• Food Science and Preservation
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• v.23 no.6
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• pp.906-912
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• 2016

${\beta}$-Glucan is a natural compound contained in cell walls of yeast or fungi, and cereal's fiber. It is also known to boost the immune system in human. Aureobasidium is a producer of water-soluble ${\beta}$-1,3/1,6-glucan. In this study, natural killer (NK) cell and macrophage activity were tested to investigate the effects of ${\beta}$-1,3/1,6-glucan isolated from A. pullulans on immune activity. Activation of NK cell was increased about 63-39% by the treatment of $10-200{\mu}g/mL$ ${\beta}$-1,3/1,6-glucan than control. Besides, only $10{\mu}g/mL$ of ${\beta}$-1,3/1,6-glucan was enough to boost activation of NK cell. Phagocytosis of macrophage was increased to 15~21% by the treatment of $10{\sim}200{\mu}g/mL$ of ${\beta}$-1,3/1,6-glucan than zymosan-treatment. In LP-BM5 proliferating inhibition test, relative mRNA level of LP-BM5 virus was decreased in ${\beta}$-1,3/1,6-glucan-treated cell about 36~74% than control. The decline of LP-BM5 mRNA level appeared to depend on the concentration of ${\beta}$-1,3/1,6-glucan. These results suggest that pure ${\beta}$-1,3/1,6-glucan from A. pullulans might be contributing to enhancement of immune activity through the activation of NK cell and phagocytosis of macrophage. Moreover, treatment of the ${\beta}$-1,3/1,6-glucan could increase the resistance to virus infection such as LP-BM5 through the restraining of the multiplication.

• Journal of Life Science
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• v.33 no.3
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• pp.295-303
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• 2023

Immune and metabolic systems are important factors in maintaining homeostasis. Immune response and metabolic regulation are highly associated, so, when the normal metabolism is disturbed, the immune response changed followed the metabolic diseases occur. Likewise, obesity is highly related to immune response. Obesity, which is caused by an imbalance in energy metabolism, is associated with metabolic diseases, such as insulin resistance, type 2 diabetes, fatty liver diseases, atherosclerosis and hypertension. As known, obesity is characterized in chronic low-grade inflammation. In obesity, the microenvironment of immune cells became inflammatory by the unique activation phenotypes of immune cells such as macrophage, natural killer cell, T cell. Also, the immune cells interact each other in cellular or cytokine mechanisms, which intensify the obesity-induced inflammatory response. This phenomenon suggests the possibility of regulating the activation of immune cells as a pharmacological therapeutic strategy for obesity in addition to the common pharmacological treatment of obesity which is aimed at inhibiting enzymes such as pancreatic lipase and α-amylase or inhibiting differentiation of preadipocytes. In this review, we summarize the activation phenotypes of macrophage, natural killer cell and T cell, and their aspects in obesity. We also summarize the pharmacological substances that alleviates obesity by regulating the activation of immune cells.

• Asian-Australasian Journal of Animal Sciences
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• v.18 no.12
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• pp.1741-1745
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• 2005

Zinc is a trace element that is associated with a stimulation of immune function and regulation of ion balance for livestock production. In this study, the effect of zinc as inhibitor to apoptosis-induced cells was examined in vitro using mammary epithelial cell line, HC11 and macrophage cell line, NCTC3749. Cell viability, measured by MTT assay, indicated that 10 g/ml of zinc had a negative impact on cellular activity and 50 ng/ml was chosen for further testing. Apoptosis was induced in cells treated with C2-ceramide in serum-free media. DNA fragmentation and gene expression of acidic sphingomyelinase (a gene responsible for the progress of apoptosis) were distinctively low in zinc treated cells compared with those in non-treated controls. In conclusion, zinc is involved in the regulation of cell proliferation and apoptosis in mammary epithelial cells and macrophages.

