• 동의생리병리학회지
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• 제21권1호
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• pp.181-189
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• 2007

To examine the effects of HHCP on atopic dermatitis and its various immunopathologic parameters was induced by DNCB in NC/Nga mice and the animals were orally administrated with HHCP. We summarized the results obtained from serum levels of IgE and the numbers of various immune cells as follow. HHCP has no cytotoxic effects at the range of concentration (1-400 ${\mu}g$/ml) on fibroblast isolated from lung of BALB/c mice. HHCP significantly lowered the serum levels of IgE compared with control at 16 and 20 week. HHCP significantly reduced the number of CD19$^+$ cell in spleen and DLN, as well as the number of B220$^+$ /IgE$^+$ cell in DLN compared with control. HHCP significantly reduced the number of ${\alpha}$${\beta}$ TCR$^+$ in spleen and DLN, the number of CD8$^+$ in spleen compared with control, and also significantly reduced the number of CD3$^+$, CCR3, CD3$^+$/CD69$^+$, CD3/ CCR3, CD4$^+$, CD3$^+$/ CD4$^+$/CD45$^+$ cell in DLN. HHCP increased the number of NK$^+$ cells in spleen compared with control, in contrast significantly decreased the number of CD11c$^+$/ Classll$^+$ cell and CD11b$^+$/Gr-1$^+$ cell in DLN. Taken together, these results suggested that HHCP has suppressive effects on atopic dermatitis through the inhibition of IgE production and modulation of immune cell population in NC/Nga mice.

• 한국약용작물학회지
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• 제16권6호
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• pp.383-389
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• 2008

This study was performed to compare effect of immune activities of Rhodiola sachalinensis by various extraction process with different temperature and extraction solvents. Experiments were performed for investigate the immune activities on human B and T cell growth and secretion of their cytokines. Also, antibodies in serum were investigated in female ICR mouse by feeding the extracts of R. sachalinensis at doses of 40, 120 and 360 mg/kg orally for 15 days. The immune cell growth and secretion of cytokines (IL-6, TNF-$\alpha$) on human B and T cells were increased by adding R. sachalinensis extracts compare to the control. Also, total serum IgG levels increased by feeding R. sachalinensis extracts. It can be conclude that optimum condition for efficient extraction of R. sachalinensis as functional material is slovent extraction process using water with ultrasonification at below $100^{\circ}C$ than typical process.

• IMMUNE NETWORK
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• 제23권4호
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• pp.31.1-31.18
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• 2023

Evidence suggests that the human respiratory tract, as with the gastrointestinal tract, has evolved to its current state in association with commensal microbes. However, little is known about how the airway microbiome affects the development of airway immune system. Here, we uncover a previously unidentified mode of interaction between host airway immunity and a unique strain (AIT01) of Staphylococcus epidermidis, a predominant species of the nasal microbiome. Intranasal administration of AIT01 increased the population of neutrophils and monocytes in mouse lungs. The recruitment of these immune cells resulted in the protection of the murine host against infection by Pseudomonas aeruginosa, a pathogenic bacterium. Interestingly, an AIT01-secreted protein identified as GAPDH, a well-known bacterial moonlighting protein, mediated this protective effect. Intranasal delivery of the purified GAPDH conferred significant resistance against other Gram-negative pathogens (Klebsiella pneumoniae and Acinetobacter baumannii) and influenza A virus. Our findings demonstrate the potential of a native nasal microbe and its secretory protein to enhance innate immune defense against airway infections. These results offer a promising preventive measure, particularly relevant in the context of global pandemics.

• 생약학회지
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• 제41권2호
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• pp.115-121
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• 2010

The present study was designed to explore an immunostimulating activity of crude extracts of Macrolepiota procera, and a combination therapy of cisplatin and Macrolepiota procera extracts which can potentiate the anti-cancer activity of cisplatin. For these, water extraction of Macrolepiota procera were performed at $4^{\circ}C$(MPE-4) and $100^{\circ}C$(MPE-100). In experimental metastasis of colon26-M3.1 cells, prophylactic intravenous administration of MPE ($80-2,000{\mu}g$/mouse) inhibited tumor metastasis compared with tumor control. Peritoneal macrophages stimulated with MPE produced IL-12 as well as induced tumoricidal activity. In an analysis of NK-cell activity, i.v. administration of MPE ($200{\mu}g$/mouse) significantly augmented NK cytotoxicity to YAC-1 tumor cells. The combination treatments of cisplatin ($20{\mu}g$) and MPE ($100{\mu}g$) exhibited prolongation of lifespan in colon26-M3.1 tumor bearing mouse. These results suggested that MPE stimulate immune system non-specifically and application as adjuvant in cancer treatment.

