Possible Role Of Interleukin-6 Research Articles

Evaluation the Possible Role of Interleukin-6 and Tumor Necrosis Factor- Alpha in Pathogenesis of Obstructive Sleep Apnea in Obese Patients: A Case-Control Study:.

According to a mounting body of evidence, recent observations have highlighted considerable association between obstructive sleep apnea (OSA) syndrome and patients' obesity and inflammation, however the exact underlying mechanisms remain to be fully understood. In this study, the relationship between OSA and Interleukin-6 and Tumor necrosis factor- alpha was assessed in obese patients and their serum concentrations were compared to non-OSA obese subjects. This case-control study was conducted on forty-six obese OSA patients (body mass indices, BMI30) and 42 obese but otherwise healthy individuals who were admitted to the pulmonary or obesity clinics of the Hazrat-e Rasool General Hospital (Tehran, Iran) between November 2019 and May 2020 were included. The participants completed the NOSAS, EPWORTH and STOPBANG questionnaires. Tumor Necrosis Factor-Alpha (TNF-α) and Interleukin-6 (IL-6) serum concentrations were determined using the enzyme-linked immunosorbent assay (ELISA) method. Compared to the non-OSA group, OSA patients had higher systolic and diastolic blood pressure, pCO2, bicarbonate (HCO3) and hemoglobin and lower high-density lipoprotein (HDL) values. IL-6 and TNF-α serum levels were not significantly different between both groups. Univariate and multivariate linear regression models showed that BMI, systolic blood pressure, pCO2 and HCO3 can positively affect the serum TNF-α and systolic blood pressure and HCO3 can also positively affect the serum IL-6 values in patients with the OSA. This investigation suggests that among the OSA patients, the heightened inflammatory profile may be influenced by the high BMI. Furthermore, the exclusive relationship between different disease biomarkers and inflammatory agents in OSA patients is intriguing and needs further research.

Assessment of the chemerin, IL-6, and IL-23 correlations and their impact on CRC progression: An observational study

Introduction: The role of proinflammatory cytokines is said to be crucial in the development of colorectal cancer (CRC). IL-6, IL-23, and chemerin have all been proven to take part in tumor growth and progression. Aim of the study: to determine the level of chemerin and the concentrations of interleukin-6 (IL-6) and interleukin- 23 (IL-23) in the tumor and margin specimens of CRC in relation to histological grade and TNM staging. Material and methods: The study involved 49 samples of tumor and margin tissues obtained from CRC patients. To assess the concentration of chemerin, IL-6, and IL-23, commercially available enzyme-linked immunosorbent assay (ELISA) kits were used. Results: There was no difference in chemerin concentration between the tumor and margin. We found significantly increased levels of IL-6 in tumor tissue compared to margin tissue and higher concentrations of IL-23 in margin tissue than in tumor tissue. Tumor levels of chemerin were significantly correlated with those of IL-23, while its margin concentrations were associated with margin concentrations of IL-6. Additionally, tumor levels of IL-23 were positively correlated with margin levels of IL-6. Conclusions: Chemerin might play an important role in CRC progression through its association with cytokine expression. More studies are needed to investigate the possible role of IL-6, IL-23, and chemerin as potential markers in the development of CRC.

The possible role of Interleukin-6 as a regulator of insulin sensitivity in patients with neuromyelitis optica spectrum disorder

BackgroundNeuromyelitis optica spectrum disorder (NMOSD) is associated with inflammatory mediators that may also trigger downstream signaling pathways leading to reduce insulin sensitivity.MethodsWe aimed to determine the risk association of hyperinsulinemia in NMOSD patients with seropositive AQP4-IgG and the serum levels of interleukin (IL)-6 and IL-17A compared with the control group.Serum levels of metabolic (Insulin, Fasting Blood Sugar (FBS), lipid profile) and inflammatory (IL-6 and IL-17) markers were assessed in 56 NMOSD patients and 100 controls.ResultsHyperinsulinemia was more prevalent in NMOSD patients independent of age, sex and body mass index (BMI) (48.2% vs. 26%, p = 0.005) compared to control group. After adjusting age, sex and BMI, there was significant association between lower insulin sensitivity (IS) and NMOSD risk (95% CI: Beta = 0.73, 0.62 to 0.86, p = 0.0001).Circulating levels of IL-6 and IL-17 were higher in NMOSD patients, and only IL-6 had an effect modifier for the association between lower insulin sensitivity and NMOSD risk.ConclusionsOur data suggests that inflammatory pathogenesis of NMOSD leads to hyperinsulinemia and increases the risk of insulin resistance.

