• Nutrition Research and Practice
• /
• v.5 no.2
• /
• pp.101-106
• /
• 2011

The hawthorn fruit (Crataegus pinnatifida Bunge var. typica Schneider) is used as a traditional medicine in Korea. The objective of this study was to understand the mechanisms of the anti-inflammatory effects of the water fractionated portion of hawthorn fruit on a lipopolysaccharide (LPS)-stimulated RAW 264.7 cellular model. The level of nitric oxide (NO) production in the water fraction and LPS-treated RAW 264.7 cells were determined with an ELISA. The cytotoxicity of the water fraction and LPS was measured with an MTT assay. Expression of nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor (TNF)-${\alpha}$, interleukin 6 (IL-6), and interleukin $1{\beta}$ (IL-$1{\beta}$) mRNA were analyzed with a reverse transcription polymerase chain reaction (RT-PCR). The water fraction of hawthorn fruit was determined to be safe and significantly inhibited NO production in LPS-stimulated RAW 264.7 cells and suppressed COX-2, (TNF)-${\alpha}$, IL-$1{\beta}$, and IL-6 expression. The observed anti-inflammatory effects of the water fraction of hawthorn fruit might be attributed to the down-regulation of COX-2, (TNF)-${\alpha}$, IL-$1{\beta}$, and IL-6 expression in LPS-stimulated RAW 264.7 cells.

• BMB Reports
• /
• v.52 no.3
• /
• pp.165-174
• /
• 2019

Interleukin-32 (IL-32) was originally identified in natural killer (NK) cells activated by IL-2 in 1992. Thus, it was named NK cell transcript 4 (NK4) because of its unknown function at that time. The function of IL-32 has been elucidated over the last decade. IL-32 is primarily considered to be a booster of inflammatory reactions because it is induced by pro-inflammatory cytokines and stimulates the production of those cytokines and vice versa. Therefore, many studies have been devoted to studying the roles of IL-32 in inflammation-associated cancers, including gastric, colon cancer, and hepatocellular carcinoma. At the same time, roles of IL-32 have also been discovered in other cancers. Collectively, IL-32 fosters the tumor progression by nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$)-mediated cytokines and metalloproteinase production, as well as stimulation of differentiation into immunosuppressive cell types in some cancer types. However, it is also able to induce tumor cell apoptosis and enhance NK and cytotoxic T cell sensitivity in other cancer types. In this review, we will address the function of each IL-32 isoform in different cancer types studied to date, and suggest further strategies to comprehensively elucidate the roles of IL-32 in a context-dependent manner.

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

• Herbal Formula Science
• /
• v.21 no.2
• /
• pp.81-89
• /
• 2013

Objectives : The purpose of this study is to observe the effect of Coptidis Rhizoma (CCE-extract of C. chinensis Rhizome) in induction of immune protein on mouse macrophages. Methods : To analyze cytokines interleukin(IL)-$1{\alpha}$, IL-3, IL-9, IL-12p40, IL-13, IL-17, Monocyte Chemoattractant Protein(MCP)-1 induced by macrophages, mouse macrophages were incubated with CCE and was measured. Results : IL-$1{\alpha}$ measurement, CCE showed significant inhibition only at concentration level of 200 ${\mu}g/mL$. IL-3, MCP-1 measurement, CCE showed significant inhibition only at concentration level of 100, 200 ${\mu}g/mL$. IL-9 measurement, CCE showed significant inhibition only at concentration level of 50 ${\mu}g/mL$. IL-13 measurement, CCE showed significant inhibition only at concentration level of 50, 100, 200 ${\mu}g/mL$. The IL-12p40, IL-17 levels indicated no changes at 25, 50, 100, 200 ${\mu}g/mL$ on mouse macrophages. Conclusions : CCE did not significantly increased inflammatory cytokines IL-$1{\alpha}$, IL-3, IL-9, IL-12p40, IL-13, IL-17, Monocyte Chemoattractant Protein(MCP)-1 on mouse macrophages. It was verified CCE does not trigger cytokine related hypersensitivity reaction of organism or exacerbation of acute/chronic inflammatory disease.

