Interleukin-6 In Patients Research Articles

Evaluation of Serum Level of Interleukin 1 in Patients Suffering from Acute Coronary Syndrome, Admitted to the CCU Ward of AmirAlmomenin Hospital of Zahedan

Background: Atherosclerosis is a disease in which the particles of fat builds up in the blood vessel’s walls. This build up leads to blood flow blockage or can cause the arteries to narrow, but until the stenosis of the vessel is not more than 70 percent, there won’t be any obvious symptoms. Symptoms are dependent on the location of the stenosis that can bring about diseases such as, Unstable Angina (UA), Myocardial Infarction with Q Wave (MIQW) and Non Q Wave (NMIQW). The most common causes of death in most developed countries is Coronary Artery Disease (CAD), and since the inflammatory factors are one of the causes of these diseases, we decided to evaluate the level of the Interleukin-1 (IL-1) in patients with acute coronary syndrome. Methods: 90 patients, suffering from the acute coronary syndrome were selected, which were previously diagnosed and referred to a cardiologist in the Imam Ali Ebneh hospital’s cardiac ward, in 2011. Five ml of periphery blood was obtained from each patient, after 24 hours of hospitalization. Using the ELISA method, the level of interleukin-1 was measured in the three groups of patients, each with symptoms of UA, MIQW and MINQW. Results: Our findings, showed the highest level of interleukin-1 in the MIQW patients, with the average of 46.55 pg/ml and, the lowest level in the MINQW patients, with the average of 28.17 pg/ml. Moreover, the average level of IL-1 in the patient’s serum with UA, is determined equal to 31.28 pg/ml. Although, there was no significant correlations between the type of MI development and UA, there was a significant correlation between the level of IL-1 and the type of MI development. Conclusion: Despite the fact, that the level of IL-1 was higher than normal in all the group types, and no significant correlation between the type of MI development and UA was found, there was statistically a significant correlation between the types of MI development and the level of IL-1.

Serum Level of Interleukin 17 in Alopecia Areata Patients and Its Relation with the Severity of the Disease: a Case Control Study

Abstract Background Alopecia Areata (AA) is one of the most common autoimmune diseases that’s characterized by hair loss on the scalp and/or body. It is an organ-specific autoimmune disease characterized by T-cell infiltrates and cytokine production. T-helper 17 (Th17) cells are crucially involved in the pathogenesis of autoimmune diseases. Objectives Our aim was to compare the serum level of interleukin-17 (IL-17) between alopecia areata patients and healthy controls to demonstrate its proposed role in the pathogenesis of alopecia areata and to correlate it with the severity of the disease. Subjects and methods The serum concentration of IL-17 was measured in 26 patients with AA and 26 healthy controls. The clinical type of AA was determined, and the severity of scalp hair loss was assessed in accordance with the Alopecia Areata Investigational Assessment Guideline criteria. Results The serum concentration of IL-17 was significantly higher in patients with AA as compared with healthy. The IL-17 concentration among cases ranged from 133.38 – 325.99 pg/ml with a median of 195.38, while among controls, the IL-17 concentration ranged from 13.59 – 225.73 pg/ml with a median of 48.42. No statistically significant difference was found in IL-17 levels regarding age, sex, clinical type, duration of disease or severity. Conclusion The significantly higher levels of serum IL-17 in patients with AA suggest a possible role of IL-17 as a proinflammatory cytokine in the pathogenesis of AA. This could point to the potential benefit of IL-17 inhibitors in recalcitrant cases of alopecia areata.

303 Maintenance of Repigmentation After Discontinuation of Ruxolitinib Cream in Patients With Vitiligo

Treatment with ruxolitinib cream (Janus kinase [JAK] 1/JAK2 inhibitor) in adult patients with vitiligo resulted in substantial repigmentation over 52 weeks in a phase 2 dose-ranging study (NCT03099304). We assessed maintenance of repigmentation among responders from the phase 2 study following ruxolitinib discontinuation after 104 weeks of treatment. Patients initially randomized to ruxolitinib cream (1.5% twice daily [BID], 1.5% once daily [QD], 0.5% QD, or 0.15% QD) with evidence of facial repigmentation at Week 24 who completed ≥1 follow-up visit 1, 3, or 6 months after an additional 52 weeks of 1.5% ruxolitinib cream BID (Weeks 52–104) were analyzed. Loss of repigmentation was defined as an increase in Vitiligo Area Severity Index score during the last follow-up visit vs Week 104 on ruxolitinib cream. The analysis included 16 patients (1.5% BID, n=3; 1.5% QD, n=5; 0.5% QD, n=3; 0.15% QD, n=5 [including 2 patients rerandomized to 1.5% BID/0.5% QD after Week 24]). Twelve patients (75.0%) maintained total body repigmentation and 13 (81.3%) maintained facial repigmentation during follow-up of 1–6 months; no patients from the 1.5% ruxolitinib BID treatment group (with 2 years’ exposure) experienced repigmentation loss. There were no significant differences in baseline serum levels of chemokine (C-X-C motif) ligand (CXCL) 9, CXCL10, or interleukin-15 in patients who experienced loss vs maintenance of repigmentation after ruxolitinib cream discontinuation. This exploratory analysis suggests that some repigmentation with ruxolitinib cream may be maintained post-discontinuation; larger follow-up studies are required to confirm these findings.