The possible role of interleukin-6 (IL-6) and survivin in the pathogenesis of embryonic damage

The possible role of interleukin-6 (IL-6) and survivin in the pathogenesis of embryonic damage

IL-6 Receptor Blockade by Tocilizumab Has Anti-absence and Anti-epileptogenic Effects in the WAG/Rij Rat Model of Absence Epilepsy.

Increased expression of interleukin-6 (IL-6) both in cerebrospinal fluid (CSF) and plasma is closely associated with convulsive epilepsy and symptom severity of depression. By comparison, at present, little is known about the role of this cytokine in childhood (non-convulsive) absence epilepsy. The aim of this work was to investigate the potential effects of acute and chronic treatment with tocilizumab (TCZ, 10 and 30mg/kg/day), on absence seizures, their development, and related psychiatric comorbidity in WAG/Rij rats. It is known that lipopolysaccharide (LPS)-induced changes in inflammatory processes increase absence epileptic activity. In order to study the central effects of TCZ, we investigated whether administration of this anti-IL-6R antibody could modulate the lipopolysaccharide (LPS) or IL-6-evoked changes in absence epileptic activity in WAG/Rij rats. Our results demonstrate that TCZ, at both doses, significantly reduced the development of absence seizures in adult WAG/Rij rats at 6months of age (1month after treatment suspension) compared with untreated controls, thus showing disease-modifying effects. Decreased absence seizure development at 6months of age was also accompanied by reduced comorbid depressive-like behavior, whereas no effects were observed on anxiety-related behavior. Acute treatment with TCZ, at 30mg/kg, had anti-absence properties lasting ~25h. The co-administration TCZ with i.c.v. LPS or IL-6 showed that TCZ inhibited the worsening of absence seizures induced by both proinflammatory agents in the WAG/Rij rats, supporting a central anti-inflammatory-like protective action. These results suggest the possible role of IL-6 and consequent neuroinflammation in the epileptogenic process underlying the development and maintenance of absence seizures in WAG/Rij rats. Accordingly, IL-6 signaling could be a promising pharmacological target in absence epilepsy and depressive-like comorbidity.

Neurons and astrocytes of the chicken hypothalamus directly respond to lipopolysaccharide and chicken interleukin-6

In 4–5-month-old chicken, intravenous injections of bacterial lipopolysaccharide (LPS) induced a dose-dependent fever response and a pronounced increase of circulating interleukin-6 (IL-6). To assess a possible role for IL-6 in the brain of birds, a hypothalamic neuro-glial primary culture from 1-day-old chicken was established. Each well of cultured hypothalamic cells contained some 615 neurons, 1350 astrocytes, and 580 microglial cells on average. Incubation of chicken hypothalamic primary cultures with 10 or 100 µg/ml LPS induced a dose-dependent release of bioactive IL-6 into the supernatant. Populations of hypothalamic neurons (4%) and astrocytes (12%) directly responded to superfusion with buffer containing 10 µg/ml LPS with a transient increase of intracellular calcium, a sign of direct cellular activation. Stimulation of hypothalamic cultures with buffer containing 50 ng/ml chicken IL-6 induced calcium signaling in 11% of neurons and 22% of astrocytes investigated. These results demonstrate that IL-6 is produced in the periphery and in the hypothalamus in response to LPS in chicken. The observed cellular responses of hypothalamic cells to chicken IL-6 indicate that this cytokine may readily be involved in the manifestation of fever in the avian hypothalamus.

Interleukin-6 in Schizophrenia-Is There a Therapeutic Relevance?

