• Asian Pacific Journal of Cancer Prevention
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• v.15 no.20
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• pp.8741-8747
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• 2014

Purpose: We aimed to investigate the associations between polymorphisms of interleukin-1A (IL-1A), IL-1B, and IL-1 receptor antagonist (IL-1RN) and prostate cancer (PCa) risk. Materials and Methods: A comprehensive search for articles of MEDLINE and EMBASE databases and bibliographies of retrieved articles published up to August 3, 2014 was performed. Methodological quality assessment of the trials was based on a standard quality scoring system. The meta-analysis was performed using STATA 12.0. Results: We included 9 studies (1 study for IL-1A, 5 studies for IL-1B, and 3 studies for IL-1RN), and significant association was found between polymorphisms of IL-1B-511 (rs16944) as well as IL-1B-31 (rs1143627) and PCa risk. IL-1B-511 (rs16944) polymorphism was significantly associated with PCa risk in homozygote and recessive models, as well as allele contrast (TT vs CC: OR, 0.74; 95%CI, 0.58-0.94; P=0.012; TT vs TC+CC; OR, 0.79; 95%CI, 0.63-0.98; P=0.033; T vs C: OR, 0.86; 95%CI, 0.77-0.96; P=0.008). The association between IL-1B-31 (rs1143627) polymorphism and PCa risk was weakly significant under a heterozygote model (OR, 1.35; 95%CI, 1.00-1.80; P=0.047). Conclusions: Sequence variants in IL-1B-511 (rs16944) and IL-1B-31 (rs1143627) are significantly associated with PCa risk, which provides additional novel evidence that proinflammatory cytokines and inflammation play an important role in the etiology of PCa.

• Tuberculosis and Respiratory Diseases
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• v.48 no.4
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• pp.464-470
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• 2000

Background : The recognition of bronchial asthma as an inflammatory disease led to the search for soluble markers that would be useful in assessing airway inflammation. Interleukin-6 (IL-6) is a representative proinflammatory cytokine that has been shown to be connected with various inflammatory diseases. IL-6 acts via specific receptors that consist of the IL-6 binding glycoprotein gp80 and the signal transducer gp130. In the search for markers of airway inflammation, delete the role of soluble interleukin-6 receptor (sIL-6R) and IL-6 in acute asthma were investigated. Methods : Serum levels of sIL-6R and IL-6 were measured in 78 acute asthmatics, in 15 patients with asymptomatic asthma and in 10 healthy control subjects by a specific ELISA using a murine antihuman IL-6R, IL-6 mAb ($Quantikine^{(R)}sIL$-6R, IL-6). Results : Serum levels of IL-6 in acute asthmatics significantly exceeded those of control subjects. The levels of sIL-6R in acute asthmatics were also significantly increased compared to those of control subjects. The serum concentrations of IL-6 obtained in acute asthmatics were elevated compared with those in asymptomatic asthmatics. However, association between eosinophilic count/IgE and IL-6/sIL-6R in acute asthma could not be found. Conclusion : Our results suggest that IL-6 may be involved in the pathogenesis of acute asthma, and serum levels of IL-6 and sIL-6R may reflect the severity of airway inflammation.

• Tuberculosis and Respiratory Diseases
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• v.73 no.6
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• pp.312-319
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• 2012

Background: Muscle wasting in sepsis is associated with increased proteolysis. Interleukin-15 (IL-15) has been characterized as an anabolic factor for skeletal muscles. Our study aims to investigate the role of IL-15 in sepsis-induced muscle atrophy and proteolysis. Methods: Mice were rendered septic either by cecal ligation and puncture or by intraperitoneal injection of lipopolysaccharide (LPS, 10 mg/kg i.p.). Expression of IL-15 mRNA and protein was determined by reverse transcriptase polymerase chain reaction and Western blot analysis in the control and septic limb muscles. C2C12 skeletal muscle cells were stimulated in vitro with either LPS or dexamethasone in the presence and absence of IL-15 and sampled at different time intervals (24, 48, or 72 hours). IL-15 ($10{\mu}g/kg$) was intraperitoneally administered 6 hours before sepsis induction and limb muscles were sampled after 24 hours of sepsis. Cathepsin L activity was determined to measure muscle proteolysis. Atrogin-1 and muscle-specific ring finger protein 1 (MuRF1) expressions in limb muscle protein lysates was analyzed. Results: IL-15 mRNA expression was significantly lower in the limb muscles of septic mice compared to that of controls. Cathepsin L activity in C2C12 cells was significantly lower in presence of IL-15, when compared to that observed with individual treatments of LPS or dexamethasone or tumor necrosis factor ${\alpha}$. Further, the limb muscles of mice pre-treated with IL-15 prior to sepsis induction showed a lower expression of atrogin-1 and MuRF1 than those not pre-treated. Conclusion: IL-15 may play a role in protection against sepsis-induced muscle wasting; thereby, serving as a potential therapeutic target for sepsis-induced skeletal muscle wasting and proteolysis.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.20
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• pp.8775-8778
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• 2014