• Biomedical Science Letters
• /
• v.26 no.4
• /
• pp.344-350
• /
• 2020

Asthma is a chronic disease and occurs in airway in the lung. The cause of the disease has not been identified, it is assumed that both genetic and environmental risk factors play an important role in the development of asthma. Interleukin (IL)-12 is a cytokine regulating T-cell and NK cell. In this study, we analyzed the genetic polymorphisms of IL-12 receptor genes (IL-12Rβ1 and IL-12Rβ2) in asthma patients and normal individuals in a Korean population. We analyzed single nucleotide polymorphisms (SNPs) in IL-12Rβ1 and IL-12Rβ2 using the genotype data of 193 asthma cases and 3,228 healthy controls from the Korea Association REsource for their correlation with asthma case. IL-12Rβ1 and IL-12Rβ2 genes showed statistically significant polymorphism association with asthma case. As a results, 16 SNPs from IL-12Rβ1 and IL-12Rβ2 genes showed statistically significant association with asthma. Among them, rs375947 SNP in IL-12Rβ1 showed the greatest statistical correlation with asthma (P-value = 0.028, Odds Ratio = 1.27, 95% Confidence Interval = 1.03~1.57). The groups with minor allele of IL-12Rβ1 and IL-12Rβ2 showed increased risk of asthma. The genotype-based mRNA expression analysis showed that the group of minor allele of IL-12Rβ1 showed decreased mRNA expression. Decreased IL-12Rβ1 expression causes decreased IL-12 signaling, and this affects developing asthma. In conclusion, the SNPs in IL-12Rβ1 and IL-12Rβ2 may contribute to development of asthma in a Korean population.

• BMB Reports
• /
• v.50 no.9
• /
• pp.472-477
• /
• 2017

The transcription repressor Bach2 has been proposed as a regulator of T cell quiescence, but the underlying mechanism is not fully understood. Given the importance of interleukin-2 in T cell activation, we investigated whether Bach2 is a component of the network of factors that regulates interleukin-2 expression. In primary and transformed $CD4^+$ T cells, Bach2 overexpression counteracted T cell receptor/CD28- or PMA/ionomycin-driven induction of interleukin-2 expression, and silencing of Bach2 had the opposite effect. Luciferase and chromatin immunoprecipitation assays revealed that Bach2 binds to multiple Maf-recognition element-like sites on the interleukin-2 proximal promoter in a manner competitive with AP-1, and thereby represses AP-1-driven induction of interleukin-2 transcription. Thus, this study demonstrates that Bach2 is a direct repressor of the interleukin-2 gene in $CD4^+$ T cells during the immediate early phase of AP-driven activation, thereby playing an important role in the maintenance of immune quiescence in the steady state.

• IMMUNE NETWORK
• /
• v.24 no.1
• /
• pp.6.1-6.17
• /
• 2024

The intricate role of innate type-2 cytokines in immune responses is increasingly acknowledged for its dual nature, encompassing both protective and pathogenic dimensions. Ranging from defense against parasitic infections to contributing to inflammatory diseases like asthma, fibrosis, and obesity, these cytokines intricately engage with various innate immune cells. This review meticulously explores the cellular origins of innate type-2 cytokines and their intricate interactions, shedding light on factors that amplify the innate type-2 response, including TSLP, IL-25, and IL-33. Recent advancements in therapeutic strategies, specifically the utilization of biologics targeting pivotal cytokines (IL-4, IL-5, and IL-13), are discussed, offering insights into both challenges and opportunities. Acknowledging the pivotal role of innate type-2 cytokines in orchestrating immune responses positions them as promising therapeutic targets. The evolving landscape of research and development in this field not only propels immunological knowledge forward but also holds the promise of more effective treatments in the future.

• Tuberculosis and Respiratory Diseases
• /
• v.41 no.2
• /
• pp.135-143
• /
• 1994

