• Biomedical Science Letters
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• v.28 no.3
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• pp.192-194
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• 2022

The trophic factor Neuregulin-1 (NRG-1) plays a critical role in the development of the peripheral nervous system and the repair of nerve injuries. The regulation of neutrophil apoptosis by cytokine secretion from structural cells is an important process in inflammatory diseases, including asthma. This study aimed to investigate the relationship between NRG-1 and the alteration of neutrophil apoptosis by the regulation of cytokine release in the human lung epithelial BEAS-2B cells. Tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) induce the increase in the release of interleukin (IL)-6, IL-8, and monocyte chemoattractant protein-1 (MCP-1). NRG-1 alone had no effect on the secretion of IL-6, IL-8, and MCP-1. However, co-treatment of TNF-α and IFN-γ with NRG-1 inhibited the secretion of IL-6, IL-8, and MCP-1 that had been increased by TNF-α and IFN-γ. Treatment with NRG-1 did not have a direct effect on neutrophil apoptosis. Co-treatment of TNF-α and IFN-γ with NRG-1 was not effective on suppression of neutrophil apoptosis due to TNF-α and IFN-γ. The supernatant of BEAS-2B cells after co-treatment of TNF-α and IFN-γ with NRG-1 suppressed the inhibition of neutrophil apoptosis that had been caused due to the supernatant treated with TNF-α and IFN-γ. Taken together, NRG-1 has an anti-inflammatory effect in an inflammatory milieu by the regulation of cytokine secretion and neutrophil apoptosis.

• Korean Journal of Pharmacognosy
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• v.48 no.1
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• pp.18-24
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• 2017

This study was conducted to determine the anti-inflammatory effect of essential oil extracted from the wood of Chamaecyparis obtusa Sieb. et Zucc. Endl. (Cupressaceae). The essential oil was extracted from the wood of C. obtusa by hydrodistillation method, and conducted the analysis on the chemical composition of the extracted C. obtusa wood oil through GC-MS. The major constituents of the oil were found to be: ${\alpha}-pinene$ (11.4%), cadinene (5.4%), ${\delta}-cadiene$ (9.0%), ${\tau}-muurolol$ (22.2%), ${\alpha}-cadinol$ (20.8%) etc. We attempted to identify the anti-inflammatory activities of the oil when it is injected in the lipopolysaccharide (LPS)-stimulated RBL-2H3 cells, along with its effects on the secretion of interleukin-4 (IL-4), interleukin-13 (IL-13), ${\beta}-hexosaminidase$. According to the cell viability analysis conducted by MTT assay, the oil in $10^{-7}{\sim}10^{-5}%$concentration showed no effect on the cell viability. After RBL-2H3 cells treated by LPS stimulation were exposed to $10^{-7}%$ concentration of C. obtusa wood oil, the expression levels of IL-4, IL-13 within the cell were observed to remarkably decrease. Also, it was attenuated the release of ${\beta}-hexosaminidase$ from mast cells to a significantly meaningful level. These results suggest that C. obtusa wood oil exerts the anti-inflammatory effect, by regulating the expression of inflammatory cytokines, which is a valuable feature to be highly utilized as the functional materials in the future.

• The korean journal of orthodontics
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• v.24 no.4 s.47
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• pp.871-883
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• 1994

