• Macromolecular Research
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• v.17 no.2
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• pp.128-132
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• 2009

Fucoidan, a sulfated polysaccharide derived from brown seaweed, is an important material valued for its various biological functions, including anti-coagulation, anti-aging, and immune system support. In this study, we examined the potential of fucoidan as a novel emulsifying agent in BSA (bovine serum albumin)-stabilized emulsion at a neutral pH. We measured the dispersed oil-droplet size, surface zeta-potential and creaming formation of 0.5 wt% BSA emulsion (20 wt% oil traction) in the absence and presence of fucoidan. The average particle size and zeta-potential value were 625.4 nm and -30.91 mV in only BSA-stabilized emulsion and 745.2 nm and -44.2 mV in 1.0 wt% fucoidan-added BSA emulsion, respectively. This result suggested that some positive charges of the BSA molecules interacted with the negative charges of fucoidan to inhibit the flocculation among the oil droplets. The creaming rate calculated from the backscattering data measured by Turbiscan dramatically decreased in 1.0 wt% fucoidan-added BSA emulsion during storage. Accordingly, the repulsion forces induced among the oil particles coated with 1.0 wt% fucoidan in emulsion solution resulted in significantly increased emulsion stability. The turbidity of the BSA-stabilized emulsion at 500 nm decreased during five days of storage. However, the fucoidan-added BSA emulsion exhibited a higher value of turbidity than the BSA-stabilized emulsion did. In conclusion, an anionic sulfated fucoidan lowered the surface zeta-potential of BSA-coated oil droplets via the electrostatic interaction, and subsequently inhibited the flocculation among the oil droplets, thereby clearly minimizing the creaming and phase separation of the emulsion.

• YAKHAK HOEJI
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• v.46 no.4
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• pp.258-264
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• 2002

Zinc plays an important role in immunobiological responses, while excessive zinc attenuates immune functions in a dose-dependent manner. Zinc excess has been reported to increase levels of plasma prostaglandin E$_2$ (PGE$_2$), which is known to inhibit production of Th (helper T) 1-associated cytokines and to induce inflammatory responses. Thus, this study was investigated the effects of indomethacin, a potent inhibitor of PGE$_2$ synthesis, on the proinflammatory cytokine and lymphokine production in ICR mice exposed to excessive zinc. Indomethacin at doses of 5 mg/kg was administered i.p. 30 minutes before zinc chloride (Zn) 30 mg/kg orally daily for 10 days. Excessive Zn remarkedly increased tumor necrosis factor (TNF)-$\alpha$ and interleukin (IL)-1$\beta$ levels in both serum and splenic supernatants compared with those in controls, while indomethacin significantly reduced the excessive Zn-induced levels of IL-1$\beta$. In serum, excessive Zn significantly decreased the levels of IL-2 and interferon (IFN)-${\gamma}$ compared with those in controls, whereas indomethacin significantly enhanced the excessive Zn-decreased levels of IFN-${\gamma}$ but did not affect the Zn-decreased levels of serum IL-2. In splenic supernatants, All of excessive Zn, indomethacin, and combination of Zn and indomethacin significantly enhanced IL-2 levels compared with those in controls, but indomethacin didn't affect the Zn-induced production of IL-2. These data, therefore, suggest that indomethacin significantly attenuated the in vivo and ex vivo IL-1$\beta$ production increased by excessive zinc and remarkedly enhanced the in vivo excessive zinc-suppressed production of IFN-${\gamma}$ but not IL-2.

• IMMUNE NETWORK
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• v.6 no.2
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• pp.76-85
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• 2006

Background: Chemotaxis is one of the cardinal functions of leukocytes, which enables them to be recruited efficiently to the right place at the right time. Analyzing chemotactic activities is important not only for the study on leukocyte migration but also for many other applications including development of new drugs interfering with the chemotactic process. However, there are many technical limitations in the conventional in vitro chemotaxis assays. Here we applied a new optical assay to investigate chemotactic activities induced in differentiated HL-60 cells. Methods: HL-60 cells were stimulated with 0.8% dimethylformamide (DMF) for 4 days. The cells were analyzed for morphology, flow cytometry as well as chemotactic activities by a time-lapse videomicroscopic assay using a chemotactic microchamber bearing a fibronectin-coated cover slip and an etched silicon chip. Results: Videomicroscopic observation of the real cellular motions in a stable concentration gradient of chemokines demonstrated that HL-60 cells showed chemotaxis to inflammatory chemokines (CCL3, CCL5 and CXCL8) and also a homeostatic chemokine (CXCL12) after DFM-induced differentiation to granulocytic cells. The cells moved randomly at a speed of $6.99{\pm}1.24{\mu}m/min$ (n=100) in the absence of chemokine. Chemokine stimulation induced directional migration of differentiated HL-60 cells, while they still wandered very much and significantly increased the moving speeds. Conclusion: The locomotive patterns of DMF-stimulated HL-60 cells can be analyzed in detail throughout the course of chemotaxis by the use of a time-lapse videomicroscopic assay. DMF-stimulated HL-60 cells may provide a convenient in vitro model for chemotactic studies of neutrophils.