Renewing interest in immune aspects of schizophrenia and new findings about the brain-fat axis encourage us to discuss the possible role of interleukin-6 (IL-6) in schizophrenia. Previously, it was suggested that a primary alteration of the innate immune system may be relevant in schizophrenia. Functional dichotomy of IL-6 suggests that this chemical messenger may be responsible for regulating the balance between pro- and anti-inflammatory responses, with tissue-specific properties at the periphery and in the central nervous system. Specific phase of this chronic and deteriorating disorder must be considered, which can involve IL-6 in acute or possible chronic inflammation and/or autoimmunity. We give an overview of IL-6 role in the onset and progression of this disorder, also considering cognitive impairment and metabolic changes in patients with schizophrenia. Data suggest that decreased serum level of IL-6 following antipsychotic therapy could be predisposing factor for the development of obesity and obesity-related metabolic disorders in schizophrenia. As we reviewed, the IL-6 plays significant role in disease genesis and progression, so the use of specific inhibitors may not only be beneficial for exacerbation and alleviation of positive symptoms, but may attenuate cognitive impairment in patients with schizophrenia.

Study of the possible role of interleukin-6 (IL-6) on embryo implantation in mice

Study of the possible role of interleukin-6 (IL-6) on embryo implantation in mice

Serum interleukin-6 concentration and association with response to hepatitis C virus therapy for chronic hepatitis C patients

Background Egypt has the highest prevalence of hepatitis C virus (HCV) in the world. Interleukin 6 (IL-6) is a pleiotropic cytokine that is elevated in chronic hepatitis C patients. IL-6 was suggested by several studies to play a major role in response to HCV therapy. Aim The aim of this work was to assess the possible role of IL-6 in the response status of patients with HCV during treatment. Moreover, we attempted to use IL-6 as a predictive factor for response in patients with chronic HCV. Patients and methods Serum concentrations of IL-6 were measured before and after treatment using a commercially available Quantikine enzyme-linked immunosorbent assay in 57 patients with chronic hepatitis C treated with sofosbuvir and simeprevir for 3 months. Results The mean values of IL-6 level in responders and nonresponders were 272.96 and 230.5 pg/ml, respectively. IL-6 levels decreased significantly after treatment in the sustained virological response group. The best cutoff point for IL-6 was 233 pg/ml with a sensitivity of 70%, a specificity of 75%, a positive predictive value of 97.2%, and a negative predictive value of 16.7%. Conclusion Virological response during HCV therapy was associated with a decrease in IL-6 level.

Infrapatellar fat pad aggravates degeneration of acute traumatized cartilage: a possible role for interleukin-6

The infrapatellar fat pad (IPFP), which is located underneath the patella, close to cartilage surfaces, functions in distributing mechanical load and has been shown to produce cytokines. This study aims to assess the involvement of the IPFP in the progression of post-traumatic osteoarthritis (OA) through investigating the crosstalk between the IPFP and injured cartilage invitro. A single blunt impact (36MPa) on healthy bovine articular cartilage explants was used to generate traumatized cartilage. Conditioned media from IPFP and traumatized cartilage (FP-CM and TC-CM) were prepared separately. After culturing in FP-CM, the posttraumatic cartilage explants were analyzed for expression of cartilage degeneration associated genes and secretion of the interleukin (IL)-6, into the culture medium. The effect of traumatized cartilage on IPFP was studied by treating IPFP-derived adipocytes and IPFP adipose-derived stromal cells (ADSC) with TC-CM followed by analysis of cytokine expression. FP-CM aggravated glycosaminoglycan (GAG) release in traumatized cartilage, but did not significantly affect healthy cartilage. FP-CM raised gene expression of cyclooxygenase-2, inducible nitric oxide synthase, and IL-6 in traumatized cartilage explants, and lowered expression of tissue inhibitor of metalloproteinases-1, 2, 3, compared to non-conditioned medium. Of particular significance is that medium IL-6 levels increased substantially in both FP-CM and FP-CM treated traumatized cartilage cultures. Extrinsic IL-6 treatment of traumatized cartilage simulated part of the effects of FP-CM. TC-CM elevated levels of IL-6 expression in IPFP derived adipocytes and ADSCs. IPFP aggravates post-traumatized cartilage degeneration, and IL-6 is a candidate tissue degeneration mediator.