Background: To explore the relationship between polymorphisms of interleukin17 (IL-17) gene(A-832G 7488A/G) and the susceptibility to silicosis, a risk factor for lung cancer. Materials and Methods: A total of 113 silicosis patients and 116 workers without silicosis were enrolled in the case-control study. IL-17A A-832G and IL-17F 7488A/G polymorphisms were evaluated by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: The frequencies of AA,GG and AG of IL-17A A-832G locus in the case and control groups were 46.9%, 8.0%, 45.1%, and 49.2%, 7.6%, 43.2%, respectively, with no significant differences (p>0.05).The GG genotype in the IL-17F (7488A/G) locus was not found. The frequencies of AA and GA of IL-17F 7488A/G locus in the case and control groups were 84.1%, 15.9% and 66.4%, 33.6%, respectively (p<0.05). Analysis of combined effects showed that the individuals with GG+AG genotype of IL-17A and GG+GA genotype of IL-17F are protected against silicosis (OR=0.469). Conclusions: IL-17F 7488A/G is associated with susceptibility to silicosis, and G allele may have a protective effect. No relationship was found between IL-17A gene polymorphisms at A-832G and silicosis.

• Physical Therapy Korea
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• v.15 no.1
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• pp.69-76
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• 2008

This study was designed to determine the effects of swimming and low power laser on rheumatoid arthritis in Sprague-Dawley rats. Rheumatoid arthritis was induced in 36 rats among 48 Sprague-Dawley rats by the subcutaneous injection of .05 $m{\ell}$ Freund's Complete Adjuvant into the right hind paw and .05 $m{\ell}$ Freund's Complete Adjuvant into the right hind knee joint capsule. A second injection was performed by the same method using .1 $m{\ell}$ Freund's Complete Adjuvant per a rat. Arthritic rats were divided into 8 groups: each 1 week and 2 weeks of arthritic swimming, arthritic laser, arthritic case control and normal group. In this study, several experimental tests were performed to determine the concentration of Interleukin-6, the space of the knee joint and the thickness of the hind paw. The concentration of Interleukin-6 and hind paw thickness decreased in the swimming group and laser group as compared to the control group. The space of the knee joint increased significantly after the swimming exercise. Swimming and low power laser therapy positively affect rheumatoid arthritis in rats affect by decreasing the concentration of Interleukin-6 and hind paw thickness, and increasing the space of the knee joint.

• Journal of Periodontal and Implant Science
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• v.44 no.3
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• pp.126-133
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• 2014

Purpose: Smokeless tobacco-based oral-use products like gutka are popular in India. Gutka usage leads to increased periodontal destruction and inflammation; however, the relevant mechanism remains unknown. This study aimed to elucidate the role of gutka in periodontitis by examining its effect on the levels of interleukin (IL) $1{\beta}$ and IL-8 from the gingival crevicular fluid (GCF). Methods: A total of 45 patients were enrolled in this study. Thirty patients with periodontitis (15 gutka chewers [GCP] and 15 nongutka chewers [NGC]) and 15 periodontally healthy controls (HC) were selected. The full-mouth plaque index (PI), gingival index (GI), probing depth (PD), clinical attachment level (CAL), and recession (RC) were recorded. The IL-$1{\beta}$ and IL-8 levels in the GCF of all subjects were assessed through an enzyme-linked immunosorbent assay (Quantikine). Results: The IL-$1{\beta}$ and IL-8 levels were not significantly higher in the GCP group (IL-$1{\beta}$, $369.01{\pm}273.44{\mu}L$; IL-8, $205.97{\pm}196.78{\mu}L$) as compared to those in the NGC group (IL-$1{\beta}$, $195.57{\pm}96.85{\mu}L$; IL-8, $178.61{\pm}149.35{\mu}L$). More gingival RC and loss of attachment was seen among the GCP group (RC: $2.02{\pm}0.31$, P=0.013; CAL: $4.60{\pm}0.56$, P<0.001) than among the NGC group (RC, $1.21{\pm}1.15$; CAL, $3.70{\pm}0.32$); however, PD was deeper among the NGC subjects (P=0.002). PI and GI were significantly higher for the periodontitis group (P<0.001) when compared to the HC, but there was no difference among gutka chewers and non-chewers (P=0.22 and P=0.89). A positive correlation was found between the IL-8 levels and the duration of gutka chewing (r=-0.64, P<0.01). Conclusions: Gutka chewing leads to increased gingival RC and clinical loss of attachment. There was no effect seen in the proinflammatory cytokine levels in the GCF of gutka users.

