Sarcopenia is an age-related, progressive skeletal muscle disorder involving the loss of muscle mass and strength. Previous studies have shown that γ-aminobutyric acid (GABA) from fermented oysters aids in regulatory T cells (Tregs) cell expansion and function by enhancing autophagy, and concomitantly mediate muscle regeneration by modulating muscle inflammation and satellite cell function. The fermentation process of oysters not only increases the GABA content but also enhances the content of branched amino acids and free amino acids that aid the level of protein absorption and muscle strength, mass, and repair. In this study, the effect of GABA-enriched fermented sarco oyster extract (FSO) on reduced muscle mass and functions via Treg modulation and enhanced autophagy in aged mice was investigated. Results showed that FSO enhanced the expression of autophagy markers (autophagy-related gene 5 [ATG5] and GABA receptor-associated protein [GABARAP]), forkhead box protein 3 (FoxP3) expression, and levels of anti-inflammatory cytokines (interleukin [IL]-10 and transforming growth factor [TGF]-β) secreted by Tregs while reducing pro-inflammatory cytokine levels (IL-17A and interferon [IFN]-γ). Furthermore, FSO increased the expression of IL-33 and its receptor IL-1 receptor-like 1 (ST2); well-known signaling pathways that increase amphiregulin (Areg) secretion and expression of myogenesis markers (myogenic factor 5, myoblast determination protein 1, and myogenin). Muscle mass and function were also enhanced via FSO. Overall, the current study suggests that FSO increased autophagy, which enhanced Treg accumulation and function, decreased muscle inflammation, and increased satellite cell function for muscle regeneration and therefore could decrease the loss of muscle mass and function with aging.
In order to investigate experimentally that the effect of aqua-acupuncture solution of Paeonia lactiflora on arthritis of mice induced by collagenII, the author performed several experimental items : that is increase, paw thickness, DTH, weight of spleen, hematological change, expression of $CD4^+$, $CD8^+$, $CD19^+$, gene expression of IL-1, IL-6, IL-12, IFN-${\gamma}$, TNF, proliferation of synovial cells and cytotoxicity. The results were obtained as follows; 1. Inhibitory effects of aqua-acupuncture solution of Paeonia lactiflora on arthritis induced by collgenII. 1) In incidence, paw edema, AI and DTH were inhibited as compared with control group. 2) The splenic weight was increased and the number of leukocytes was decreased as compared with control group. 3) The number of $CD4^+$, $CD8^+$ activated cells and surface-receptor expression were increased as compared with control group. 4) In hematological change, total protein, creatinine and LDH were decreased significantiy as compared with control group. 2. FACS analysis on normal BABL/c of spenic cells treated with aqua-acupuncture solution of Paeonia lactiflora. 1) Aqua-acupuncture solution of Paeonia lactiflora activated adhesive splenic cells of mice morphologically in vitro. 2) Aqua-acupuncture solution of Paeonia dactiflora enhanced the gene expression of IL-12 and also enhanced that of interferon-${\gamma}$ remarkably. 3) Aqua-acupuncture solution of Paeonia lactiflora reduced the number of $CD4^+$, $CD8^+$, $CD19^+$ activated cells and their surface-receptor expression as compared with control group. 3. Effects of aqua-acupuncture solution of Paeonia lactiflora on human synovial cells. 1) In cytotoxicity against synovial cells, aqua-acupuncture solution of Paeonia lactiflora didn't show cytotoxicity at concentration of $10-100{\mu}g/m{\ell}$ but showed significantly at concentration of $200-400{\mu}g/m{\ell}$ as compared with control group. 2) Aqua-acupuncture solution of Paeonia lactiflora reduced the gene expression of IL-6, IL-$1{\beta}$ and TNF-${\alpha}$. 3) Aqua-acupuncture solution of Paeonia lactiflora inhibited proliferation of synovial cells at concentration of 100 and $200{\mu}g/m{\ell}$.