• Biomolecules & Therapeutics
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• 제26권2호
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• pp.210-217
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• 2018

Neuroinflammation is an immune response within the central nervous system against various proinflammatory stimuli. Abnormal activation of this response contributes to neurodegenerative diseases such as Parkinson disease, Alzheimer's disease, and Huntington disease. Therefore, pharmacologic modulation of abnormal neuroinflammation is thought to be a promising approach to amelioration of neurodegenerative diseases. In this study, we evaluated the synthetic flavone derivative 3',4'-dihydroxyflavone, investigating its anti-neuroinflammatory activity in BV2 microglial cells and in a mouse model. In BV2 microglial cells, 3',4'-dihydroxyflavone successfully inhibited production of chemokines such as nitric oxide and prostaglandin $E_2$ and proinflammatory cytokines such as tumor necrosis factor alpha, interleukin 1 beta, and interleukin 6 in BV2 microglia. It also inhibited phosphorylation of mitogen-activated protein kinase (MAPK) and nuclear factor $(NF)-{\kappa}B$ activation. This indicates that the anti-inflammatory activities of 3',4'-dihydroxyflavone might be related to suppression of the proinflammatory MAPK and $NF-{\kappa}B$ signaling pathways. Similar anti-neuroinflammatory activities of the compound were observed in the mouse model. These findings suggest that 3',4'-dihydroxyflavone is a potential drug candidate for the treatment of microglia-related neuroinflammatory diseases.

• 혜화의학회지
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• 제4권2호
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• pp.335-336
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• 1996

Artemisinin, a new antimalarial to treat patients infected with strains of Plasmodium jalciparum, derived from the plant Artemisia annua Linn, has immunopharmacologic actions such as enhence the PHA -induced lymphocyte transformation rate, increased the weight of spleen but reduced the weight of thymus, reduced phagocytic function of peritoneal macrophage, remarkably reduced the level of serum IgG and hemolysin fonning capacity (sentitized with SRBC), inhibited the activity of Ts cells of donor mice by supraoptimal immunuization(SOI), but enhenced activity of Ts cells of recipient mice by SOI. These results suggested that Ts cells may be the target cells of artemisinin. To the serum complement C3 level of plasmodium berghei-infeted mice, artemisinin (i. m,) could remarkly increase it. The artemisinin also obviously reduced the prostaglandin E(PGE) in the mouse hind paw swelling induced by carrageenin. Numerous studies have demonstrated that pharmacologic doses of PGE attenuate the development of immunocomplex nephritis. Some autologous immune mechanisms may be invoolved In the pathogensis of some types of glomurulonephritis. Glomerular abnormalities can be induced in animals by variety of immunological manipulations. The resulting disorder has many clinical and pathogical similarities to the disease in human. Our purpose was therefore to test the ability of the artemisinin to lessen the severity of rabbit IgG accelerated nephrotoxic serum glomerulonephritis in mice model. Mice which had treated with rabbit IgG and NTS, administrated with saline, showed Significant inceases of urinary protein, cholesterol level, and decrease of serum albumin in NS group. On the contrary, By i.g. adminstration of artemisinin at dose of 12.5, 25 and 50 mg/kg for 14 days after NTS injection, shown that artemisinin inhibited the nephritic changes in some parameters by means of urinary protein(p<0.05, p<0.01) and serum choleterol(p<0.05, p<0.01) and albumin (p<0.05, p<0.01), blood urea nitrogen (p<0.05, p<0.01), serum albumin(p<0.05, p<0.01); Cyclophosphamide(i.p. 10mg/kg for 14d) had almost same effect as the artemisinin had. Morphological studies shown that The picture of kidney from the mouse with NTS-nephritis accerated with rabbit IgG, treated with i.g. saline as the control, the mesangiocapillary were enlarged and proliferated; There were inflammatory cells infiltrating around the glomeruli; The ethelial cell were proliferated in the wall of Bowman's capsule. Histopatholological picture of kidney from the NTS-nephritis accerated with rabbit IgG mouse treated with i.p. 10mg/kg cyclophosphamide as the positive control. No siginicant histopathological evidence were found. Treaded with i.p. 12.5mg/kg artemisinine, the picture shown that mesangiocapillary were lightly proliferated; There were inflammatory cells infiltrating around the glomeruli; Treaded with i.p. 25mg/kg artemisinine, The picture shown that the mesangiocapillary were lightly proliferated; Treaded with i.p. 50mg/kg artemisinine, The picture shown that both the mesangiocapillary proliferated and the inflammatory cells infiltrating around the glomeruli are less than treated with saline, 12.5 and 25 mg/kg artemisinine. On the basis of these studies we conclude that the artemisinin can relieve pathological change caused by NTS-nephritis aacerated with rabbit IgG.