Закономірності зміни концентрацій ІЛ-17А, ІЛ-10 та ІЛ-2 у крові людей із гніздовою алопецією до та після лікування збагаченою тромбоцитами плазмою

Alopecia areata is a heterogeneous disease characterized by nonscarring hair loss. It affects 1-2% of the population of both genders and occurs in all age groups. According to the recent studies, helper T cells 1, helper T cells 2, helper T cells 17, and regulatory T cells may be the main possible initiators of alopecia areata. The purpose of the study was to determine the concentrations of serum interleukin-17A, interleukin-10 and interleukin-2 in patients with alopecia areata, and to study the relationship between their levels before and after treatment with platelet-rich plasma. Materials and methods. The study involved 37 patients with alopecia areata aged (35.7±8.9) years and 30 people of the control group aged (37.4±7.9) years. People with alopecia areata were injected with platelet-rich plasma. For this, immediately before administration, venous blood was taken from the patients from the cubital vein into a special tube for the preparation of platelet-rich plasma. Platelet-rich plasma was injected into the lesions at the rate of 0.2 ml/cm2 using an insulin syringe and a 30 G needle, once every 2 weeks for 16 weeks. The patients were examined before the treatment and in 3, 6 and 17 months. The concentrations of interleukin-17A, interleukin-2 and interleukin-10 were determined in blood serum before treatment and after 3, 6 and 17 months of observation by the Sandwich-ELISA method (enzyme-linked immunosorbent assay). Interleukin-17A, interleukin-2 and interleukin-10 in the blood serum in the control group were also determined. The software program SPSS 22.0 was used for the statistical analysis. The normality distribution was tested by Shapiro-Wilk’s method. Independent Student’s t-test for unpaired samples was used to compare mean values between groups. The p-value < 0.05 was considered significant. Results and discussion. The results obtained in our study showed that the concentrations of the pro-inflammatory cytokines interleukin-17A and interleukin-2 were significantly higher in persons with alopecia areata before treatment. After 17 months of therapy with platelet-rich plasma, serum interleukin-17A and interleukin-2 levels approached the control level. Conclusion. There was no difference in the concentration of anti-inflammatory interleukin-10 between patients with alopecia areata and healthy people. In the course of treatment, the concentration of interleukin-10 increased after 3 and 17 months of therapy

Analysis of Serum Interleukin-37 Level and Prognosis in Patients with ACS.

Objective To explore the level of serum interleukin-37 in patients with acute coronary syndrome (ACS) and its prognostic value. Methods Altogether, 121 continuous ACS cases from September 2017 to June 2020 were selected as the research group (RG), and 107 healthy individuals during the same period were obtained as the control group (CG). ELISA was applied to test IL-37 in the serum of the CG and the RG. Chemiluminescence immunoassay was applied to test NT-pro BNP and hs-cTnI in each group and immune scattering turbidimetry to test hs-CRP. The correlation of IL-37 with serum NT-pro BNP, hs-cTnI, and CRP was analyzed, and the value of IL-37 in diagnosis and prognosis prediction of patients with ACS was tested. Logistic regression was applied to test the independent risk factors affecting poor prognosis of patients with ACS. Results IL-37 was poorly expressed in patients with ACS, which had a high diagnostic value for ACS (sensitivity: 94.39%, specificity: 74.38%, and area under curve: 0.945). There was a negative correlation of IL-37 with serum NT-pro BNP, hs-cTnI, and CRP. IL-37 in patients with poor prognosis was markedly declined compared with that of patients with good prognosis, and the predicted AUC was 0.965. Logistic regression revealed that low IL-37, diabetes, high CRP, NT-pro BNP, and hs-cTnI in the blood were independent risk factors for poor prognosis in patients with ACS. Conclusion IL-37 is low expressed in patients with ACS, which has a good diagnostic and prognostic value for ACS, and may be applied as an important marker for the prediction of patients with ACS.

Evaluation of Interleukin 33 and ST2 Serum Concentration in Active Tuberculosis Patients

The aim of this study was to determine the serum levels of ST2 protein and interleukin-33 in patients affected to tuberculosis and compare them with the control group. In the present study, at first 30 patients affected to TB were randomly selected and 52 healthy individuals, who were matched with respect to their age and gender, included in the study as the control group. After that, the serum levels of sST2 and IL33 were measured by ELISA sandwich method using commercial Quantikine Human ELISA kit (R&D Systems). The data were finally analyzed by SPSS software. IL-33 levels in the TB group were higher than the healthy controls and a statistically significant difference was observed in the IL-33 levels between the two groups (P = 0.021). Moreover, IL-33R (ST2) was slightly increased in the TB patients compared to the healthy controls, although statistical analysis showed no significant difference between the two groups (P = 0.083). Regarding the high normal variation of sST2 and the limitations of the present study, it is recommended that future studies of sST2 be performed in with higher number of TB patients.

