COPD患者C反应蛋白、TNF-α、IL-8、IL-6临床研究

目的：探讨血清中C反应蛋白（CRP）、肿瘤坏死因子-α（TNF-α）、白介素-8（IL-8）、白介素-6（IL-6）的水平变化在慢性阻塞性肺疾病（COPD）的发生发展中的作用及临床意义。方法：采用酶联免疫吸附法及全自动生化仪对35例COPD患者急性发病期和缓解期血清中的CRP、TNF-α、IL-8和IL-6浓度进行检测。结果：①COPD缓解期CRP、TNF-α、IL-8和IL-6含量显著低于急性期,但仍高于对照组（P〈0.05）。②吸烟因素可增加COPD患者血清中CRP、TNF-α、IL-8和IL-6含量。③血清中CRP、TNF-α、IL-8和IL-6含量与肺功能指标FEV1%和FEV1/FVC%呈负相关。结论：CRP、TNF-α、IL-8和IL-6参与了COPD患者气道炎症反应,可能与疾病的严重程度有关,可作为判断预后的辅助指标;吸烟可能是COPD发生发展的重要因素。     

Adiponectin,TNF-α and inflammatory cytokines and risk of type 2 diabetes: A systematic review and meta-analysis

AimsThere has been growing evidence that adiponectin, tumor necrosis factor-α (TNF-α) and inflammatory cytokines involved in insulin resistance and may be attractive candidates for assessing risk of the incident type 2 diabetes (T2DM). A systematic review and meta-analysis of prospective studies was conducted to assess the associations of levels of serum adiponectin, TNF-α and inflammatory markers (Interleukin-1 beta (IL-1β), Interleukin-6 (IL-6), Interleukin-18 (IL-18), C-reactive protein (CRP)) with risk of T2DM.Materials/methodsWe searched PubMed, ISI Web of Knowledge, EMBASE, and Cochrane Library databases up until February 1, 2016 for eligible studies which were matched to search subjects. Either fixed-effects or random-effects models were used to estimate the summary risk incorporated between study variations.Results19 studies comprising a total of 39,136 participants and 7924 cases were included in the meta-analysis. Our findings showed that an obvious association of elevated CRP levels with T2DM risk (relative risk [RR] 1.48 [95% CI 1.26–1.71]), with the absence of publication bias. For IL-6, the meta-analysis involved 16 cohorts with a total of 24,929 participants and 4751 cases. Using data from all trials, a strong positive correlation (1.32 [1.14, 1.51]) was observed between basal plasma IL-6 and T2DM, whereas relatively lower relation between TNF-α (1.16 [0.87, 1.45]), IL-18 (1.45 [1.16, 1.73]), IL-1β (0.87, [0.59, 1.15]) and independently increased risk to occurrence of T2DM. Conversely, we also found that the level of adiponectin decreased significantly in patients with T2DM. Sensitivity analyses further supported the associations.ConclusionsThis meta-analysis indicates that T2DM risk as whole was strongly associated with elevated levels of inflammatory cytokines (IL-1β, IL-6, IL-18, CRP), TNF-α and low levels of adiponectin. Despite an overall detectable association in the meta-analysis, considerable heterogeneity existed between studies. Further work is needed, it seems clear that a complex interplay of inflammation and the development of DM. Moreover, these biomarkers are predictors of T2DM subjects and should take more attention to measure levels of these as well as to target therapy/interventions.     

Levels of Amyloid Beta-42, Interleukin-6 and Tumor Necrosis Factor-Alpha in Alzheimer’s Disease and Vascular Dementia

Amyloid β42 (Aβ42) and proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) have been suggested to contribute to the pathogenesis of Alzheimer's disease (AD) and vascular dementia (VaD). Our aim was to examine whether the changes in these parameters would be able to discriminate the patients with AD from those with VaD and from healthy individuals. We have analyzed the levels of Aβ42, IL-6 and TNF-α in the serum of newly diagnosed 28 AD patients, 16 VaD patients and 26 healthy non-demented controls. We also investigated whether there is an association between Aβ42, IL-6 and TNF-α levels and mini-mental state examination (MMSE) scores and body mass indexes (BMI) of patients. Our data showed a significant decrease in serum Aβ-42 levels in AD patients compared to VaD patients and controls. Levels of IL-6 and TNF-α were not different between AD patients, VaD patients and controls. We observed a correlation between Aβ-42 levels and MMSE scores and BMI levels in both AD and VaD patients. However, Aβ-42 levels were not correlated with IL-6 and TNF-α levels. Significantly lower levels of Aβ42 found in the serum of AD patients than that of VaD patients and controls suggests that it can be a specific biochemical marker for AD.     

