• Journal of Yeungnam Medical Science
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• v.24 no.2
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• pp.129-136
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• 2007

Purpose : To evaluate the chemokine expression in children with a non-productive cough. Materials and Methods : Six children with a non-productive cough who visited Yeungnam University Hospital were evaluated for the mRNA expression of interferon-${\gamma}$-inducible protein 10(IP-10), macrophage cationic protein 1 and 3 (MCP-1, 3), interleukin (IL)-8, regulated upon activation in normal T cells expressed and secreted (RANTES), eotaxin and growth-related oncogene-${\alpha}$ (Gro-${\alpha}$) using the reverse transcription polymerase chain reaction. Results : The chemokines IP-10 and MCP-3 were expressed in all samples. The chemokine RANTES was expressed in five cases, and IL-8 was expressed in three among them. However, eotaxin, Gro-${\alpha}$ and MCP-1 were not expressed at all. The expression of chemokine MCP-3, RANTES and IL-8 were suppressed after the resolution of coughing in just one available case. Conclusion : The chemokines MCP-3, RANTES and IL-8 may contribute to airway inflammation in children with a non-productive cough, whereas IP-10 is of secondary importance in this condition.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.5
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• pp.503-511
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• 2018

Lysophosphatidic acid (LPA) is known to play a critical role in breast cancer metastasis to bone. In this study, we tried to investigate any role of LPA in the regulation of osteoclastogenic cytokines from breast cancer cells and the possibility of these secretory factors in affecting osteoclastogenesis. Effect of secreted cytokines on osteoclastogenesis was analyzed by treating conditioned media from LPA-stimulated breast cancer cells to differentiating osteoclasts. Result demonstrated that IL-8 and IL-11 expression were upregulated in LPA-treated MDA-MB-231 cells. IL-8 was induced in both MDA-MB-231 and MDA-MB-468, however, IL-11 was induced only in MDA-MB-231, suggesting differential LPARs participation in the expression of these cytokines. Expression of IL-8 but not IL-11 was suppressed by inhibitors of PI3K, NF-kB, ROCK and PKC pathways. In the case of PKC activation, it was observed that $PKC{\delta}$ and $PKC{\mu}$ might regulate LPA-induced expression of IL-11 and IL-8, respectively, by using specific PKC subtype inhibitors. Finally, conditioned Medium from LPA-stimulated breast cancer cells induced osteoclastogenesis. In conclusion, LPA induced the expression of osteolytic cytokines (IL-8 and IL-11) in breast cancer cells by involving different LPA receptors. Enhanced expression of IL-8 by LPA may be via ROCK, PKCu, PI3K, and NFkB signaling pathways, while enhanced expression of IL-11 might involve $PKC{\delta}$ signaling pathway. LPA has the ability to enhance breast cancer cells-mediated osteoclastogenesis by inducing the secretion of cytokines such as IL-8 and IL-11.

• 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

• International Journal of Oral Biology
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• v.36 no.1
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• pp.23-29
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• 2011

Porphyromonas gingivalis, one of the major periodontal pathogens, is implicated in the initiation and progression of periodontal disease. The initial stages of periodontal inflammation are accompanied by vascular hyperpermeability. In our present study, we report that the P. gingivalis lipopolysaccharide (LPS) increases the mRNA expression of interleukin-8 (IL-8), a major inducer of vascular permeability, in vascular endothelial cells. P. gingivalis LPS also stimulated the induction of IL-8 secretion in endothelial cells. The P. gingivalis LPS-induced expression of IL-8 was primarily modulated by nuclear factor-${\kappa}$B(NF-${\kappa}$B). P. gingivalis LPS significantly enhanced the vascular permeability both in vitro and in vivo, and a blockade of the IL-8 receptor decreased the P. gingivalis LPS-induced vascular permeability. Taken together, these results suggest that P. gingivalis LPS increases vascular permeability through the NF-${\kappa}$B-dependent production of IL-8 in vascular endothelial cells.

• Tuberculosis and Respiratory Diseases
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• v.78 no.1
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• pp.8-17
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• 2015