This experiment was designed to study possible roles of $interleukin-1\beta$, interleukin-6 and tumor necrosis $factor-\alpha$ in bone remodeling by measuring their effects on $PGE_2,\; LTB_4$ and collagenase production when they were administered to human periodontal ligament fibroblasts. Human periodontal ligament fibroblasts were collected from first premolars extracted for orthodontic treatment. They were incubated in the environment of $37^{\circ}C,\;5\%\;Co^2,\;and\;100\%$ humidity. They were treated with $0.25\%$ trypsin-EDTA solution and centrifuged. PDL cells in the fifth to seventh passage were used for the experiment. Cells were seeded onto the culture dishes and when they were successfully attached, human recombinant $interleukin-1\beta$, interleukin-6, and tumor necrosis $factor-\alpha$ were administered, alone or in combination. They were incubated for 4, 8 and 24 hours and the levels of $PGE_2,\;LTB_4$ and collagenase released into the culture media were assessed by enzymeimmunoassay and collagenase activity assay. The conclusions are as follows: 1. $IL-1\beta\;and\;TNF-\alpha$ were very active in stimulating the production of $PGE_2$ and collagenase by human periodontal ligament fibroblasts, while IL-6 increased $LTB_4$ production. 2. $IL-1\beta$ significantly increased $PGE_2$, but $LTB_4$ Production was not increased. $IL-1\beta$ is thought to act mainly via the cyclooxygenase pathway of arachidonic acid metabolism. 3. IL-6 tended to inhibit $IL-1\beta$ in the production of $PGE_2$ and collagense whereas IL-6 and $TNF-\alpha$ showed auditive effect in the level of $PGE_2$. The above cytokines increased the release of at least one of $PGE_2,\;LTB_4$ and collagenase. It suggests that cytokines are involved in bone remodeling process by stimulating PDL fibroblasts to produce various bone-resorptive agents. The roles of cytokines in bone remodeling as a whole would need further study.

• Proceedings of the Korean Society of Life Science Conference
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• 2003.10a
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• pp.77-77
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• 2003

• IMMUNE NETWORK
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• v.13 no.5
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• pp.213-217
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• 2013

Enterotoxigenic Bacteroides fragilis (ETBF) is a human gut commensal bacteria that causes inflammatory diarrhea and colitis. ETBF also promotes colorectal tumorigenesis in the Min mouse model. The key virulence factor is a secreted metalloprotease called B. fragilis toxin (BFT). BFT induces E-cadherin cleavage, cell rounding, activation of the ${\beta}$-catenin pathway and secretion of IL-8 in colonic epithelial cells. However, the precise mechanism by which these processes occur and how these processes are interrelated is still unclear. E-cadherin form homophilic interactions which tethers adjacent cells. Loss of E-cadherin results in detachment of adjacent cells. Prior studies have suggested that BFT induces IL-8 expression by inducing E-cadherin cleavage; cells that do not express E-cadherin do not secrete IL-8 in response to BFT. In the current study, we found that HT29/C1cells treated with dilute trypsin solution induced E-cadherin degradation and IL-8 secretion, consistent with the hypothesis that E-cadherin cleavage causes IL-8 secretion. However, physical damage to the cell monolayer did not induce IL-8 secretion. We also show that EDTA-mediated disruption of E-cadherin interactions without E-cadherin degradation was sufficient to induce IL-8 secretion. Finally, we determined that HT29/C1 cells treated with LiCl (${\beta}$-catenin activator) induced IL-8 secretion in a dose-dependent and time-dependent manner. Taken together, our results suggest that BFT induced IL-8 secretion may occur by the following process: E-cadherin cleavage, disruption of cellular interactions, activation of the ${\beta}$-catenin pathway and IL-8 expression. However, we further propose that E-cadherin cleavage per se may not be required for BFT induced IL-8 secretion.

• Clinical and Experimental Pediatrics
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• v.51 no.10
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• pp.1096-1101
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• 2008