• IMMUNE NETWORK
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• v.11 no.4
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• pp.216-222
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• 2011

Background: The ligand for CD137 (CD137L; also called 4-1BBL) is mainly expressed on activated APCs such as dendritic cells, B cells and macrophages. Even though CD137L functions as a trigger of the CD137 signaling pathway for T cell activation and expansion, engagement of CD137L can deliver a signal leading to the production of proinflammatory cytokines in macrophages. Methods: We generated cell-permeable TAT-CD137L cytoplasmic domain fusion protein (TAT-CD137Lct) and examined its ability to initiate the CD137L reverse signaling pathway. Results: Treatment of TAT-CD137Lct induced the production of high levels of IL-6 and TNF-${\alpha}$ mRNAs and proteins in peritoneal macrophages. TAT-CD137Lct increased phosphorylation of Erk, p38 MAPK and Jnk, and activated transcription factors C/EBP and CREB. However, TAT-CD137Lct did not visibly affect the degradation of the inhibitor of NF-${\kappa}B$ ($IkB{\alpha}$). We further demonstrated that JNK activation was required for TAT-CD137Lct-induced production of TNF-${\alpha}$, while activation of Erk and p38 MAPK were involved in IL-6 and TNF-${\alpha}$ production. Conclusion: Our results suggest that TATCD137Lct is an effective activator for the CD137L reverse signaling pathway.

• International Journal of Oral Biology
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• v.36 no.2
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• pp.91-101
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• 2011

MspTL is the major surface protein of Treponema lecithinolyticum associated with periodontitis and endodontic infections. Our recent investigation revealed that MspTL induces proinflammatory cytokines and intercellular adhesion molecule 1 in THP-1 cells and periodontal ligament cells. In this study we conducted oligonucleotide microarray analysis to investigate the global transcriptional regulation in THP-1 cells stimulated with purified recombinant MspTL. MspTL upregulated the expression of 90 genes in THP-1 cells at least four fold, and the functions of these genes were categorized into adhesion, apoptosis/antiapoptosis, cell cycle/growth/differentiation, chemotaxis, cytoskeleton organization, immune response, molecular metabolism, proteolysis, signaling, and transcription. The majority of the modified genes are known to be NF-${\kappa}B$-responsive and interferon-stimulated genes (ISGs). The expression of 12 selected genes was confirmed by real-time RT-PCR. Because prostaglandin $E_2(PGE_2)$ is an important inflammatory mediator and Cox-2 was found to be induced by MspTL in the microarray analysis, we determined the level of $PGE_2$ in the culture supernatants of MspTL-treated cells and found that MspTL significantly increased $PGE_2$. Our results provide insight into the gene regulation of host cells in response to MspTL, and may contribute to the understanding of the molecular mechanism in periodontitis.

• YAKHAK HOEJI
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• v.51 no.6
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• pp.482-489
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• 2007

Kaempferitrin, isolated from Kenaf (Hibiscus cannabinus), was examined to evaluate its modulatory effects on antigen-presenting cell functions of macrophages/monocytes such as phagocytosis of foreign materials, up-regulation of costimulatory molecules (CD40, CD80 and CD86), adhesion molecule activation, and antigen processing and presentation. Kaempferitrin strongly blocked up-regulation of CD40, CD80 and CD86, but not pattern recognition receptor (PRR) (e.g., TLR2). It also suppressed functional activation of CD29 (${\beta}1$-integrins), as assessed by cell-cell adhesion assay, required for T cell-antigen-presenting cell (APC) interaction. Furthermore, this compound did not block a simple activation of CD29, as assessed by cell-fibronectin adhesion assay. However, the compound did not diminish phagocytic uptake, an initial step for antigen processing, and ROS generation in RAW264.7 cells. In particular, to understand molecular mechanism of kaempferitrin-mediated inhibition, the regulatory role of LPS-induced signaling events was examined using immunoblotting analysis. Interestingly, this compound dose dependently suppressed the phosphorylation of $I{\kappa}B{\alpha}$, Src, Akt and Syk, demonstrating that it can negatively modulate the activation of these signaling enzymes. Therefore, our data suggested that kaempferitrin may be involved in regulating APC function-relevant immune responses of macrophages and monocytes by regulating intracellular signaling.

• Proceedings of the KOR-BRONCHOESO Conference
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• 1993.05a
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• pp.92-92
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• 1993

It is generally agreed that cellular immune functions are damaged by radiation therapy(RT). However, the exact effects of RT on peripheral lymphocytes are not yet clear. Authors previously reported the radiation effects on lymphocytes subpopulations, but these results merely showed the alteration of proportion of lymphocytes subpopulations after RT. So we try to evaluate the number of lymphocytes in each subpopulations as well as the proportion of subpopulations, and the recovery patterns of these alterations by time duraion after RT. The result shows that the proportion of subpopulations and number of lymphocytes in each subpopulations are decreased after RT except natural killer cells(NK cells), which proportion is increased but number is not changed, and these changes are stationary continued for post RT 6 months and then gradually recovered. However, the radiation effects on peripheral lymphocytes still remain after one year.