• 한방안이비인후피부과학회지
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• 제28권1호
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• pp.68-84
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• 2015

Object : The object of this study was effected of composed of 4 herbal medicines(Rubus coreanus, Rehmanniae Radix, Houttuynia cordata, Betulae cortex) on acute atopic dermatitis mice. Methods : BALB/c mice were divided 4 groups ; normal group, negative control group of acute atopic dermatitis mice induced by DNCB, treated apply to the back skin with the herbal medicine group, and treated orally with herbal medicine group. Treated with herbal medicine and DNCB during 2 weeks. After treated, measured WBCs, RBCs, and platelet in the blood, and analysed mRNA expression of spleen. Result : Composed herbal medicines could reduce WBCs, lymphocytes, monocytes, neutrophils, and eosinophils in the mouse blood. And, could down TNF-${\alpha}$ levels in spleen. In the skin tissue histology results, herbal medicines reduce the cells and T cells. Conclusion : Composed herbal medicines help to another inflammatory disease because they reduce the cells and T cells in the skin tissues. And they have inhibitory effects of TNF-${\alpha}$ mRNA expression, and Th 2 immune responses. Therefore herbal medicines use for an acute atopic dermatitis treatment.

• IMMUNE NETWORK
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• 제13권1호
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• pp.10-15
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• 2013

Aluminum hydroxide (alum) is the most widely used adjuvant in human vaccines. Nevertheless, it is virtually unknown whether alum acts on B cells. In the present study, we explored the direct effect of alum on Ig expression by murine B cells in vitro. LPS-activated mouse spleen B cells were cultured with alum, and the level of isotype-specific Ig secretion, IgG1 secreting cell numbers, and Ig germ-line transcripts (GLT) were measured using ELISA, ELISPOT, and RT-PCR, respectively. Alum consistently enhanced total IgG1 production, numbers of IgG1 secreting cells, and $GLT{\gamma}1$ expression. These results demonstrate that alum can directly cause IgG1 isotype switching leading to IgG1 production.

• IMMUNE NETWORK
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• 제1권2호
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• pp.162-169
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• 2001

Background: Nitric oxide (NO), a cytotoxic molecule is produced in various tissues including tumor cells during interleukin-2 (IL-2) therapy . Lymphokine-activated killer (LAK) cells are induced during IL-2 therapy, and have cytotoxic activity against tumor cells. The current study investigated the effects of NO synthesized in target cells or exposure of target cells to NO on the sensitivity of target cells to LAK cell cytotoxicity. Methods: Cytotoxicity was measured using 4 h chromium release assays. LAK cells which were induced by a 4 day incubation of BALB/c mouse splenocytes with IL-2 (6,000 IU/mL) were employed as effector cells. RD-995 skin tumor cells originated from a C3H/HeN mouse were employed as target cells. NO synthesis in target cells was induced by a 24 h incubation of RD-995 cells with $IFN{\gamma}$ (25 U/mL), TNF (50 U/mL) and IL-1 (20 U/mL). S-nitrosyl acetylpenicillamine (SNAP), an NO donor, was used to expose target cells to NO. $N^G$-monomethyl-L-arginine (MLA) and carboxy-PTIO were added during cytotoxicity assays to inhibit NO synthesis, and to scavenge NO produced by target cells, respectively. Results: Sensitivity of NO-producing RD-995 cells to LAK cell cytotoxicity was decreased by addition of MLA and carboxy-PTIO during cytotoxicity assays. However, the two reagents had no effect on the sensitivity of non-NO-producing RD-995 cells. Pretreatment of RD-995 target cells with SNAP increased the sensitivity in comparison with untreated cells. Conclusions: Sensitivity of target cells to LAK cell cytotoxicity is increased by target cell NO synthesis or exposure to NO. Further studies are needed to evaluate whether these in vitro results have relevance to in vivo phenomena.

• Journal of Microbiology and Biotechnology
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• 제24권8호
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• pp.1133-1142
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• 2014

Interleukin-32 (IL-32) is a cytokine and inducer of various proinflammatory cytokines such as $TNF{\alpha}$, IL-$1{\beta}$, and IL-6 as well as chemokines. There are five splicing variants (${\alpha}$, ${\beta}$, ${\gamma}$, ${\delta}$, and ${\varepsilon}$) and IL-$32{\gamma}$ is the most active isoform. We generated human IL-$32{\gamma}$ transgenic (IL-$32{\gamma}$ TG) mice to express high level of IL-$32{\gamma}$ in various tissues, including immune cells. The pathology of sepsis is based on the systemic inflammatory response that is characterized by upregulating inflammatory cytokines in whole body, particularly in response to gram-negative bacteria. We investigated the role of IL-$32{\gamma}$ in a mouse model of experimental sepsis by using lipopolysaccharides (LPS). We found that IL-$32{\gamma}TG$ mice resisted LPS-induced lethal endotoxemia. IL-$32{\gamma}$ reduced systemic cytokines release after LPS administration but not the local immune response. IL-$32{\gamma}TG$ increased neutrophil influx into the initial foci of the primary injected site, and prolonged local cytokines and chemokines production. These results suggest that neutrophil recruitment in IL-$32{\gamma}TG$ occurred as a result of the local induction of chemokines but not the systemic inflammatory cytokine circulation. Together, our results suggest that IL-$32{\gamma}$ enhances an innate immune response against local infection but inhibits the spread of immune responses, leading to systemic immune disorder.