• BMB Reports
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• v.33 no.2
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• pp.148-154
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• 2000

The glycation process plays an important role in accelerated atherosclerosis in diabetes, and the uptake of atherogenic lipoproteins by macrophage in the intima of the vessel wall leads to foam cell formation, an early sign of atherosclerosis. Besides the lipolytic action on the plasma triglyceride component, lipoprotein lipase (LPL) has been reported to enhance the cholesterol uptake by arterial wall cells. In this study, some properties of LPL-mediated low-density lipoprotein (LDL) uptake and the effect of LDL glycation were investigated in RAW 264.7 cell, a murine macrophage cell line. In the presence of LPL, $^{125}I$-LDL binding to RAW 264.7 cells was increased in a dose-dependent manner. At concentrations greater than $20\;{\mu}g/ml$ of LPL, LPL-mediated LDL binding was increased about 17-fold, achieving saturation. Without LPL, both very low-density lipoprotein (VLDL) and high-density lipoprotein (HDL) were ineffective in blocking the binding of $^{125}I$-LDL to Cells. However, LPL-enhanced LDL binding was inhibited about 50% by the presence of VLDL, while no significant effect was observed with HDL. Heat inactivation of LPL caused a 30% decrease of LDL binding. In the presence of LPL, the cells took up 40% of cell-bound native LDL. No significant difference was observed in cell binding between native and glycated LDL. However, the uptake of glycated LDL was significantly greater than that of native LDL, reaching to 70% of the total cell bound glycated LDL. These results indicate that LPL can cause the significant enhancement of LDL uptake by RAW 264.7 cells and the enhanced uptake of glycated LDL in the presence of LPL might play an important role in the accelerated atherogenesis in diabetic patients.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.1
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• pp.27-38
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• 2021

Excessive salt intake induces hypertension, but several gamma-aminobutyric acid (GABA) supplements have been shown to reduce blood pressure. GABA-salt, a fermented salt by L. brevis BJ20 containing GABA was prepared through the post-fermentation with refined salt and the fermented GABA extract. We evaluated the effect of GABA-salt on hypertension in a high salt, high cholesterol diet induced mouse model. We analyzed type 1 macrophage (M1) polarization, the expression of M1 related cytokines, GABA receptor expression, endothelial cell (EC) dysfunction, vascular smooth muscle cell (VSMC) proliferation, and medial thicknesses in mice model. GABA-salt attenuated diet-induced blood pressure increases, M1 polarization, and TNF-α and inducible nitric oxide synthase (NOS) levels in mouse aortas, and in salt treated macrophages in vitro. Furthermore, GABA-salt induced higher GABAB receptor and endothelial NOS (eNOS) and eNOS phosphorylation levels than those observed in salt treated ECs. In addition, GABA-salt attenuated EC dysfunction by decreasing the levels of adhesion molecules (E-selectin, Intercellular Adhesion Molecule-1 [ICAM-1], vascular cell adhesion molecule-1 [VCAM-1]) and of von Willebrand Factor and reduced EC death. GABA-salt also reduced diet-induced reductions in the levels of eNOS, phosphorylated eNOS, VSMC proliferation and medial thickening in mouse aortic tissues, and attenuated Endothelin-1 levels in salt treated VSMCs. In summary, GABA-salt reduced high salt, high cholesterol diet induced hypertension in our mouse model by reducing M1 polarization, EC dysfunction, and VSMC proliferation.