Type 2-diabetes is associated with elevated levels of TNF-alpha, IL-6 and adiponectin and low levels of leptin in a population of Mexican Americans: a cross-sectional study

The goal of the study was to determine the association between diabetes and inflammation in clinically diagnosed diabetes patients. We hypothesized that low-grade inflammation in diabetes is associated with the level of glucose control. Using a cross-sectional design we compared pro- and anti-inflammatory cytokines in a community-recruited cohort of 367 Mexican Americans with type 2-diabetes having a wide range of blood glucose levels. Cytokines (IL-6, TNF-α, IL-1β, IL-8) and adipokines (adiponectin, resistin and leptin) were measured using multiplex ELISA. Our data indicated that diabetes as whole was strongly associated with elevated levels of IL-6, leptin, CRP and TNF-α, whereas worsening of glucose control was positively and linearly associated with high levels of IL-6, and leptin. The associations remained statistically significant even after controlling for BMI and age (p = 0.01). The association between TNF-α, however, was attenuated when comparisons were performed based on glucose control. Strong interaction effects between age and diabetes and BMI and diabetes were observed for IL-8, resistin and CRP. The cytokine/adipokine profiles of Mexican Americans with diabetes suggest an association between low-grade inflammation and quality of glucose control. Unique to in our population is that the chronic inflammation is accompanied by lower levels of leptin.     

慢性肾小球肾炎患者治疗前后血清CRP和VEGF浓度变化及临床意义

目的：研究慢性肾小球肾炎（CNG）中血清C反应蛋白（CRP）和血管内皮生长因子（VEGF）的浓度变化及其临床意义。方法：采用ELISA法测定35例正常对照组与41例慢性肾小球肾炎患者治疗前后血清IL-6和VEGF的浓度,同时放射免疫分析法测定血清TNF-α浓度,免疫比浊法测定血清CRP与尿Alb浓度。结果：①治疗前后CNG患者血清中IL-6、TNF-α和CRP较正常对照组均显著升高（P〈0.05或P〈0.01）,但治疗后IL-6、TNF-α和CRP水平显著低于治疗前（P〈0.01）,且血清CRP与IL-6和TNF-α呈正相关（P〈0.01）。②治疗后,CNG患者血清VEGF水平与尿Alb含量较治疗前明显降低（P〈0.05或P〈0.01）,仍显著高于正常对照组（P〈0.05或P〈0.01）,且血清VEGF与尿Alb水平呈正相关（P〈0.01）。结论：CRP、IL-6和TNF-α参与了CNG患者慢性炎症反应,VEGF则与蛋白尿的产生密切相关,治疗前后血清CRP和VEGF检测对于慢性肾小球肾炎的病情了解及临床疗效评估均具有重要的临床价值。     

腹部外伤患者术后感染与血清炎症因子的关联性研究

本研究旨在探讨外伤术后腹腔感染患者血清降钙素原(PCT)、肿瘤坏死因子-α(TNF-α)、C-反应蛋白(CRP)和白细胞介素6 (IL-6)的水平变化与感染程度的相关性,为外伤术后腹腔感染临床治疗、抗菌药物应用提供依据。本研究选取我院2015年1月至2017年5月收治的腹部外伤手术患者150例,其中术后发生感染患者83例,未感染组,未发生感染患者67例,为非感染组。通过检测其术前术后及进行抗感染治疗后的PCT、TNF-α、CRP、IL-6水平,对腹腔感染标本进行菌种鉴定,并分析PCT、TNF-α、CRP、IL-6水平变化与腹腔感染的相关性,本研究发现,感染组患者术后各时间段血清PCT、TNF-α、CRP、IL-6水平明显较术前升高(p<0.05);且在术后12 h、24 h、72 h的PCT、TNF-α、CRP、IL-6水平明显高于未感染组(p<0.05);感染患者标本共检出76株不同的菌株,革兰阴性杆菌45株,革兰阳性菌22株,真菌9株;PCT、TNF-α、CRP在术后12 h、24 h、72 h检出感染的阳性率与病原学诊断结果相关性较高,血清IL-6则在术后72 h检出感染的阳性与病原学诊断相关性较高。本研究初步得出结论,临床检测血清PCT、TNF-α、CRP和IL-6均有助于鉴别是否存在外科腹腔感染,对抗菌药物的应用有一定的指导作用。     