Estimation of serum Alpha feto-protein (AFP), interlukin-6 and Des-?-carboxyprothrombin (DCP) in case of hepatocellular carcinoma

Background: Hepatocellular carcinoma (HCC) is one the most common primary malignancy of the liver and represents the third leading cause of cancer-related deaths worldwide. Incidence rates are highest in East Asia and Sub-Saharan Africa. A number of evidence suggests a possible role of interleukin-6 (IL-6), ?-Fetoprotein (AFP) and Des-?-carboxyprothrombin (DCP) in the pathogenesis of hepatocellular carcinoma (HCC). The high DCP may be related to increase tumour behaviour, such as the presence of vascular invasion and intrahepatic metastasis of HCC cells. Patients and methods: We studied IL-6, AFP and DCP in patients with HCC or in healthy controls. AFP was measured by chemiluminescent immunoassay; Serum IL-6 and DCP were measured by enzyme linked immunosorbent assay in 30 patients with primary hepatocellular carcinoma and 30 normal subjects.Results: IL-6, AFP and DCP were found high in the serum of patients initially diagnosed with HCC (18±9.8), (315.99±594.62) and (26.15±5.01) respectively compared with healthy subjects (4.29±2.10), (3.13±1.27) and (4.25±1.22). A significant positive correlation was found between mean levels of IL- 6 & AFP in HCC (P < 0.05), Combination of IL-6, AFP and DCP improved the sensitivity in diagnosing HCC or predicting future HCC development. Conclusions: IL-6, DCP along with AFP could be considered a promising tumor marker for HCC. DCP is a well recognized tumor marker for the screening and diagnosis of HCC. In particular, the diagnostic value of the test is significantly increased when combined with AFP.Bangladesh Journal of Medical Science Vol.15(2) 2016 p.230-233

IL-6 Blockade as a Therapeutic Approach for Duchenne Muscular Dystrophy

Duchenne muscular dystrophy (DMD) is a recessive X-linked form of genetic muscle disease affecting approximately 1 in 3500 males (Flanigan, 2014). Boys with DMD carry mutations in the dystrophin gene resulting in defective or absent dystrophin protein. Both skeletal and cardiac muscles undergo progressive damage in this disease, with most boys confined to wheelchairs by age 12. There is currently no cure for DMD and affected patients die from respiratory failure, cardiomyopathy, or other complications at an average age of 25 years. In this issue of EBioMedicine, Pelosi and colleagues present evidence that blockade of interleukin-6 (IL-6) ameliorates muscle destruction and weakness in a mouse model of DMD and suggest that this may represent a novel therapeutic approach in humans. In DMD, dystrophin deficiency disrupts the dystrophin–glycoprotein complex, leading to muscle fiber necrosis as well as a prominent inflammatory response. Although the inflammatory response may play a role in muscle repair, accumulating evidence suggests that it also contributes to muscle damage (Spencer and Tidball, 2001). In the 1970s, recognition of this inflammatory response prompted Drachman and colleagues to treat DMD patients with glucocorticoids (Drachman et al., 1974). The improvements these investigators noted in some DMD patients in an open-label trial have subsequently been confirmed in randomized, placebo-controlled clinical trials (Manzur et al., 2008). However, glucocorticoids, which remain the only available treatment for DMD, have relatively modest effect on the course of this fatal disease. Furthermore, these drugs have significant side effects including weight gain, osteoporosis, and increased risk of infection. Clearly, more effective and safer treatments for DMD are desperately needed. In an article in this issue of EBioMedicine, Pelosi and colleagues observe that the inflammatory cytokine IL-6 is expressed at high levels in the serum of boys with DMD as well as in inflammatory cells infiltrating their muscle tissue. Moreover, serum IL-6 levels were increased in untreated DMD patients compared to those receiving treatment with glucocorticoids. Taken together, these observations suggested that IL-6 might play a role in mediating muscle damage through the inflammatory response. In order to further study the possible role of IL-6 in mediating muscle damage, these investigators utilized the mdx mouse model of DMD. These mice lack functional dystrophin and, like boys with DMD, develop a progressive muscular dystrophy that includes a prominent inflammatory response. As in boys with DMD, Pelosi and colleagues demonstrated that circulating levels of IL-6 are increased and cells expressing high levels of IL-6 infiltrate the diaphragm muscles of mdx mice. To test whether blockade of IL-6 would ameliorate the dystrophic process in mdx mice, these mice were treated with an antibody recognizing the IL-6 receptor. Compared to untreated mdx mice, mice treated with the neutralizing antibody had decreased myofiber necrosis, improved functional performance after exercise on a treadmill, and evidence of a decreased inflammatory response in their muscle tissue. Based on their findings, Pelosi and colleagues suggest that IL-6 inhibitors, which are already approved for children with systemic juvenile idiopathic arthritis, should be considered for use in boys with DMD. However, optimism about their potential effectiveness is tempered by at least five considerations. First, another recent study by Kostek et al. showed that IL-6 blockade increased muscle inflammation and did not significantly improve muscle function in mdx mice (Kostek et al., 2012). These conflicting results may be due to differences in the dosing regimens used in each study. If that's the case, it remains unclear what the appropriate dosing regimen would be for DMD patients. Second, boys with DMD frequently die as a result of cardiomyopathy and the effect of IL-6 on cardiac muscle has not been studied. Third, in addition to promoting a potentially harmful inflammatory milieu, IL-6 has also been reported to play a role in muscle regeneration by promoting myoblast differentiation (Serrano et al., 2008); any therapeutic intervention aimed at blocking IL-6 in humans should consider this dual role of IL-6. Fourth, although mdx mice have been used extensively to understand the pathophysiology of DMD, they have limitations as a model for testing the effectiveness of therapeutic interventions (Partridge, 2013). Indeed, the literature includes numerous examples of drugs that improved outcomes in mouse models but did not have a similar effect in humans. And finally, any therapy for DMD that does not involve repletion of dystrophin is unlikely to cure this fatal disease. Despite these caveats, IL-6 blockade certainly warrants further study as a potential treatment modality for patients with DMD.