• Journal of Microbiology and Biotechnology
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• v.17 no.7
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• pp.1120-1126
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• 2007

This study was performed to screen probiotic bifidobacteria for their ability to bind and neutralize lipopolysaccharides (LPS) from Escherichia coli and to verify the relationship between LPS-binding ability, cell surface hydrophobicity (CSH), and inhibition of LPS-induced interleukin-8 (IL-8) secretion by HT-29 cells of the various bifidobacterial strains. Ninety bifidobacteria isolates from human feces were assessed for their ability to bind fluorescein isothiocyanate (FITC)-labeled LPS from E. coli. Isolates showing 30-60% binding were designated LPS-high binding (LPS-H) and those with less than 15% binding were designated LPS-low binding (LPS-L). The CSH, autoaggregation (AA), and inhibition of LPS-induced IL-8 release from HT-29 cells of the LPS-H and LPS-L groups were evaluated. Five bifidobacteria strains showed high levels of LPS binding, CSH, AA, and inhibition of IL-8 release. However, statistically significant correlations between LPS binding, CSH, AA, and reduction of IL-8 release were not found. Although we could isolate bifidobacteria with high LPS-binding ability, CSH, AA, and inhibition of IL-8 release, each characteristic should be considered as strain dependent. Bifidobacteria with high LPS binding and inhibition of IL-8 release may be good agents for preventing inflammation by neutralizing Gram-negative endotoxins and improving intestinal health.

• Journal of Chest Surgery
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• v.33 no.1
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• pp.1-6
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• 2000

Background: TNF-$\alpha$ plays a major role in producing left ventricular dysfunction cardio-myopathy pulmonary edema and inhibits the compensatory mechanism of congestive heart failure. IL-6 is an acute reactant of immune reaction and also known to control immune reaction but its function in the myocyte was not clearly investigated. Author's performed this experiment to investigate the contents of TNF-$\alpha$ and IL-6 on the assumption that TNF-$\alpha$ and IL-6 may reside in nonfailing heart that has gone cardiac surgery and play some role in cardiac function. Material and Method : Right auricular tissues were sampled from 12 patients who had undergone total corrective surgery for both congenital and acquired heart diseases from January 1998 to June 1998 in Kosin Universcfy Gospel hospital. The quantitive analysis of TNF-$\alpha$ and IL-6 were assessed by ELISA method in right auricular tissue. Hemodynamic values about the pressure of ventricle atrium aorta pulmonary artery and cardiac index pulmonary and systemic vascular resistance and cardiac output were measured by echocardiography and cardiac catheterization and biochemical analyses of LDH & AST were done before operation. statistical analysis was by Paired Student t-test. Patients were divided into children(under 15 years olds) and adults groups and the data was compared beween two groups. Conclusion: Mild pulmonary hypertension and increased pulmonary vascular resistance were existed in both group. The contents of tissue TNF-$\alpha$ IL-6 in each group were independent of each data.

• Archives of Pharmacal Research
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• v.29 no.1
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• pp.1-15
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• 2006

Vascular endothelial cell injury or dysfunction has been implicated in the onset and' progression of cardiovascular diseases including atherosclerosis. A number of previous studies have demonstrated that the pro-oxidative and pro-inflammatory pathways within vascular endothelium play an important role in the initiation and progression of atherosclerosis, Recent evidence has provided compelling evidence to indicate that interleukin-4 (IL-4) can induce proc inflammatory environment via oxidative stress-mediated up-regulation of inflammatory mediators such as cytokine, chemokine, and adhesion molecules in vascular endothelial cells. In addition, apoptotic cell death within vascular endothelium has been hypothesized to be involved in the development of atherosclerosis. Emerging evidence has demonstrated that IL-4 can induce apoptosis of human vascular endothelial cells through the caspase-3-dependent pathway, suggesting that IL-4 can increase endothelial cell turnover by accelerated apoptosis, the event which may cause the dysfunction of the vascular endothelium. These studies will have a high probability of revealing new directions that lead to the development of clinical strategies toward the prevention and/or treatment for individuals with inflammatory vascular diseases including atherosclerosis.

• Restorative Dentistry and Endodontics
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• v.28 no.5
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• pp.409-418
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• 2003

본 연구는 치수 염증 시 IL-8과 MCP-1 분비에서 neuropeptide의 역할에 대해 관찰하고자 발거된 건전한 치아를 수직 파절시켜 치수조직을 채취하여 배양된 치수세포 및 혈관내피세포(ECV 304세포)를 각기 다른 농도의 Substance P(SP)로 12시간 자극하였고, 24시간 동안 4시간 간격으로 시간대별로 자극하였으며, 또 치수세포를 Calcitonin gene-related peptide (CGRP)로 12시간 자극하였다. 이들 세포를 SP길항제 (Spantide)로 15분간 차단한 후 SP로 12시간 재 자극하였으며, SP와 CGRP혼합액을 12시간 자극하였다. 상기의 실험 후 부유물로 ELISA를 시행하여 IL-8과 MCP-1의 분비 량을 측정하였다. 치수세포는 SP로 자극 시 IL-8이 현저히 증가한 반면, CGRP는 효과가 없었으며, SP와 CGRP를 혼합자극 시 시너지 효과 또한 없었고, Spantide는 치수세포의 IL-8과 MCP-1의 분비를 차단시켰다. 치수세포를 SP로 24시간 동안 4시간 간격으로 자극 시 8시간 후 최대의 IL-8은 분비량 나타내었으며, 8시간과 12시간 사이에서 최대의 MCP-1 분비량을 나타내었다. ECV 304세포를 SP로 자극 시 IL-8과 MCP-1 분비량이 미약하게 증가하였으며, Spantide는 ECV 304세포의 IL-8과 MCP-1 분비를 억제시켰다.