膝关节炎患者关节置换术后细菌感染严重程度与IL-1β、TNF-α、IL-6水平的相关性

目的探讨膝关节炎患者关节置换术后细菌感染严重程度与IL-1β、TNF-α、IL-6水平的相关性。方法选取2016年8月至2018年8月于我院进行治疗的70例膝关节炎关节置换术后细菌感染患者作为试验组,参照Michel Lequesen推荐的膝关节炎严重性判断标准将膝关节炎关节置换术后细菌感染患者分为极严重组、非常严重组、严重组、中度组和轻度组。选取同期来我院体检中心进行体检的健康者50例为对照组。采用全自动生化免疫分析仪测定血清IL-1β、IL-6及TNF-α水平。结果试验组患者血清IL-1β、TNF-α、IL-6水平均明显高于对照组(均P<0.05)。极严重组患者血清IL-1β、TNF-α、IL-6水平显著高于非常严重组、严重组、中度组和轻度组(均P<0.05)。非常严重组患者血清IL-1β、TNF-α、IL-6水平显著高于严重组、中度组和轻度组(均P<0.05)。严重组患者血清IL-1β、TNF-α、IL-6水平显著高于中度组和轻度组(均P<0.05)。IL-1β、TNF-α、IL-6水平与膝关节炎关节置换术后细菌感染严重程度呈显著正相关(均P<0.05)。结论膝关节炎关节置换术后细菌感染患者血清IL-1β、TNF-α、IL-6水平明显升高,并且病情越严重,IL-1β、TNF-α、IL-6水平越高。     

Investigation of relationship between IL-6 gene variants and hypertension in Turkish population

Hypertension (HT) is a common and life threating health problem worldwide leading to stroke, heart attack and renal failure. It is characterized by elevated blood pressure forced heart load. Human interleukin-6 (IL-6) and C- reactive protein (CRP) are known to be involved in inflammatory processes. IL-6 gene is a polymorphic gene which −174 G/C is a common and −572 G/C is a rare polymorphisms identified in promoter region. Publications on IL-6 gene polymorphisms raised the question whether this gene polymorphisms lead to susceptibility to HT or not. To investigate the effects of IL-6 gene −174 G/C (rs 1800795) and −572 G/C (rs1800796) polymorphisms on plasma IL-6 and CRP levels and their associations with hypertension disease in Turkish population we analyzed −174 G/C and −572 G/C polymorphisms and plasma IL-6 and CRP levels in 111 healthy controls and 108 hypertension patients from Adıyaman, Turkey. We determined the genotypes using polymerase chain reaction-restriction fragment length polymorphism and analyzed plasma levels of IL-6 by ELISA and CRP by automated standard biochemical methods. We have found no statistically significant differences between IL-6 gene −174 G/C and −572 G/C genotypes and allelic frequencies and IL-6 and CRP plasma levels and HT (p > 0.05). No CC genotype was found in control subjects for −572 G/C polymorphism. In conclusion, we found relation to −174 G/C and −572 G/C gene variants between neither IL-6 and CRP levels nor hypertension. The −572 G allele and GG genotype are predominant in Turkish population in Adıyaman, Turkey whereas the CC genotype is very rare.     