Estimation of Serum Alpha Feto-Protein (AFP), Interlukin-6 and Des-􀀁-Carboxyprothrombin (DCP) in Case of Hepatocellular Carcinoma.

Background : Hepatocellular carcinoma (HCC) is one the most common primary malignancy of the liver and represents the third leading cause of cancer-related deaths worldwide. Incidence rates are highest in East Asia and Sub-Saharan Africa. A number of evidence suggests a possible role of interleukin-6 (IL-6), α-Fetoprotein (AFP) and Des-γ-carboxyprothrombin (DCP) in the pathogenesis of hepatocellular carcinoma (HCC). The high DCP may be related to increase tumour behaviour, such as the presence of vascular invasion and intrahepatic metastasis of HCC cells. Patients and Methods : We studied IL-6, AFP and DCP in patients with HCC or in healthy controls. AFP was measured by chemiluminescent immunoassay; Serum IL-6 and DCP were measured by enzyme linked immunosorbent assay in 30 patients with primary hepatocellular carcinoma and 30 normal subjects. Results : IL-6, AFP and DCP were found high in the serum of patients initially diagnosed with HCC (18±9.8), (315.99±594.62) and (26.15±5.01) respectively compared with healthy subjects (4.29±2.10), (3.13±1.27) and (4.25±1.22). A significant positive correlation was found between mean levels of IL- 6 & AFP in HCC (P < 0.05), Combination of IL-6, AFP and DCP improved the sensitivity in diagnosing HCC or predicting future HCC development. Conclusions : IL-6, DCP along with AFP could be considered a promising tumor marker for HCC. DCP is a well recognized tumor marker for the screening and diagnosis of HCC. In particular, the diagnostic value of the test is significantly increased when combined with AFP.