Purpose : Patients with chronic granulomatous disease (CGD) have genetic mutations in a component of the NADPH oxidase enzyme that is necessary for the generation of the superoxide anion. The profound defect in innate immunity is reflected by the patients susceptibility to catalase-positive bacteria and fungi. In addition, CGD patients display signs of persistent inflammation, which is not associated only with deficient superoxide anion production. The aim of this study was to elucidate the cytokine responses in CGD patients after $TNF-{\alpha}$ stimulation. Methods : Heparinized blood samples were collected from 8 CGD patients and 10 healthy volunteers. Monocytes ($1{\times}10^6cell/well$) isolated by the magnet cell isolation system were incubated with a constant amount of $TNF-{\alpha}$ (10 ng/mL) at $37^{\circ}C$ for 6 h. Incubated cells were harvested at 60-min intervals for IL-8 and IL-10 mRNA analysis, and the supernatant was collected at the same intervals to determine IL-8 and IL-10 expression. Monocytes from healthy volunteers were also incubated with antioxidants followed by $TNF-{\alpha}$ stimulation for IL-8 and IL-10 expression. Results : In CGD patients, a high expression of IL-8 together with a significantly higher IL-10 expression than in the healthy controls was seen after $TNF-{\alpha}$ stimulation. Moreover, normal monocytes treated with antioxidants exhibited increased IL-8 responses. Conclusion : The absence of phagocyte-derived reactive oxidants in CGD might be associated with a dysregulated production of pro- and antiinflammatory cytokines. Additional research related to reactive oxidants is needed to clarify the role of cytokines in CGD patients.

• Biomedical Science Letters
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• v.14 no.4
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• pp.219-223
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• 2008

The present study was designed to clarify whether scuba diving at 5 meters of seawater influences cerebral hemodynamics, hematological and biochemical variables. Twenty healthy young men well trained scuba diving participated in this study. The blood flow velocity in the right and left middle cerebral arteries (L-MCAV and R-MCAV), blood pressure (BP), heart rate (HR), CBC and differential count, prothrombin time (PT), activated partial thromboplastin time (aPTT), biochemical variables, D-dimer and interleukin-8 (IL-8) levels were determined before, immediately after scuba diving for 30 min, and after 30 min of rest (Pre-scuba, Scuba and R-30m, respectively). L-MCAV and R-MCAV tended to increase, but the only significant increase was in L-MCAV in Scuba. SBP and HR significantly declined in R-30m compared with those of Pre-scuba and the Scuba. IL-8 levels were elevated in Scuba and R-30m compared with that of Pre-scuba. In Scuba and R-30m, hematological variables except PT and biochemical parameters excluding glucose and lactic acid did not significantly changed in comparison with those of Pre-scuba. PT level at Scuba and glucose level at R-30m significantly declined in Scuba, while lactate level at R-30m increased compared with each in Pre-scuba. However, PT level at Scuba was within a normal range. These results suggest that scuba diving at 5 m of seawater for 30 min has no adverse effects, is safe and useful for improving health. However, further study must be performed to clarify the mechanism of elevated IL-8 level following scuba diving.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.24 no.4
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• pp.377-383
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• 2021

Purpose: We investigated the association of effector memory (EM) CD8⁺ T cell and CD4⁺ T cell immunity with metabolic syndrome (MS). Methods: Surface and intracellular staining of peripheral blood mononuclear cells was performed. Anti-interleukin-7 receptor-alpha (IL-7Rα) and CX3CR1 antibodies were used to stain the subsets of EM CD8⁺ T cells, while anti-interferon-gamma (IFN-γ), interleukin-17 (IL-17), and forkhead box P3 (FOXP3) antibodies were used for CD4⁺ T cell subsets. Results: Of the 47 obese children, 11 were female. Children with MS had significantly higher levels of serum insulin (34.8±13.8 vs. 16.4±6.3 µU/mL, p<0.001) and homeostasis model assessment of insulin resistance (8.9±4.1 vs. 3.9±1.5, p<0.001) than children without MS. Children with MS revealed significantly higher frequencies of IL-7Rα^low CD8⁺ T cells (60.1±19.1% vs. 48.4±11.5%, p=0.047) and IL-7Rα^lowCX3CR1⁺ CD8⁺ T cells (53.8±20.1% vs. 41.5±11.9%, p=0.036) than children without MS. As the serum triglyceride levels increased, the frequency of IL-7Rα^lowCX3CR1⁺ and IL-7Rα^highCX3CR1^- CD8⁺ T cells increased and decreased, respectively (r=0.335, p=0.014 and r=-0.350, p=0.010, respectively), in 47 children. However, no CD4⁺ T cell subset parameters were significantly different between children with and without MS. Conclusion: In obese children with MS, the changes in immunity due to changes in EM CD8⁺ T cells might be related to the morbidity of obesity.