Background: AMP-activated protein kinase (AMPK) not only functions as an intracellular energy sensor and regulator, but is also a general sensor of oxidative stress. Furthermore, there is recent evidence that it participates in limiting acute inflammatory reactions, apoptosis and cellular senescence. Thus, it may oppose the development of chronic obstructive pulmonary disease. Methods: To investigate the role of AMPK in cigarette smoke-induced lung inflammation and emphysema we first compared cigarette smoking and polyinosinic-polycytidylic acid [poly(I:C)]-induced lung inflammation and emphysema in $AMPK{\alpha}1$-deficient ($AMPK{\alpha}1$-HT) mice and wild-type mice of the same genetic background. We then investigated the role of AMPK in the induction of interleukin-8 (IL-8) by cigarette smoke extract (CSE) in A549 cells. Results: Cigarette smoking and poly(I:C)-induced lung inflammation and emphysema were elevated in $AMPK{\alpha}1$-HT compared to wild-type mice. CSE increased AMPK activation in a CSE concentration- and time-dependent manner. 5-Aminoimidazole-4-carboxamide-1-${\beta}$-4-ribofuranoside (AICAR), an AMPK activator, decreased CSE-induced IL-8 production while Compound C, an AMPK inhibitor, increased it, as did pretreatment with an $AMPK{\alpha}1$-specific small interfering RNA. Conclusion: $AMPK{\alpha}1$-deficient mice have increased susceptibility to lung inflammation and emphysema when exposed to cigarette smoke, and AMPK appears to reduce lung inflammation and emphysema by lowering IL-8 production.

• Animal Bioscience
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• v.35 no.6
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• pp.892-901
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• 2022

Objective: This study was performed to investigate the potential effect of wheat phytase on long-chain inorganic polyphosphate (polyP)-mediated interleukin 8 (IL-8) signaling in an intestinal epithelial cell line, HT-29 cells. Methods: Cell viability and the release of the pro-inflammatory cytokine IL-8 in HT-29 cells exposed to polyP1150 (average of 1,150 phosphate residues) treated with or without wheat phytase were measured by the EZ-CYTOX kit and the IL-8 ELISA kit, respectively. Also, the activation of cellular inflammatory factors NF-κB and MAPK (p38 and ERK 1/2) in HT-29 cells was investigated using ELISA kits. Results: PolyP1150 negatively affected the viability of HT-29 cells in a dose-dependent manner. However, 100 mM polyP1150 dephosphorylated by wheat phytase increased cell viability by 1.4-fold over that of the intact substrate. Moreover, the 24 h exposure of cells to enzyme-treated 50 mM polyP1150 reduced the secretion of IL-8 and the activation of NF-κB by 9% and 19%, respectively, compared to the intact substrate. PolyP1150 (25 and 50 mM) dephosphorylated by the enzyme induced the activation of p38 MAPK via phosphorylation to 2.3 and 1.4-fold, respectively, compared to intact substrate, even though it had little effect on the expression of ERK 1/2 via phosphorylation. Conclusion: Wheat phytase could attenuate polyP1150-induced IL-8 release in HT-29 cells through NF-κB, independent of MAP kinases p38 and ERK. Thus, wheat phytase may alleviate inflammatory responses including hypercytokinemia caused by bacterial polyP infection in animals. Therefore, wheat phytase has the potential as an anti-inflammatory therapeutic supplement in animal husbandry.

• Journal of Pharmacopuncture
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• v.7 no.2
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• pp.19-28
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• 2004

봉독은 관절염 치료를 비롯한 여러 질환에 그 응용범위가 넓어지고 있으며 기전규명과 새로운 치료효과 개발을 위한 연구가 필요하다. 연골의 파괴는 진행된 각종 관절병증의 공통 병리기전이며 연골세포의 기능이상은 이 기전에 중요한 의미를 지닌다. 사람 연골세포의 특성을 유지하고 있는 HTB-94 연골육종세포를 배양하고 봉독을 처치했을 때의 유전자 발현양상을 microarray를 이용하여 관찰하였다. 대조군에 비해 4배 이상 발현의 차이가 있는 경우를 유의한 것으로 보았을 때 microarray의 344개 유전자중 봉독처치시 발현이 증강되는 유전자는 없었으며 발현이 억제되는 유전자는 interleukin 6 receptor, interleukin 1 alpha, tissue inhibitor of metalloproteinase 1, matrix metalloproteinase 1, tumor necrosis factor (ligand) superfamily, members 4, 8 and 12, and caspases 2, 6, and 10등 35개가 관찰되었다. Microarray를 통한 유전자발현 분석을 통해 관절염에 대한 봉독치료의 기전을 시사하는 유용한 자료를 얻을 수 있었으며 앞으로 보다 넓은 범위에 대한 연구가 필요할 것이다.

• Journal of Microbiology and Biotechnology
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• v.18 no.8
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• pp.1423-1426
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• 2008

Nuruk, which is a natural inoculator and source of amylolytic enzymes, is used in Korean traditional rice wine. A methanol extract of nuruk (NE) attenuated lipopolysaccharide (LPS)-induced nitrite and interleukin (IL)-6 in RAW 264.7 cells. Both the n-hexane and water fractions from NE (MEH and MW, respectively) inhibited the production of nitrite and IL-6 in RAW 264.7 cells. MEH and MW also inhibited the LPS-induced inducible nitric oxide synthase expression. Further, and MEH protected against the LPS-induced activation of p38 mitogen-activated protein kinase. Together, these results indicate that nuruk may contribute to the anti-inflammatory and cancer-preventive effects of Korean traditional rice wine.

