major component found in Viscum album var. (coloratum), displaying anti-cancer and immunostimulating activities. Even though it has been shown to boost host immune defense mechanisms, the regulatory roles of KML on the functional activation of macrophages have not been fully elucidated. In this study, regulatory mechanism of KML on macrophage-mediated immune responses was examined in terms of KML-mediated signaling event. KML clearly induced mRNA expression of tumor necrosis factor (TNF)-$\alpha$, the generation of reactive oxygen species (ROS) and phagocytic uptake in RAW264.7 cells. All of these events were strongly suppressed by U0126, whereas TNF-$\alpha$ mRNA was not diminished by SB203580 and SP600125, indicating ERK as a central enzyme managing KML-induced up-regulation of macrophage functions. Indeed, KML strongly induced the phosphorylation of ERK in a time-dependent manner without altering its total level. Therefore, these data suggest that ERK may be a major signaling enzyme with regulatory property toward various KML-mediated macrophage responses.