Objective To examine the levels of interferon-gamma; (INF-gamma;), tumor necrosis factor-alpha; (TNF-alpha;) and interleukin-6(IL-6) in serum of patients with acute uveitis before and after treatment, and to explore the possible roles of those cytokines in the initiation and progression of the uveitis. Methods A series of 75 patients with acute uveitis,and 30 healthy persons from our hospital were investigated. The levels of INF-gamma;, TNF-alpha; and IL-6 in acute phase and convalescent phase were measured by the enzymelinked immunosorbent assay. Result The serum levels of INF-gamma;, TNF-alpha; and IL-6 in acute phase were significantly higher than that of the convalescent phase and the healthy controls (F=65.805/50.418/155.381, P=0.000). A significant negative correlation was found between the serum levels of INF-gamma;, TNF-alpha; and IL-6 in acute phase with their initial visual acuity(r=-0.656, -0.592 and -0.653, Plt;0.01). There was also a positive correlation among the serum levels of INF-gamma;, TNF-alpha; and IL-6(r=0.340, 0.467 and 0.338, Plt;0.05). Conclusions There are high serum levels of INF-gamma;, TNF-alpha; and IL-6 in patients with acute uveitis, and the cytokines levels were decreased after the treatment. The results suggested that the INF-gamma;, TNF-alpha; and IL-6 involved in initiation and progression of uveitis.
Objective To evaluate the role of interleukin-10 (IL-10) in acute pancreatitis. Methods Thirty mongrel dogs were divided into three groups based on the severity: acute edematous pancreatitis (AEP) group (n＝11), acute hemorrhagic necrotizing pancreatitis (AHNP) group (n＝12), and control group (n＝7). Serum level of IL-10 was determined with enzyme-linked immuno-sorbent assay (ELISA). Results Within 24 hours, AEP group had serum level of IL-10 significantly higher than that of AHNP group. Control group had no detectable serum IL-10. No significant difference was observed between AEP group and AHNP group at 48 hours. Conclusion The finding of low values of serum IL-10 suggests that there may be more consumption in AHNP group than in AEP group and it may be beneficial to decrease the severity of experimental acute pancreatitis.
Objective To investigate the effects of tobacco smoke exposure on histone deacetylase 2 (HDAC2),interleukin-8(IL-8)and tumor necrosis factor-α(TNF-α)expression in peripheral blood of patients with lung adenocarcinoma and analyze the relationships among them. Methods Seventy-three cases diagnosed as lung adenocarcinoma were collected in the First Affiliated Hospital and Affiliated Tumor Hospital of Guangxi Medical University from April 2014 to March 2015.All patients underwent lung function test preoperatively.Fourteen healthy volunteers without tobacco smoke exposure and chronic obstructive pulmonary disease (COPD)were recruited as healthy control.According to the lung function and tobacco smoke exposure,all cases were divided into four groups,ie. a healthy control group (group A,14 cases),a group without tobacco smoke exposure and COPD(group B,19 cases),a group with tobacco smoke exposure and without COPD(group C,33 cases),and a group with tobacco smoke exposure and COPD(group D,21 cases).The expressions of HDAC2 mRNA,IL-8 mRNA and TNF-α mRNA in peripheral blood mononuclear cells (PBMCs)were detected by real-time polymerase chain reaction (PCR).The contents of IL-8 and TNF-α in serum were detected by ELISA. Results Compared with group A,the HDAC2 mRNA expression in PBMCs had no difference in group B(P>0.05),and was down-regulated significantly in group C and D (P<0.05),which in group D was the most obvious.Compared with group A,the expressions of IL-8 mRNA and TNF-α mRNA in PBMCs and the contents of IL-8 and TNF-α in serum were significantly higher in all lung adenocarcinoma patients(all P<0.05),and the up-regulation was more obvious in group D.The relative expression of HDAC2 mRNA in PBMCs showed no significant difference with respect to age,gender or TNM stage (P>0.05).IL-8 and TNF-α in PBMCs and serum showed no significant difference with respect to age and gender (P>0.05),and were higher in the patients with TNM stage Ⅲ lung adenocarcinoma than those with stage Ⅰ and Ⅱ(P<0.05),with no obvious difference between stage Ⅰ and stage Ⅱ (P>0.05). Conclusion Tobacco smoke exposure causes lower expression of HDAC2 and over-expression of IL-8 and TNF-α in peripheral blood of patients with lung adenocarcinoma,can aggravate inflammatory response especially when complicated with COPD,which may be related to the prognosis of lung adenocarcinoma.