IL-6, but not TNF-α, increases plasma YKL-40 in human subjects

Plasma levels of YKL-40 are elevated in patients with systemic infection, inflammatory disorders and cancer. Both monocytes/macrophages, neutrophils, and cancer cells have the capacity to produce YKL-40, but the regulation during the inflammatory response is unknown. To study the possible role of interleukin-6 (IL-6) and tumor necrosis factor (TNF)-α in the regulation of YKL-40 plasma levels, we included healthy men, who received either recombinant human (rh)IL-6 ( n = 6), rhTNF-α ( n = 8) or vehicle ( n = 7) for 3 h. The plasma levels of IL-6 and TNF-α reached ∼150 and ∼18 pg/ml, respectively, during the infusions. Following the IL-6 infusion, the plasma level of YKL-40 increased from ∼30 to ∼57 ng/ml ( p < 0.05) at 24 h, and returned to normal values after 48 h. The plasma level of YKL-40 did not change during TNF-α infusion or infusion of vehicle. These data demonstrate that IL-6, but not TNF-α, has a key-role in the regulation of plasma YKL-40 levels during inflammation.

Voluntary exercise protects hippocampal neurons from trimethyltin injury: Possible role of interleukin-6 to modulate tumor necrosis factor receptor-mediated neurotoxicity

In the periphery, exercise induces interleukin (IL)-6 to downregulate tumor necrosis factor (TNF), elevate interleukin-1 receptor antagonist (IL-1RA), decreasing inflammation. Exercise also offers neuroprotection and facilitates brain repair. IL-6 production in the hippocampus following exercise suggests the potential of a similar protective role as in the periphery to down-regulate TNFα and inflammation. Using a chemical-induced model of hippocampal dentate granule cell death (trimethyltin, TMT 2.4mg/kg, ip) dependent upon TNF receptor signaling, we demonstrate neuroprotection in mice with 2weeks access to running wheel. Exercise attenuated neuronal death and diminished elevations in TNFα, TNF receptor 1, myeloid differentiation primary response gene (MyD) 88, transforming growth factor β, chemokine (C–C motif) ligand 2 (CCL2), and CCL3. Elevated mRNA levels for IL-1α, IL-1RA, occurred with injury and protection. mRNA and protein levels of IL-6 and neuronal expression of IL-6 receptor α, were elevated with injury and protection. Microarray pathway analysis supported an up-regulation of TNFα cell death signaling pathways with TMT and inhibition by exercise. IL-6 pathway recruitment occurred in both conditions. IL-6 downstream signal events differed in the level of STAT3 activation. Exercise did not increase mRNA levels of brain derived neurotrophic factor, nerve growth factor, or glial derived neurotrophic factor. In IL-6 deficient mice, exercise did not attenuate TMT-induced tremor and a diminished level of neuroprotection was observed. These data suggest a contributory role for IL-6 induced by exercise for neuroprotection in the CNS similar to that seen in the periphery.

Interleukin‐6 (G‐174C) and tumour necrosis factor‐alpha (G‐308A) gene polymorphisms in geriatric patients with chronic periodontitis

Periodontitis is a chronic inflammatory disease, and genetic factors may have an important role in its severity. Polymorphisms in the promoter regions of the interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) genes have been reported to cause changes in the production of these cytokines. The aim of this study was to evaluate the possible role of IL-6 (G-174C) and tumour necrosis factor (G-308A) polymorphisms, in the severity of chronic periodontitis in an elderly population. In this study, a group of 65 elderly women, comprising 17 patients with moderate chronic periodontitis, 21 with severe chronic periodontitis and 27 healthy patients were selected. DNA was isolated from all subjects, and polymerase chain reaction was used to study the IL-6 and TNF-alpha gene polymorphisms. The results of this study showed a significant difference in the allele and genotype frequencies of IL-6 gene polymorphism between patients with periodontal disease and controls. Subjects carrying the G/G genotype of IL-6 were most severely affected by periodontitis. The TNF-alpha gene polymorphism showed no association with chronic periodontitis between patients and controls. The results suggest that the IL-6 gene polymorphism may be associated with chronic periodontitis, and that TNF-alpha gene polymorphism may not be involved in the progression of chronic periodontitis in the population of elderly Brazilian women.