• BMB Reports
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• v.57 no.8
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• pp.375-380
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• 2024

Early proatherogenic inflammation constitutes a significant risk factor for atherogenesis development. Despite this, the precise molecular mechanisms driving this pathological progression largely remain elusive. Our study unveils a pivotal role for the microRNA miR-328-5p in dampening endothelial inflammation by modulating the stability of JUNB (JunB proto-oncogene). Perturbation of miR-328-5p levels results in heightened monocyte adhesion to endothelial cells and enhanced transendothelial migration, while its overexpression mitigates these inflammatory processes. Furthermore, miR-328-5p hinders macrophage polarization toward the pro-inflammatory M1 phenotype, and exerts a negative influence on atherosclerotic plaque formation in vivo. By pinpointing JUNB as a direct miR-328-5p target, our research underscores the potential of miR-328-5p as a therapeutic target for inflammatory atherosclerosis. Reintroduction of JUNB effectively counteracts the anti-atherosclerotic effects of miR-328-5p, highlighting the promise of pharmacological miR-328-5p targeting in managing inflammatory atherosclerosis.

• Journal of Ginseng Research
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• v.13 no.1
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• pp.24-29
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• 1989

The tumoricidal activity of marine macrophage against K562 tumor cells was studied in the presence of lipopolysaccharide(LPS) and ginseng saponin. 1 The tumoricidal activity was increased more by LPS treatment with ginseng saponin (44% in 24 hours) than by LPS only (22% in 24 hours). In the case of diol saponin, the tumoricidal activity was increased as much as 35% at concentrations of 10-3 to 1034%. Triol saponin increased the tumoricidal activity more than LPS only treatment at each concentration . 2. When total, dial and triol saponin were added to K.562 tumor cell in various concentration without macrophage, it was found that the ginseng saponin hall no tumoricidal effect. This result suggests that ginseng saponin increases the tumoricidal activity of K562 tumor celts through the tumoricidal activity of the macrophage.

• Tuberculosis and Respiratory Diseases
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• v.46 no.3
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• pp.327-337
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• 1999

Background: Reactive oxygen species are involved in multi-stage process of carcinogenesis. The moot of cancer cell lines and cancer cells in tumor tissue produce reactive oxygen species and on the other hand, the activities of catalase, Mn- and CuZn-superoxide dismutase in tumor cells are usually low. These persistent oxidative stress in tumor tissue facilitates tumor invasion and metastasis. 12-kDa thioredoxin, which regulates the intracellular redox potential with glutathione and glutaredoxin is involved in cell activation, proliferation, differentiation and redox-mediated apoptosis. It is also purified as 14-kDa and 10-kDa eooinophilic cytotoxic enhancing factor(ECEF) from human histiocytic cell(U937) and 10-kDa ECEF has more than 20 times eosinophilic stimulation activity than 14-kDa ECEF. It has been reported that adult T-cell leukemia, squamous cell carcinoma of uterine cervix, and hepatocellular carcinoma show increased amounts of human thioredoxin and thioredoxin mRNA is increased in lung cancer. In this study, we investigated the expression of conventional antioxidant enzymes such as catalase, CuZn-SOD, and glutathione peroxidase and thioredoxin in lung cancer tissue compared to adjacent normal lung tissue and the induction of thioredoxin in macrophage cells after treatment of oxidative stress and endotoxin Methods: We measured the amount of conventional antioxidant enzymes such as catalase, CuZn-SOD, and glutathione peroxidase and thioredoxin in lung cancer tissue compared to adjacent normal lung tissue by immunoblot analysis and the induction of thioredoxin in mouse monocyte-macrophage cells(RAW 264.7) by treatment of 5 ${\mu}M$ menadione and 1 ${\mu}g/ml$ endotoxin Results: On immunoblot analysis, the expression of 12-kDa thioredoxin was increased in lung cancer tissue compared to paired normal lung tissue. but the expression of catalase and CuZn-SOD were decreased in lung cancer tissue compared to paired normal tissue and the expression of glutathione peroxidase in lung cancer was variable. The expression of truncated thioredoxin was also increased in lung cancer. When mouse monocyte-macrophage cells were treated with 5 ${\mu}M$ menadione and 1 ${\mu}g/ml$ endotoxin, the expression of thioredoxin was peaked at 12 hrs and sustained to 48 hrs. Conclusion: In contrast with other conventional antioxidants, the expression of 12-kDa and truncated thioredoxin in lung cancer were increased and it is closely associated with persistent oxidative stress in tumor microenvironment. Considering especially the biological functions of truncated thioredoxin, the increased amount of truncated thioredoxin has significant role in tumor growth through cell proliferation.