Pigment epithelium-derived factor (PEDF) blocks the interleukin-6 signaling to C-reactive protein expression in Hep3B cells by suppressing Rac-1 activation

There is a growing body of evidence to show that that C-reactive protein (CRP), an acute phase reactant, is one of the most valuable predictors of future cardiovascular events. Since CRP proteins directly contribute to the development and progression of atherosclerosis as well, reduction of CRP levels may be a novel therapeutic target for the treatment of cardiovascular disease. In this study, we examined whether pigment epithelium-derived factor (PEDF) could block the interleukin-6-induced CRP expression in cultured human hepatoma cells and the way that it might achieve this effect. PEDF inhibited the IL-6-induced CRP expression in Hep3B cells at both mRNA and proteins levels. PEDF suppressed the intracellular reactive oxygen species generation in IL-6-exposed Hep3B cells. Anti-oxidants mimicked the effects of PEDF. PEDF was also found to inhibit the IL-6-elicited Rac-1 activation, whereas dominant-negative Rac-1 dose-dependently decreased the CRP mRNA levels. PEDF blocked the IL-6-induced STAT3 phosphorylations and NF-kappaB p65 activity in Hep3B cells. Our present study suggests that PEDF could be one of the potent suppressors of CRP production by the liver and may play a protective role against atherosclerosis.     

Longitudinal changes in serum proinflammatory markers across pregnancy and postpartum: Effects of maternal body mass index

BackgroundThe maternal immune system undergoes substantial changes to support healthy pregnancy. Although obesity is a primary driver of inflammation and predictive of perinatal complications, additive effects of pregnancy and obesity on changes in inflammatory processes are not well delineated.MethodsThis study examined serum proinflammatory markers interleukin(IL)-6, IL-8, tumor necrosis factor (TNF)-α, IL-1β, and C-reactive protein (CRP) during each trimester of pregnancy and 4–6 weeks postpartum among 57 women.ResultsOverall, IL-6 showed an increasing trend across pregnancy and significant increase at postpartum. Similarly, TNF-α increased significantly across gestation, with a further increase at postpartum. Both IL-8 and IL-1β showed a U-shaped curve, decreasing from early to later pregnancy, and increasing at postpartum. Finally, serum CRP decreased significantly across pregnancy, with further decreases at postpartum. Maternal obesity predicted higher IL-6 at each study visit. Obese women showed a trend toward elevated serum CRP during pregnancy, and significantly higher levels at postpartum.DiscussionThe course of pregnancy and postpartum is characterized by significant changes in serum proinflammatory mediators. Obese women show elevations in serum proinflammatory markers relative to normal weight women during pregnancy and postpartum. Further research is needed to determine the extent to which obesity-induced inflammation affects maternal and fetal health.     

A polymorphism in the visfatin gene promoter is related to decreased plasma levels of inflammatory markers in patients with coronary artery disease

Visfatin, a newly identified proinflammatory adipokine, has been linked to coronary artery disease (CAD). The ?1535C>T polymorphism (rs61330082) located in the visfatin gene promoter is reportedly associated with proinflammatory status. However, it is unclear whether this polymorphism correlates with plasma levels of inflammatory markers including visfatin, hs-CRP, IL-6 and TNF-?? in CAD patients. The present study was to investigate the potential association of the ?1535C>T polymorphism with plasma levels of visfatin, IL-6, C reactive protein (hs-CRP) and TNF-?? in patients with CAD. We conducted a hospital based study with 171 CAD patients to examine the association between the ?1535C>T polymorphism and plasma levels of visfatin, hs-CRP, IL-6 and TNF-??. Plasma visfatin levels were markedly different between patients with stable angina pectoris (SAP, 11.91 ± 0.70 ng/l) and those with unstable angina pectoris (UAP, 17.49 ± 0.20 ng/l) or acute myocardial infarction (AMI, 16.63 ± 0.22 ng/l; SAP versus UAP or AMI, P < 0.05). Compared with the CC genotype, variant genotypes CT and TT correlated with significantly lower levels of visfatin, hs-CRP, IL-6 and TNF-?? in the SAP group (P < 0.05), with lower levels of hs-CRP and IL-6 in the UAP group (P < 0.05), and with lower levels of visfatin in the AMI group (P < 0.05) after adjustment for age, gender, smoking, hypertension, diabetes, dyslipidemia and medication. Our results suggest that the ?1535C>T polymorphism is associated with decreased plasma levels of inflammatory markers in CAD patients, reflecting that this polymorphism might provide a useful marker for predicting the development of CAD events.     