• Journal of Animal Science and Technology
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• v.56 no.7
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• pp.23.1-23.7
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• 2014

Background: Scanning of the genome for selection signatures between breeds may play important role in understanding the underlie causes for observable phenotypic variations. The discovery of high density single nucleotide polymorphisms (SNPs) provide a useful starting point to perform genome-wide scan in pig populations in order to identify loci/candidate genes underlie phenotypic variation in pig breeds and facilitate genetic improvement programs. However, prior to this study genomic region under selection in commercially selected Berkshire and Korean native pig breeds has never been detected using high density SNP markers. To this end, we have genotyped 45 animals using Porcine SNP60 chip to detect selection signatures in the genome of the two breeds by using the $F_{ST}$ approach. Results: In the comparison of Berkshire and KNP breeds using the FDIST approach, a total of 1108 outlier loci (3.48%) were significantly different from zero at 99% confidence level with 870 of the outlier SNPs displaying high level of genetic differentiation ($F_{ST}{\geq}0.490$). The identified candidate genes were involved in a wide array of biological processes and molecular functions. Results revealed that 19 candidate genes were enriched in phosphate metabolism (GO: 0006796; ADCK1, ACYP1, CAMK2D, CDK13, CDK13, ERN1, GALK2, INPP1; MAK, MAP2K5, MAP3K1, MAPK14, P14KB, PIK3C3, PRKC1, PTPRK, RNASEL, THBS1, BRAF, VRK1). We have identified a set of candidate genes under selection and have known to be involved in growth, size and pork quality (CART, AGL, CF7L2, MAP2K5, DLK1, GLI3, CA3 and MC3R), ear morphology and size (HMGA2 and SOX5) stress response (ATF2, MSRB3, TMTC3 and SCAF8) and immune response (HCST and RYR1). Conclusions: Some of the genes may be used to facilitate genetic improvement programs. Our results also provide insights for better understanding of the process and influence of breed development on the pattern of genetic variations.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.6
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• pp.463-468
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• 2012

Type 1 diabetes (T1D) is caused by dysregulation of the immune system in the pancreatic islets, which eventually leads to insulin-producing pancreatic ${\beta}$-cell death and destabilization of glucose homeostasis. One of the major characteristics of T1D pathogenesis is the production of inflammatory mediators by macrophages that result in destruction or damage of pancreatic ${\beta}$-cells. In this study the inflammatory microenvironment of T1D was simulated with RAW264.7 cells and MIN6 cells, acting as macrophages and pancreatic ${\beta}$-cells respectably. In this setting, peroxiredoxin-1, an anti-oxidant enzyme was knocked down to observe its functions in the pathogenesis of T1D. RAW264.7 cells were primed with lipopolysaccharide and co-cultured with MIN6 cells while PRX-1 was knocked down in one or both cell types. Our results suggest that hindrance of PRX-1 activity or the deficiency of this enzyme in inflammatory conditions negatively affects pancreatic ${\beta}$-cell survival. The observed decrease in viability of MIN6 cells seems to be caused by nitric oxide production. Additionally, it seems that PRX-1 affects previously reported protective activity of IL-6 in pancreatic ${\beta}$ cells as well. These results signify new, undiscovered roles for PRX-1 in inflammatory conditions and may contribute toward our understanding of autoimmunity.

• Korean Journal of Acupuncture
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• v.37 no.3
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• pp.145-158
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• 2020

Objectives : Mast cells, the multifunctional immune cells which can be activated by various stimulations, have been in the limelight recently at the fields of acupuncture research. This study aimed to investigate the association between the distribution of mast cell and acupoint specificity. We focused on the characteristics of mast cell distribution of acupoints in normal, pathologically sensitized, and acupoint-stimulated state. Methods : Literature searches were performed on PubMed and EMBASE for dates ranging to February 2019, by using terms "acupuncture", "moxibustion", "acupoint", "mast cell". Finally, 18 papers were collected by inclusion and exclusion criteria. To assess the quality of included studies, modified SYRCLE's risk of bias tool for animal studies was used. Results : Overall, the studies showed that the number of the mast cells was higher in acupoints than non-acupoints. After pathological sensitization, increasing tendency towards the mast cell number was reported in acupoints. The increase of mast cells was also observed after acupuncture or moxibustion. However, when the acupoint stimulation was repeated for several days in pathological models, the results did not show consistent tendency. In quality assessments, most of the studies showed unclear risk of bias. Conclusions : The studies showed a consistent trend about the association with mast cell distribution and acupoint specificity. However, we could not certainly affirm the relationship due to insufficient qualities of included studies. Not only the distribution but also the functions should be considered in further researches to identify the relationship between mast cells and acupuncture effect.