Recent studies have suggested that oral bacteriotherapy with probiotics might be useful for preventing and managing childhood atopic dermatitis (AD). The purpose of this investigation was to evaluate the efficacy and safety of oral treatment with probiotics for adolescent and adult AD patients as well as for childhood AD patients. Sixty-four patients with mild to moderate AD were recruited for treatment with a mixture of four probiotic strains (Lactobacillus rhamnosus, Lactobacillus plantarum, Lactobacillus casei, and Biftdobacterium lactis) twice daily for 8 weeks. The degree of pruritus was determined by a 10-point visual analog scale every other week, and the patients' global assessments of their clinical responses (i.e., better, unchanged, or worse) was done at the end of intervention. The clinical severity of the eczema was evaluated by eczema area and severity index (EASI) score every other week. As laboratory markers, total immunoglobulin E (IgE), eosinophil cationic protein (ECP) in the serum, and cytokine production [interleukin-4 (IL-4), interleukin-10 (IL-10), and $interferon-{\gamma}\;(IFN-{\gamma})$ by the peripheral blood mononuclear cells (PBMCs) were measured at the beginning and at the end of intervention. Of the 64 enrolled AD patients, only 50 patients finally completed the 8-week study. After 8-week treatment with probiotics, the EASI score was significantly improved (p<0.0001), 50% of the patients experienced improvement of their eczema, and significant improvement of the pruritus was also observed (p=0.0002). The effect was more pronounced for the patients with very high IgE levels (>1,000 ku/l) or for the patients with moderate disease severity. There was no significant difference in the therapeutic effects between the childhood AD and adolescent and adult AD patients. There were no significant changes of cytokines, as well as the total IgE and ECP levels, in the patients' serum. Treatment with the mixture of four probiotic strains was generally well tolerated. Our results suggest that the treatment with the mixture of four probiotic strains is beneficial for the management of the adolescent and adult AD patients, as well as for the childhood AD patients.
Oral administration of antigen has long been considered as a promising alternative for the treatment of chronic autoimmune diseases including rheumatoid arthritis (RA), and oral application of type II collagen (CII) has been proven to improve pathogenic symptoms in RA patients without problematic side effects. To further current understandings about the immune suppression mechanisms mediated by orally administered antigens, we examined the changes in IgG subtypes, T-cell proliferative response, and proportion of interleukin (IL)-10 producing Th subsets in a time course study of collagen induced arthritis (CIA) animal models. We found that joint inflammation in CIA mouse peaked at 5 weeks after first immunization with CII, which was significantly subdued in mice pre-treated by repeated oral administration of CII. Orally tolerized mice also showed increase in their serum level of IgG1, while the level of IgG2a was decreased. T-cell proliferation upon CII stimulation was also suppressed in lymph nodes of mice given oral administration of CII compared to non-tolerized controls. When cultured in vitro in the presence of CII, T-cells isolated from orally tolerized mice presented higher proportion of $CD4^+IL-10^+$ subsets compared to non-tolerized controls. Interestingly, such increase in IL-10 producing cells were obvious first in Peyer's patch, then by 5 weeks after immunization, in mesenteric lymph node and spleen instead. This result indicates that a particular subset of T-cells with immune suppressive functions might have migrated from the original contact site with CII to inflamed joints via peripheral blood after 5 weeks post immunization.
Journal of the Korean Society of Food Science and Nutrition
/
v.43
no.3
/
pp.349-354
/
2014
Elevation of intracellular calcium ($Ca^{{+}{+}}$) triggers degranulation of mast cells by bypassing receptor activation. Flos Sophora japonica L. has been used as a natural dying source and has been reported to have biological activities such as anti-inflammatory and anti-allergic effects through $Fc{\varepsilon}RI$ and IgE crosslinking. In the present investigation, we report the regulatory effect of ethanolic extract of Flos Sophora japonica L. (S.F) on allergic mediators produced by $Ca^{{+}{+}}$ ionophore activation in mast cells. S.F significantly inhibited calcium ionophore (A23187)-induced interleukin (IL)-4 and tumor necrosis factor (TNF)-${\alpha}$ production as well as mast cell degranulation. Furthermore, administration of S.F suppressed allergic reactions in a 2,4-dinitrofluorobenzene (DNFB)-induced allergic dermatitis mouse model. Both oral administration and ear painting using 50 mg/kg of S.F significantly reduced levels of cytokines such as IL-4, TNF, and interferon-${\gamma}$ in ear tissues compared to the DNFB alone-treated group. Serum IgE level in the S.F-treated group also decreased compared to the DNFB alone-treated group. Weights of spleens and lymph nodes in the S.F-treated groups also decreased compared to the control group. Considering the data, we conclude that S.F mediates its anti-allergic effects not only through $Fc{\varepsilon}RI$ stimulation but also $Ca^{{+}{+}}$ influx in mast cells.