Polymorphisms in the TNF-α and IL-10 gene promoters and risk of psoriasis and correlation with disease severity

Several cytokines were assumed to play an essential role in the induction and the pathogenesis of psoriasis. The aim of this work was to investigate the role of TNF-α-308 and IL-10-1082 polymorphisms and their serum levels in the pathogenesis of psoriasis and determine their relation to disease severity. 110 Psoriasis patients and 120 healthy volunteers were genotyped for TNF-α-308 and IL-10-1082 polymorphism by polymerase chain reaction. Serum level of TNF-α and IL-10 were measured by ELISA. Our study demonstrated an association of IL-10-1082 polymorphism and psoriasis and between TNF α-308 polymorphism and psoriasis disease and severity. Serum TNF α increased in patients, while serum IL-10 decreased in patients with significant correlation between serum TNF-α and psoriasis severity. These results indicated that TNF-α-308 and IL-10-1082 polymorphisms imparted significant risk towards the development of psoriasis.     

Synergistic effect of anti and pro-inflammatory cytokine genes and their promoter polymorphism with ST-elevation of myocardial infarction

Background

The single-gene approach in association studies of polygenic diseases such as acute myocardial infarction (AMI) is likely to provide limited value. Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) plasma levels may be genetically influenced.

Aim

We evaluate the impact of single nucleotide polymorphism of the promoter region of these genes, as well as reciprocal interaction of these genes with ST-elevation of myocardial infarction (STEMI).

Methods

In a case–control study 500 STEMI patients and 500 age- and sex-matched controls were studied. Three single-nucleotide polymorphism genotypes were evaluated by polymerase chain reaction and restriction enzyme analysis and assessed their association with STEMI. The synergistic effects of IL-6, TNF-α and IL-10 gene polymorphisms were evaluated by using logistic regression analysis.

Results

We found that IL-6 and TNF-α concentrations of studied population were significantly different (p < 0.0001) in each genotype of IL-6 − 174G>C and TNF-α − 308G>A gene polymorphisms respectively. A significant association was found in multivariate analysis for the IL-6 − 174G>C [odds ratio (OR): 0.390; 95% confidence interval (CI): 0.176–0.865, p = 0.020] and TNF-α − 308G>A [OR: 0.372; 95% CI: 0.171–808, p = 0.012] gene polymorphisms with STEMI. In contrast, IL-10 − 592C>A gene polymorphism was no longer significant in the multivariate model (OR: 0.678; 95% CI: 0.288 to 1.594, p = 0.373) whereas significant in univariate analysis (OR: 0.697; 95% CI: 0.523–0.929, p = 0.014).

Conclusions

Our findings suggest that IL-6, TNF-α and IL-10 gene polymorphisms all contribute in the association with STEMI whereas the association persisted only for IL-6 and TNF-α but not for IL-10 gene polymorphism with this disease in the multivariate analysis.     

TNF-α、IL-6、IL-8和sICAM-1与嗜肺军团菌感染关系的研究

目的探讨细胞因子IL-6、IL-8、TNF-α和黏附分子sICAM-1在嗜肺军团菌（Lp）感染者血清中的表达情况及其临床意义。方法用ELISA法检测30例Lp感染者和40例健康体检者血清中IL-6、IL-8、TNF-α、sICAM-1的含量并进行对比。结果Lp感染者血清中TNF-α、IL-6、IL-8、sICAM-1均表现出急性期〉恢复期,且急性期TNF-α、IL-8、sICAM-1浓度均较正常对照组明显增高,P〈0．05,IL-6与IL-8、TNF-α、sICAM-1及TNF-α与sICAM-1的改变存在明显的正相关。结论Lp感染者血清中IL-6、IL-8、TNF-α、sICAM-1含量出现表达异常,并随着病情程度的不同改变不同,对临床病情的监测、治疗、疗效判断、预后估计有重要的临床意义。     