• Journal of Community Nutrition
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• v.7 no.1
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• pp.42-48
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• 2005

This study was done to investigate effects of antioxidant supplementation on phytohemagglutinin (PHA) -stimulated interleukin-2 (IL-2) production by peripheral blood mononuclear cells (PBMCs) in elderly women. This study was designed as a placebo-controlled, single-blinded, randomized intervention trial. Twenty four elderly women aged over 60 years, visitings social welfare center in Seoul were divided into 3 groups, placebo (n = 8), vitamin C supplemented (n = 8) , and vitamin E supplemented (n = 8) groups. Experimental groups were given either 1000mg of L-ascorbic acid or 400 ill of d- $\alpha$-tocopherol for 4 weeks. There was no significant difference in antioxidant vitamins intakes and their plasma levels among pre-intervention groups. Plasma vitamin C or E levels was significantly increased after vitamin C or E sup-plementations. The increases of plasma thiobarbituric acid-reactive substance (TBARS) levels in the placebo group were significantly higher than those of the supplemented 2 groups. There were no significant differences in the changes of plasma IL-2 level between pre- and post-intervention among the 3 groups. However there was a significant increase in PHA­stimulated IL-2 production by PBMCs after 4-week vitamin E or vitamin C supplementation. Particularly, vitamin E supplemented group showed a higher PHA-stimulated IL-2 production than vitamin C supplemented group. These results indicate that vitamin E or vitamin C supplementation might enhance mitogen-stimulated cytokine production by immune cells, which could be one of the factors to improve health status in the elderly.

• Clinical and Experimental Pediatrics
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• v.52 no.2
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• pp.234-241
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• 2009

Purpose : We investigated the relationship between thyroid hormone and serum tumor necrosis factor (TNF-${\alpha}$), interleukin (IL-6) and N-terminal fragment of pro-brain natriuretic peptide (NT-proBNP) in patients with Kawasaki disease (KD). Methods : Serum levels of thyroid hormone, TNF-${\alpha}$, IL-6, and NT-proBNP were measured in 52 KD patients in the acute and subacute phase and 10 patients with acute febrile illness (control group). TNF-${\alpha}$ and IL-6 were determined by sandwich enzyme-linked immunosorbent assay (ELISA). Echocardiography was performed to detect coronary artery lesions (CAL) in KD patients. Results : Low $T_3$ syndrome occurred in 63.5% of KD patients. $T_3$ in the acute phase of KD was lower than that in the control. In KD patients, $T_3$ was lowered in the acute phase and elevated in the subacute phase, whereas TNF-${\alpha}$, IL-6 and NT-proBNP were elevated in the acute phase and decreased in the subacute phase. NT-proBNP, and IL-6 were higher in patients with low $T_3$ than in those with normal $T_3$. In addition, $T_3$ inversely correlated with IL-6 and NT-proBNP. Of the 4 patients with CAL, 3 had very low $T_3$. Compared with intravenous immunoglobulin (IVIG)-responsive patients, IVIG-resistant patients had lower $T_3$ and higher IL-6 and NT-proBNP. Conclusion : $T_3$ decreases in the acute phase of KD and normalizes in the subacute phase without thyroid hormone replacement. Low $T_3$ may be partially induced by IL-6 rather than TNF-${\alpha}$, and is strongly associated with high NT-proBNP. $T_3$ in KD may be used for the differential diagnosis, monitoring the activity of the disease, and predicting the severity of inflammation.