Background/Objectives: Maintenance of cellular function in culture is vital for transfer and development following adoptive immunotherapy. Dual properties of IL-21 in activating T cells and reducing activation induced cell death led us to explore the mechanism of action of IL-21 enhanced proliferation and cytotoxic potential of CIK cells. Method: CIK cells cultured from PBMCs of healthy subjects were stimulated with IL-21 and cellular viability and cytotoxicity to K562 cells were measured. To elucidate the mechanism of action of IL-21, mRNA expression of cytotoxic factors was assessed by RT-PCR and protein expression of significantly important cytotoxic factors and cytokine secretion were determined through flow cytometry and ELISA. Western blotting was performed to check the involvement of the JAK/STAT pathway following stimulation. Results: We found that IL-21 did not enhance in vitro proliferation of CIK cells, but did increase the number of cells expressing the CD3+/CD56+ phenotype. Cytotoxic potential was increased with corresponding increase in perforin ($0.9831{\pm}0.1265$ to $0.7592{\pm}0.1457$), granzyme B ($0.4084{\pm}0.1589$ to $0.7319{\pm}0.1639$) and FasL ($0.4015{\pm}0.2842$ to $0.7381{\pm}0.2568$). Interferon gamma and TNF-alpha were noted to increase ($25.8{\pm}6.1ng/L$ to $56.0{\pm}2.3ng/L$; and $5.64{\pm}0.61{\mu}g/L$ to $15.14{\pm}0.93{\mu}g/L$, respectively) while no significant differences were observed in the expression of granzyme A, TNF-alpha and NKG2D, and NKG2D. We further affirmed that IL-21 signals through the STAT-3 and STAT-5b signaling pathway in the CIK cell pool. Conclusion: IL-21 enhances cytotoxic potential of CIK cells through increasing expression of perforin, granzyme B, IFN-gamma and TNF-alpha. The effect is brought about by the activation of STAT-3 and STAT-5b proteins.
Recently, we reported that immunostimulation of primary rat cortical astrocyte caused stimulation of glucose deprivation induced apoptotic cell death. To enhance the understanding of the mechanism of the potentiated cell death of clucose-deprived astrocyte by immunostimulation, we investigated the effect of immunostimulation on the glucose deprivation induced cell death of rat C6 glioma cells. Co-treatment of C6 glioma cells with lipopolysaccharide (LPS, $1\;{\mu}\textrm{g}/ml$) and interferon ${\gamma}(IFN{\gamma},\;100U/ml)$ is serum free condition caused marked elevationo f nitric oxide production ($>50\;{\mu}M$). In this condition, glucose deprivation caused significant release of lactate dehdrogenase (LDH) from C6 glioma cells while control cells did not show LDH release. To investigate whether elevated level of nitric oxide is responsible for the enhanced LDH release in glucose-deprived condition, C6 glioma cells were treated with 3-morphorinosydnonimine (SIN-1) and it was observed that SIN-1 caused increase in LDH release from glucose-deprived C6 glioma cells. Treatment of C6 glioma cells with $25\;{\mu}M$ of pyrrolidinedithiocarbamate (PDTC) which inhibit Nuclear factor kB (NF-kB) activation, caused complete inhibition of nitric oxide production. Treatment of C6 glioma cells with NO synthase inhibitors, $N^{G}$-nitro-L-arginine (NNA) or L-$N{\omega}$-nitro-L-arginine methyl ester (L-NAME), caused inhibition of nitric oxide production and also glucose deprivation induced cell death of cytokine-stimulated C6 glioma cells. In addition, diaminohydroxypyrimidine (DAHP, 5 mM) which inhibits the synthesis of tetrahydrobiopterine (BH4), one of essential cofactors for iNOS activity, caused complete inhibition of NO production from immunostimulated C6 glioma cells. The results from the present study suggest that immunostimulation causes potentiation of glucose deprivation induced death of C6 glioma cells which is mediated at least in part by the increased production of nitric oxide. The vulnerability of immunostimulated C6 glioma cells to hypoglycemic insults may implicate that the elevated level of cytokines in various ischemic and neurodegenerative diseases may play a role in their pathogenesis.