Inflammatory response and neutrophil functions in players after a futsal match

Inflammatory response and neutrophil functions in players after a futsal match. J Strength Cond Res 26(9): 2507-2514, 2012-Futsal players suffer injuries resulting from muscle fatigue and contact or collision among players. Muscle lesions can be detected by measuring muscle lesion markers such as creatine kinase (CK) and lactate dehydrogenase (LDH) in plasma. After an initial lesion, there is an increase in the plasma levels of C-reactive protein (CRP) and proinflammatory cytokines. These mediators may activate neutrophils and contribute to tissue damage and increase susceptibility to invasive microorganisms. In this study, we investigated the effect of a futsal match on muscle lesion markers, cytokines, and CRP in elite players. The basal and stimulated neutrophil responsiveness after a match was also evaluated based on measurements of neutrophil necrosis, apoptosis, phagocytic capacity, reactive oxygen species (ROS) production, and cytokines (tumor necrosis factor-alpha [TNF-α], interleukin [IL]-8, IL-1β, IL-10, and IL-1ra) production. Blood samples were taken from 16 players (26.4 ± 3.2 years, 70.2 ± 6.9 kg, 59.7 ± 5.1 ml·kg·min, sports experience of 4.4 ± 0.9 years) before and immediately after a match. Exercise increased the serum activities of CK (2.5-fold) and LDH (1.3-fold). Playing futsal also increased the serum concentrations of IL-6 (1.6-fold) and CRP (1.6-fold). The TNF-α, IL-1β, IL-8, IL-1ra, and IL-10 serum levels were not modified in the conditions studied. The futsal match induced neutrophil apoptosis, as indicated by phosphatidylserine externalization (6.0-fold). The exercise induced priming of neutrophils by increasing ROS (1.3-fold), TNF-α (5.8-fold), and IL-1β (4.8-fold) released in nonstimulated cells. However, in the stimulated condition, the exercise decreased neutrophil function, diminishing the release of ROS by phorbol myristate acetate-stimulated neutrophils (1.5-fold), and the phagocytic capacity (1.6-fold). We concluded that playing futsal induces inflammation, primes and activates neutrophils, and reduces the efficiency of neutrophil phagocytosis immediately after a match.     

Gene polymorphisms in pro-inflammatory cytokines are associated with systemic inflammation in patients with severe periodontal infections

The inflammatory response to chronic infections such as periodontitis may be central to the systemic implications of these diseases. This study examined the possible association between specific gene polymorphisms and the systemic inflammatory response in individuals suffering from severe generalized periodontitis. Ninety-four subjects with periodontitis were genotyped for polymorphisms in IL-1A (-889), IL-1B (-511, +3954), TNF-A (-308), IL-6 (-174) and TLR4 (-299, -399) genes. We found that the genotypes for IL-1A or IL-6 are associated with higher levels of serum IL-6 (P < 0.03) and serum CRP (P < 0.05), similarly the TNF-A genotype is associated with higher levels of serum IL-6 (P < 0.05) after correction for age, body mass index, gender, ethnicity and cigarette smoking. Systemic inflammatory responses are higher in severe periodontitis patients carrying rare alleles for functional inflammatory gene polymorphisms. These results suggest that cytokine genotypes are important determinants of the systemic inflammatory response in subjects with periodontitis. Genetic polymorphism therefore, may in part explain the reported association between periodontitis and systemic disease.     

Serum TNF-α, sTNFR1, IL-6, IL-8 and IL-10 levels in Weil's syndrome

Studies on cytokine levels in Weil's syndrome are lacking. In this study, TNF-α, sTNFR1, IL-6, IL-8 and IL-10 levels were measured in 44 serum samples of patients diagnosed with Leptospira interrogans serovar icterohaemorrhagiae infection. TNF-α levels linked with pulmonary hemorrhagic implications, while elevated sTNFR1 and IL-10 levels linked with fatal cases. IL-6 and IL-8 did not seem to affect the outcome of the disease. Immune response pattern in Weil's syndrome bears resemblance to other patterns described for hemorrhagic fevers. IL-10/TNF-α ratio is proposed as a marker for prognosis.     