• Journal of Food Hygiene and Safety
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• v.28 no.4
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• pp.342-348
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• 2013

The following study was presented to investigate the anti-inflammatory effect of peel extracts (PE) from three citrus fruits: Citrus unshiu, Citrus limonia Osbeck and Citrus hallabong. According to this study, cytotoxicity, NO-production and protein levels of iNOS (inducible nitric oxide synthase) in macrophage cell were analyzed, which had been incubated in murine macrophage cell line RAW 264.7 cell of PE from those three citrus fruits. According to Citrus unshiu peel extracts (CUP), Citrus limonia Osbeck peel extracts (CHP) and Citrus hallabong peel extracts (CLP) treatment, the result showed that there was no cell growth inhibited below 2 mg/mL. Comparing the NO-production of the cell with LPS (100 ng/mL) and the treatment without LPS, significant increase of NO-production was detected. However NO-production also showed decrease trend, as the concentration increased. For each treatment, at the concentration of 1 mg/mL, NO-ihibitory activity showed significant result with following order: CUP > CHP > CLP. According to the result from Western blot, the inhibitory activities of iNOS protein from CUP and CHP showed fairly similar performances. Also inhibitory activity of COX-2 showed the following order: CUP > CHP> CLP. There was no doubt that all the treatments of CUP, CHP and CLP have anti-inflammatory effect and also that the inhibitory activity of the CUP treatment was the strongest among those three.

• BMB Reports
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• v.28 no.6
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• pp.527-532
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• 1995

Human taurine transporter has 12 transmembrane domains and its molecular weight is 69.6 kDa. The long cytoplasmic carboxy and amino termini might function as regulatory attachment sites for other proteins. Six potential protein kinase C phosphorylation sites have been reported in human taurine transporter. In this report, we studied the effects of phorbol 12-myristate 13-acetate (PMA) and glucocorticoid hormone on taurine transportation in the RAW 264.7, mouse macrophage cell line. When the cells were incubated with $[^{3}H]taurine$ in the presence or absence of $Na^+$ ion for 40 min at $37^{\circ}C$, the [$[^{3}H]taurine$ uptake rate was 780-times higher in the $Na^{+}-containing$ buffer than in the $Na^{+}-deficient$ buffer, indicating that this cell line expresses taurine transporter protein on the cell surface. THP1, a human promonocyte cell line, also showed a similar property. The $[^{3}H]taurine$ uptake rate was not influenced by the inflammatory inducing cytokines such as interleukin-1, gamma-interferon or interleukin-1+gamma-interferon, but was decreased by the PMA in the RAW 264.7 cell line. This suggests that activation of protein kinase C inhibits taurine transporter activity directly or indirectly. The inhibition of $[^{3}H]taurine$ uptake by PMA was time-dependent. Maximal inhibition occurred in one hr stimulation with PMA Increasing the treatment time beyond one h reduced the $[^{3}H]taurine$ uptake inhibition due to the depletion or inactivation of protein kinase C. The cell line also showed concentration-dependent $[^{3}H]taurine$ uptake under PMA stimulation. The phorbol-ester caused 23% inhibition at the concentration of 1 ${\mu}m$ PMA. The inhibition was significant even at a concentration as low as 10 nM PMA The reduced $[^{3}H]taurine$ uptake could be recovered by treatment with glucocorticosteroid hormone. Dexamethasone led to recover of the reduced taurine uptake induced by phorbol-ester, recovering maximally after one hr. This may suggest that macrophage cells require higher taurine concentration in a stressed state, for the secretion of glucocorticoid hormone is increased by hypothalamo-pituitary-adrenocortical (HPA) axis activation in the blood stream.