Circulating interleukin-6 as a tumor marker for hepatocellular carcinoma

BackgroundA large amount of evidence suggests a possible role of interleukin-6 (IL-6) in the pathogenesis of hepatocellular carcinoma (HCC). Patients and methodsWe studied both IL-6 and A1FP in patients with HCC, non-neoplastic liver disease or in healthy controls. ResultsIL-6 titers were four-fold higher in cancer than in cirrhotic patients and 25-fold higher than in healthy controls. As for alpha1-fetoprotein (A1FP) titers, the highest levels were observed in cancer patients. Receiver operating characteristic (ROC) curves analysis demonstrated that IL-6 is significantly more discriminant than A1FP, with ‘optimal’ cut-off values of 7.9 pg/ml (sensitivity = 0.83, specificity = 0.83, efficiency = 0.83). The ROC curves used to distinguish HCC from cirrhotic patients only, showed higher discriminant power of IL-6 versus A1FP titers, with a new cut-off value of 12 pg/ml (sensitivity = 0.73, specificity = 0.87, efficiency = 0.8). Discriminant analysis on HCC and non-HCC subjects yielded sensitivity, specificity and efficiency rates of 77%, 93% and 88%, respectively. The overall efficiency of the two tests combined was 82%. ConclusionsIL-6 could be considered a promising tumor marker for HCC. In particular, the diagnostic value of the test is significantly increased when combined with A1FP.

Possible Role of Interleukin-6 in Rheumatoid Arthritis

Possible Role of Interleukin-6 in Rheumatoid Arthritis

Elevated intravitreal interleukin-6 levels in patients with proliferative diabetic retinopathy

Background: We conducted this study to elucidate the possible role of interleukin-6 (IL-6) in the pathogenesis of proliferative diabetic retinopathy (PDR). Methods: Together with pertinent clinical and laboratory data, intravitreal and serum concentrations of IL-6 were determined in 8 patients with PDR by means of enzyme-linked immunosorbent assay (ELISA). The results were compared with data from 8 nondiabetic control subjects undergoing vitrectomy. Results: Significantly higher intravitreal IL-6 concentrations were found in patients with PDR (mean [SD], 755 [177] pg/mL) compared with control subjects (93 [151] pg/mL) ( p = 0.001). The serum IL-6 levels in the PDR group were lower than the measurable threshold of the ELISA kit (<0.16 pg/mL). Diabetic patients with macular edema had a higher mean (SD) level of intravitreal IL-6 (896 [73] pg/mL) compared with patients without macular edema (613 [119] pg/mL) (Mann-Whitney U test, p = 0.03). Correlation analysis did not reveal any significant association between intravitreal IL-6 levels and patient age, duration of either diabetes mellitus or vitreous hemorrhage, panretinal photocoagulation, type of current medical therapy, hyperglycemia, or the biochemical indicators of renal function. Interpretation: IL-6, a proinflammatory cytokine, may have a role in PDR. Intraocular production of IL-6 appears to be responsible for the elevated intravitreal levels observed.

Elevated intravitreal interleukin-6 levels in patients with proliferative diabetic retinopathy

Background: We conducted this study to elucidate the possible role of interleukin-6 (IL-6) in the pathogenesis of proliferative diabetic retinopathy (PDR). Methods: Together with pertinent clinical and laboratory data, intravitreal and serum concentrations of IL-6 were determined in 8 patients with PDR by means of enzyme-linked immunosorbent assay (ELISA). The results were compared with data from 8 nondiabetic control subjects undergoing vitrectomy. Results: Significantly higher intravitreal IL-6 concentrations were found in patients with PDR (mean [SD], 755 [177] pg/mL) compared with control subjects (93 [151] pg/mL) (p = 0.001). The serum IL-6 levels in the PDR group were lower than the measurable threshold of the ELISA kit (<0.16 pg/mL). Diabetic patients with macular edema had a higher mean (SD) level of intravitreal IL-6 (896 [73] pg/mL) compared with patients without macular edema (613 [119] pg/mL) (Mann-Whitney U test, p = 0.03). Correlation analysis did not reveal any significant association between intravitreal IL-6 levels and patient age, duration of either diabetes mellitus or vitreous hemorrhage, panretinal photocoagulation, type of current medical therapy, hyperglycemia, or the biochemical indicators of renal function. Interpretation: IL-6, a proinflammatory cytokine, may have a role in PDR. Intraocular production of IL-6 appears to be responsible for the elevated intravitreal levels observed.