ObjectiveTo address the effect and mechanism of interleukin 17 (IL-17) on the proliferation, migration and apoptosis of human retinal vascular endothelial cells (HREC). MethodsIL-17 receptor (IL-17R) mRNA and protein expression in human retinal vascular endothelial cells (HREC) were quantified by reverse transcription polymerase chain reaction (RT-PCR) and Western blot. Cell proliferation of HREC was examined using CCK-8 assay in the presence of different concentrations of IL-17. Cell migration of HREC was detected using wound scratch assay. Flow cytometry was used to test the effect of IL-17 on the apoptosis of HREC. The effects of IL-17 on HREC expression of basic fibroblast growth factor (bFGF), Caspase-3 and thrombospondin-1 (TSP-1) were quantified by reverse transcriptase polymerase chain reaction (RT-PCR). The effect of IL-17 on HREC expression of Caspase-3 was examined using Western blot. ResultsIL-17 receptor (IL-17R) expressed in HREC as quantified by RT-PCR and Western blot. The proliferation of HREC in the presence of IL-17 was promoted in a dosage-dependent manner (t=-3.235, -6.276;P=0.032, 0.000). Wound scratch assay showed a significant increase in the migrated distance of HREC with IL-17 stimulation under the concentration of 100μg/L(t=-3.551, -2.849; P=0.006, 0.019), 200μg/L(t=-10.347, -4.519; P=0.000, 0.001) and 500μg/L (t=-3.541, -2.607; P=0.008, 0.036). The intervention of 200μg/L IL-17 can effectively inhibit the apoptosis of HREC, compared with the control group using flow cytometry (t=5.682, P=0.047). RT-PCR results showed that IL-17 can promote the expression of bFGF and inhibit the expression of Caspase-3 and TSP-1. Western blot result also showed that IL-17 can suppress the protein expression of Caspase-3. ConclusionThe mechanism of IL-17 promoting proliferation, migration but suppress apoptosis of HREC may via regulating the expression of bFGF and Caspase-3.
目的 通过检测浸润性乳腺癌中白细胞介素18（IL-18）和血管内皮生长因子（VEGF）的表达情况，探讨其表达相关性及与临床病理学参数的关系。 方法 应用免疫组织化学法检测IL-18和VEGF在42例浸润性乳腺癌组织和12例正常乳腺组织中的表达情况。 结果 IL-18和VEGF在42例浸润性乳腺癌中的表达阳性率均显著高于12例正常乳腺组织（P＜0.05）。且在42例浸润性乳腺癌组织中，IL-18阳性组中VEGF阳性率（87.1%）显著高于IL-18阴性组中VEGF阳性率（12.9%），差异有统计学意义（P＜0.05）。在亚组分析中，IL-18的表达只与有无腋窝淋巴结转移有相关性（P＜0.05），而VEGF的表达与有无腋窝淋巴结转移和TNM分期有相关性（P＜0.05）。 结论 在浸润性乳腺癌中，IL-18的表达上调与VEGF的表达上调显著相关，IL-18可能具有促进肿瘤新生血管形成的作用。
ObjectiveTo investigate the overall accuracy of interleukin-12 (IL-12) for diagnosis of tuberculous pleurisy. MethodsWe searched in PubMed, Embase, Web of Science, China National Knowledge Infrastructure databases, WanFang Data, and VIP Information for qualified studies that reported diagnostic accuracy of IL-12 for tuberculous pleurisy up to February 2014. The methodological quality of each study was evaluated by Quality assessment of diagnostic accuracy studies. Statistical analyses were performed by Meta-Disc 1.4 software and the pooled sensitivity, specificity and other diagnostic indexes. Meta-analysis of the reported accuracy of each study and summary receiver operating characteristic (SROC) curve were also performed. ResultsEight studies met the inclusion criteria for the analysis. The summary estimates for IL-12 in the diagnosis of tuberculous pleurisy were:sensitivity 0.80 [95% CI (0.76, 0.84)], specificity 0.76 [95% CI (0.71, 0.81)], positive likelihood ratio 3.23 [95% CI (2.26, 4.60)], negative likelihood ratio 0.30 [95% CI (0.20, 0.45)], diagnostic odds ratio 13.57 [95% CI (6.66, 27.64)], and the area under the curve of SROC was 0.86. ConclusionIL-12 plays a valuable role in the diagnosis of tuberculous pleurisy, and IL-12 may be a useful diagnostic marker for tuberculous pleurisy.
Objective To explore the effect of IL-10 on the inhibition of early proinflammatory cytokine release in intraabdominal infection and early sepsis. Methods Forty eight SD rats were randomized into 4 groups, 12 in each group, ①sham operation group, ②control group, ③prophylactic group, ④therapeutic group. Group 1 underwent laparotomy only, group 2 received laparotomy and cecal ligation plus punctures (CLP) with saline injected once every 3 hrs, group 3 underwent CLP and IL-10 injection intraperitoneally 1 hr before surgery and once every 3 hrs following operation, group 4 received CLP and IL-10 injection once every 3 hrs after operation. At 3 and 9 hr points, rats were sacrificed and blood samples were taken for measurement of inflammatory cytokines. Results Almost no inflammatory cytokines were detected in sham group, CLP produced a significant rise in serum TNF-α (tumor necrosis α), IL-1, IL-6 (interleukin 1,6) in control group, IL-10 reduced the rise of inflammatory cytokines significantly. Conclusion IL-10 could inhibit the early inflammatory cytokine release in rat model of sepsis. Suggesting it may attenuate the severity of inflammation.