Exposure to Zinc Oxide Nanoparticles Induces Neurotoxicity and Proinflammatory Response: Amelioration by Hesperidin

Zinc oxide nanoparticles (ZnONPs) are widely used in food packaging and may enter the body directly if exposed. Hereby, in this study, the oral administration was selected as the route of exposure for rats to nanoparticles and the effect of hesperidin (HSP, 100 mg/kg bwt) was evaluated on ZnONP (600 mg/kg bwt)-induced neurotoxicity in rats. ZnONPs were characterized using transmission electron microscopy. Neurotoxicity was observed as seen by elevation in serum inflammatory markers including tumor necrosis factor alpha (TNF-α), interleukin 1 (IL-1β), interleukin-6 (IL-6), C-reactive protein (CRP), and activities of catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH) content in rat brains. Pretreatment of rats with HSP in ZnONP-treated group elevated activities of antioxidant enzymes. HSP also caused decrease in TNF-α, IL-1β, IL-6, and CRP levels which was higher in the ZnONP-treated group. The results suggest that HSP augments antioxidant defense with anti-inflammatory response against ZnONP-induced neurotoxicity. The increased antioxidant enzymes enhance the antioxidant potential to reduce oxidative stress.     

Cytokines genes polymorphisms in chronic hepatitis C: Impact on susceptibility to infection and response to therapy

BackgroundCytokines play a key role in the regulation of immune responses. In hepatitis C virus infection, the production of abnormal cytokine levels appears to contribute in the progression of the disease, viral persistence, and affects response to therapy. Cytokine genes polymorphisms located within the coding/regulatory regions have been shown to affect the overall expression and secretion of cytokines. The aim of the study was to evaluate the association of of IL28B rs12979860, TGF-β1-509, TNF-α 308, and IL-10-1082 polymorphisms with the susceptibility to hepatitis C virus genotype 4 infection and response to pegylated interferon-α and ribavirin therapy.MethodsIL28B, TGF-β1 and TNF-α genes polymorphisms were genotyped using polymerase chain reaction (PCR)-based restriction fragment length polymorphism assay while IL-10 gene polymorphism was detected by sequence specific primer-PCR in 220 healthy individuals and 440 hepatitis C infected patients (220 sustained virological response and 220 non-responder to combination therapy).ResultsIL28 B CT and TT, TGF-β1 CT and TT and TNF-α AG and AA genotypes were significantly associated with susceptibility to hepatitis C infection and response to therapy. While no association was found between IL-10 gene polymorphism and susceptibility to HCV infection and response to treatment.ConclusionsThese results suggested that inheritance of IL28B CT and TT, TGF-β1 CT and TT and TNF-α AG and AA genotypes which appear to affect the cytokine production may be associated with susceptibility to HCV infection and resistance to combined antiviral therapy.     

Association of TNF-α polymorphisms (−857, −863 and −1031), TNF-α serum level and lipid profile with acne vulgaris

BackgroundAcne is an inflammatory condition principally affected by genetic and dietary factors. Investigation into functional polymorphisms of TNF-α gene and their association with acne vulgaris will be helpful in exploring genetic influence on skin immune mediated inflammatory events. In the present study, we analyzed association of TNF-α gene polymorphisms, its expression levels and lipid profiles in a large cohort of acne patients and controls.MethodsWe used PCR-RFLP to study association of TNF-α polymorphisms at −857C/T, −863C/A and −1031 T/C sites with acne vulgaris. Lipid profiles were measured using enzymatic end-point method. The serum levels of TNF-α and apolipoprotein a were measured using ELISA. NIH, LDlink was used to investigate patterns of linkage disequilibrium across south Asian reference genome (Punjabi from Lahore Pakistan).ResultsWe found that TNF-α −863 polymorphism is strongly associated with acne in overall population as well as in gender and severity based groups of acne patients. Polymorphisms at −863 and −1031 position were in linkage disequilibrium. Importantly, TNF-α serum level was significantly increased in acne patients with severe disease symptoms. Furthermore, levels of total cholesterol (TC) and triglycerides (TG) were significantly increased, whereas high density lipoprotein cholesterol (HDL-C) level was significantly decreased in acne patients. The levels of apolipoprotein a varied widely in studied populations and no significant difference was found in the analyzed groups.ConclusionIn conclusion, we found that TNF-α expression increases in acne patients affected by TNF-α polymorphisms, and that the lipid profile is specifically disrupted in acne patients.