• Journal of Korean Neurosurgical Society
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• v.57 no.4
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• pp.235-241
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• 2015

Objective : Magnetic resonance imaging (MRI) of chronic subdural hematoma (CSDH) detects various patterns, which can be attributed to many factors. The purpose of this study was to measure the level of interleukin-6 (IL-6), interleukin-8 (IL-8), and highly specific protein [beta-trace protein (${\beta}TP$)] for cerebrospinal fluid (CSF) in CSDHs, and correlate the levels of these markers with the MRI findings. Methods : Thirty one patients, treated surgically for CSDH, were divided on the basis of MRI findings into hyperintense and non-hyperintense groups. The concentrations of IL-6, IL-8, and ${\beta}TP$ in the subdural fluid and serum were measured. The ${\beta}TP$ was considered to indicate an admixture of CSF to the subdural fluid if ${\beta}TP$ in the subdural fluid $({\beta}TP_{SF})/{\beta}TP$ in the serum $({\beta}TP_{SER})>2$. Results : The mean concentrations of IL-6 and IL-8 of the hyperintense group (n=17) of T1-WI MRI were $3975.1{\pm}1040.8pg/mL$ and $6873.2{\pm}6365.4pg/mL$, whereas them of the non-hyperintense group (n=14) were $2173.5{\pm}1042.1pg/mL$ and $2851.2{\pm}6267.5pg/mL$ (p<0.001 and p=0.004). The mean concentrations of ${\beta}TP_{SF}$ and the ratio of ${\beta}TP_{SF}/{\beta}TP_{SER}$ of the hyperintense group (n=13) of T2-WI MRI were $7.3{\pm}2.9mg/L$ and $12.6{\pm}5.4$, whereas them of the non-hyperintense group (n=18) were $4.3{\pm}2.3mg/L$ and $7.5{\pm}3.9$ (p=0.011 and p=0.011). Conclusion : The hyperintense group on T1-WI MRI of CSDHs exhibited higher concentrations of IL-6 and IL-8 than non-hyperintense group. And, the hyperintese group on T2-WI MRI exhibited higher concentrations of ${\beta}TP_{SF}$ and the ratio of ${\beta}TP_{SF}/{\beta}TP_{SER}$ than non-hyperintense group. These findings appear to be associated with rebleeding and CSF admixture in the CSDHs.

• Tuberculosis and Respiratory Diseases
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• v.47 no.2
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• pp.161-171
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• 1999

Background: Interleukin-12 (IL-12) can induce antitumor effects in vivo. This antitumor effect is associated with T cell infiltration but the effect of IL-12 on the steps of T cell migration into the tumor tissue has not been fully elucidated. This study focused on the effect of IL-12 on the tumor growth and the metastasis and on the expression of E-selectin, an adhesion molecule which is activated endothelial specific in its expression. In addition, we studied whether the expression of E-selectin is associated with the TNF-$\alpha$, a cytokine that its production is increased by IL-12 and has functions inducing a variety of adhesion molecules. Methods: Mice of C57BL/6 strain were injected with Lewis lung cancer cells followed by either IL-12, TNF-$\alpha$, or normal saline by intraperitoneal route. Twenty eight days after tumor cell inoculation, metastatic nodules of lung were enumerated and immunohistochemical staining of the subcutaneous tumors were performed with monoclonal antibodies to CD4, CD8, CD16, and E-selectin. In IL-12 treated mice, the subcutaneously implanted Lewis lung tumors were decreased in size and the metastases were also decreased in number compared to control mice. On tumor tissues, increased infiltration of CD4+, CD8+, and CD16+ cells were oberved in IL-12 treated mice compared to control mice. In control mice, E-selectin was absent on tumor vessels, but the expression of E-selectin was increased on tumor vessels of IL-12 treated mice. Administration of TNF-$\alpha$ increased not only the expression of E-selectin but also infiltrations of CD4+, CD8+, and CD16+ cells on tumor tissues. Conclusions: These results demonstrate that IL-12 inhibits tumor growth and metastases through infiltrations of inflammatory cells in mouse model of Lewis lung carcinoma and E-selectin may playa role in inflammatory cell recruitment on tumor tissue following IL-12 administration. Also, TNF-$\alpha$ may have a role as a mediator responsible for the IL-12 induced expression of E-selectin.