Background: The cell mediated immunity has an important role in the pathogenesis of tuberculosis. sIL-2R has been known as a sensitive marker of T lymphocyte activation Elevated serum levels of sIL-2R have been found in patients with lymphoproliferative disorders, organ transplantation, autoimmune diseases, and various granulomatous diseases. Elevated levels of sIL-2R have been also found in the serum and pleural fluid of the patients with tuberculosis. To evaluate the diagnostic value of sIL-2R in the differentiation of tuberculous pleurisy and nontuberculous pleurisy. We measured the level of sIL-2R in the sera and pleural fluids of 12 patients with tuberculous pleurisy and 32 patients with nontuberculous pleurisy. Method: Samples of pleural fluid and serum were centrifuged at 2500 rpm for 10 min to remove cell pellets. Soluble IL-2R was measured with a sandwitch enzyme immunoassay using the Cellfree(r) Interleukin-2 Receptor Test kit(T-cell science,Inc. Cambridge, MA). Results: The results obtained were as follows: 1) The sIL-2R level in pleural fluid of the patients with tuberculous pleurisy was higher than that of patients with nontuberculous pleurisy(P<0.005). 2) When the sIL-2R level above 5,000 u/ml in pleural fluid was used as the cut-off value to diagnose tuberculous pleurisy, it had a sensitivity of 84.6% and a specificity of 90.9%. 3) The sIL-2R level in the sera of the patients with tuberculous pleurisy was higher than that of patients with bacterial pleural effusions and normal control group(P<0.05) and there was no difference of levels compared with malignant pleural effusions and transudative pleural effusions(P>0.05). 4) In patients with tuberculous pleurisy, the mean concentration of sIL-2R in pleural fluid was higher than that in serum(P<0.005). Conclusion: These findings suggest that the measurement of elevated levels of pleural fluid sIL-2R in tuberculous pleurisy may be useful in the differential diagnosis between patients with tuberculous pleurisy and nontuberculous pleurisy.

• Journal of Pharmacopuncture
• /
• v.5 no.1 s.8
• /
• pp.135-151
• /
• 2002

Objective: This study was eanied out to investigate the effects of Raphani Semen on immuno-response in the mouse model of allergic asthma. Methods: In this study, BALB/C mice were divided into 6 groups: Normal (Non-treated group), Control (Group with not treated after allergic sensitization and induction by ovalbumin), Treat I (Group with the oral administration of saline after allergic sensitization and induction by ovalbumin), Treat n (Allergic asthma group treated with acupuncture (BL 13)), Treat III (Allergic asthma group treated with the oral administration of Raphani Semen) and Treat lV (Allergic asthma group treated with the herbal-acupuncture of Raphani Semen (BL 13)). The effect on cytokine was assessed by measuring cytokine (lL-2, IL-4, IL-5, IL-10, IL-12, IFN-r) in bronchoalveoar lavage fluid(ELISA). ResuJts : The results obtained as follows: 1. The production of Interleukin-2 was decreased significantly in Treat I group, Treat n group and Treat IV group as compared with Control group. 2. The production of Interleukin-4 was decreased significantly in Treat I group, Treat II group and Treat IV group as compared with Control group. Among them. the production of Interleukin-4 was decreased remarkably in Treat IV group as compared with other groups. 3. The production of Interleukin-5 was decreased significantly in Treat I group and Treat IV group as compared with Control group. 4. The production of Interleukin-10 was decreased significantly in Treat I group and Treat III group as compared with Control group. 5. The production of Interleukin-12 was all decreased significantly in Treat I group, Treat n group, Treat m group and Treat IV group as compared with Control group. 6. The production of Intelferon- showed no significant changes in Treat I group, Treat n group. Treat m group and Treat Ⅳ group as compared with Control group. Conclusion: These results show that the production of Interleukin-4, 5 was decreased significantly in aJlergic asthma group treated with the herbal-acupuncture of Raph Semen (BL 13), It is known that inactivity of Th2 cell constrained the revelation and controlled hypersenstive action. As to this mechanism, it is suggested that the herbal-acupuncture of Raphani Semen(BL 13) constrained the revelation of allergic asthma.

• Journal of Life Science
• /
• v.20 no.4
• /
• pp.474-480
• /
• 2010

Rutin, a group II phospholipase $A_2$ ($PLA_2$) inhibitor, was tested on interleukin-1 (IL-1) induced acute lung injury (ALI) in male Sprague-Dawley rats. Rutin did not alter the increased lung myeloperoxidase activity by IL-1. However, the number of neutrophils in bronchoalveolar lavage fluid (BALF) and IL-1 induced lung leak were decreased by rutin (p<0.001). Simultaneously, rutin decreased lung $PLA_2$ activity, which was increased by IL-1 (p<0.001). The reduction of neutrophilic respiratory burst by the inhibition of $PLA_2$ was confirmed by group II $PLA_2$ inhibitors such as rutin, manoalide and scalaradial. The increased level of cytokine-induced neutrophilic chemoattractant (CINC) in BALF by IL-1 was not affected by rutin. Ultrastructural changes of ALI and increased generation of free radicals in the lung by IL-1 were found, and rutin ameliorated these pathological findings. Taken together, rutin seems to be effective in decreasing IL-1 induced ALI through inhibition of group II $PLA_2$.