The study was conducted to investigate the role of vitamin E in the high altitude hypoxia-induced damage to the intestinal barrier in rats. Sprague-Dawley rats were divided into control (Control), high altitude hypoxia (HH), and high altitude hypoxia + vitamin E (250 mg/kg $BW^*d$) (HV) groups. After the third day, the HH and HV groups were placed in a hypobaric chamber at a stimulated elevation of 7000 m for 5 days. The rats in the HV group were given vitamin E by gavage daily for 8 days. The other rats were given equal volume saline. The results showed that high altitude hypoxia caused the enlargement of heart, liver, lung and kidney, and intestinal villi damage. Supplementation with vitamin E significantly alleviated hypoxia-caused damage to the main organs including intestine, increased the serum superoxide dismutase (SOD) (p< 0.05), diamino oxidase (DAO) (p< 0.01) levels, and decreased the serum levels of interleukin-2 (IL-2) (p< 0.01), interleukin-4 (IL-4) (p<0.001), interferon-gamma ($IFN-{\gamma}$) (p<0.01) and malondialdehyde (MDA) (p<0.001), and decreased the serum erythropoietin (EPO) activity (p<0.05). Administration of vitamin E significantly increased the S-IgA (p<0.001) in ileum and significantly improved the expression levels of occludin and $I{\kappa}B{\alpha}$, and decreased the expression levels of hypoxia-inducible factor 1 alpha and 2 alpha ($HIF-1{\alpha}$ and $HIF-2{\alpha}$), Toll-like receptors (TLR4), P-$I{\kappa}B{\alpha}$ and nuclear factor-${\kappa}B$ p65(NF-${\kappa}B$ P65) in ileum compared to the HH group. This study suggested that vitamin E protectis from intestinal injury caused by high altitude hypoxia environment. These effects may be related to the HIF and TLR4/NF-${\kappa}B$ signaling pathway.
Heo, Seong Beom;Lim, Sun Woo;Jhun, Joo Yeon;Cho, Mi La;Chung, Byung Ha;Yang, Chul Woo
Journal of Ginseng Research
/
v.40
no.1
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pp.18-27
/
2016
Background: It is not clear whether ginseng affects cyclosporine A (CsA)-induced desirable immunosuppressive action. In this study, we evaluated the immunological influence of combined treatment of ginseng with CsA. Methods: Using CD4+ T cells from mouse spleens stimulated with the T cell receptor (TCR) or allogeneic antigen-presenting cells (APCs), we examined the differentiation of naïve T cells into T helper 1 (Th1), Th2, Th17, and regulatory T cells (Tregs), and their cytokine production during treatment by Korean Red Ginseng extract (KRGE) and/or CsA. The influence of KRGE on the allogeneic T cell response was evaluated by mixed lymphocyte reaction (MLR). We also evaluated whether signal transducer and activator of transcription 3 (STAT3) and STAT5 are implicated in this regulation. Results: Under TCR stimulation, KRGE treatment did not affect the population of CD4+interferon gamma ($IFN{\gamma}$)+ and CD4+interleukin (IL)-4+ cells and their cytokine production compared with CsA alone. Under the Th17-polarizing condition, KRGE significantly reduced the number of CD4+IL-17+ cells and CD4+/phosphorylated STAT3 (p-STAT3)+ cells, but increased the number of CD4+CD25+forkhead box P3 (Foxp3)+ cells and CD4+/p-STAT5+ cells compared with CsA alone. In allogeneic APCs-stimulated CD4+ T cells, KRGE significantly decreased total allogeneic T cell proliferation. Consistent with the effects of TCR stimulation, KRGE reduced the number of CD4+IL-17+ cells and increased the number of CD4+CD25+Foxp3+ cells under the Th17-polarizing condition. Conclusion: KRGE has immunological benefits through the reciprocal regulation of Th17 and Treg cells during CsA-induced immunosuppression.
Objective : The aim of the study is to investigate the effect of electro-acupuncture (EA) on ST36 to modulate immune reaction in BALB/c mice immunized intraperitoneally with 2,4-dinitrophenylated keyhole limpet protein(DNP-KLH). Methods : Experimental mice were divided into four groups : 1) Normal group was not performed by any operation. 2) IM(Immunized) group was immunized intraperitoneally with DNP-KLH and aluminum hydroxide without electro-acupunture stimulation. 3) IM-EA(immunized-elctro- acupuncture) group was performed by successive electro-acupuncture on the ST36 acupoint after immunization. 4) IM-NA(immunized-naloxone) group was performed by immunization and electro-acupuncture with same method, but naloxone was injected intraperitoneally 30 minutes before eletro-acupuncture to inhibit the opiate receptor in spleen. Serum total immunoglobulin I(IgE) and antigen-specific IgE was measured in each group. The expression of interferon-${\gamma}$ and interleukin-4 mRNA in spleen was researched by real-time RT-PCR Results : Serum total-IgE and antigen-specific IgE were significantly decreased only in IM-EA group. The expression of interleukin-4 in spleen cell was significantly reduced not only in IM-EA group, but also in IM-EA group. Conclusions : Above results indicate that the mechanism of immunomodulatory effect of electro-acupuncture is related to opioid system especially in B-cell immune reaction. Further research on the T-cell immunity is necessary to explain the mechanism of immunomodulatory effect of electro-acupuncture.
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