The mineralocorticoid receptor blocker spironolactone lowers plasma interferon-γ and interleukin-6 in patients with type 2 diabetes and treatment-resistant hypertension.

The mineralocorticoid receptor antagonist spironolactone lowers blood pressure in patients with resistant hypertension despite antihypertensive treatment with angiotensin-converting inhibitors (ACEi) and angiotensin-II receptor blockers (ARB). In preclinical studies, spironolactone suppresses pro-hypertensive interleukin 17A (IL-17A). Plasma samples were analysed from a randomized, double-blind placebo-controlled trial with spironolactone given to patients with type 2 diabetes mellitus (T2DM) and resistant hypertension on three antihypertensive drugs. We tested the hypothesis that spironolactone-induced antihypertensive effects are associated with suppression of IL-17A and related cytokines. Interferon-γ (IFN-γ), IL-17A, tumor necrosis factor-α (TNF-α), IL-6, IL-1β and IL-10 were assessed in plasma with immunoassay in samples before and after 16 weeks of treatment with placebo or spironolactone (12.5-25-50 mg/day). Spironolactone significantly reduced plasma IFN-γ and IL-6 while IL-17A, TNF-α, IL-1β and IL-10 were unchanged. IL-6 was more sensitive to higher doses of spironolactone. At baseline, serum aldosterone correlated positively with diastolic night blood pressure. Urine albumin/creatinine-ratios correlated positively with plasma IL-6 at baseline. There were no relations between aldosterone and cytokine concentrations at baseline; between cytokine concentration and blood pressure at baseline; and between cytokine concentration decrease and blood pressure decrease, except for IFN-γ, after treatment. The spironolactone-induced elevation in plasma potassium related inversely to blood pressure but not to changes in cytokines. In macrophages in vitro, spironolactone suppressed lipopolysaccharide (LPS)-induced TNF-α, IL-6, IL-1β and IL-10 levels. The antihypertensive action of spironolactone in resistant hypertensive patients is associated with suppressed IFN-γ and IL-6 and not IL-17A. Spironolactone exerts anti-inflammatory actions in vivo on macrophages and T-cells.

Dynamics of interleukin-17 in patients with multiple sclerosis and two-phase model of disease patho-genesis

Objective. To study the concentration of the pro-inflammatory cytokine interleukin-17 in the blood serum of patients with multiple sclerosis.
 Materials and methods. 68 patients with multiple sclerosis were examined. The severity of neurological deficit was assessed by EDSS and MSFC. The concentration of interleukin-17 in the blood serum was determined by the method of enzyme-linked immunosorbent assay.
 Results. It was found that in patients with multiple sclerosis, the concentration of interleukin-17 in the blood serum, normal in the group as a whole, was induced by the effect of immunomodulatory therapy as well as the decrease in the activity of inflammatory processes with an increase in the duration of disease.
 Conclusions. It was found that MDDMS therapy is most effective in the early stages of the disease; in the later stages, activities associated with neurotrophic support play a special role.

Cytokine status in middle-aged men with acute coronary syndrome after coronary artery stenting

Background. Inflammatory cytokines and growth factors are involved in various mechanisms of coronary artery disease. Clinical studies have shown the correlation between the increase in the level of proinflammatory cytokines and the severity of coronary artery disease, while the data on the role of proinflammatory interleukin IL-8 and anti-inflammatory interleukin IL-4 are contradictory. The aim of the study is to assess the levels of proinflammatory cytokines (IL-8, TNF-) and anti-inflammatory interleukin (IL-4) in patients with various forms of coronary artery disease who underwent coronary artery stenting. Materials and methods. By the method of enzyme-linked immunosorbent assay, the levels of cytokines were determined in 30 patients with acute coronary syndrome who underwent primary stenting of the coronary arteries and in 24 patients with chronic coronary syndrome who had previously had myocardial infarction with stenting of an infarction-associated artery, who were admitted to the clinic for staged stenting of the coronary arteries. Results. In patients with chronic coronary syndrome the levels of IL-4 a do not exceed the reference values, in patients with acute coronary syndrome the levels of IL-4 there was an increase 3,70 0,24 and 240,85 49,25 pg/ml, р 0,001. In patients with chronic coronary syndrome the levels of IL-8 a do not exceed the reference values, in patients with acute coronary syndrome the levels of IL-8 there was an increase 7,34 1,29 and 110,33 27,67 pg/ml, р 0,001. Conclusion. Most likely the increase in the level of IL-4 has a compensatory character and, along with a slight increase in TNF-, can be considered as a positive factor stabilizing the course of the disease. There may be some relationship between of the increase in the level of interleukins in patients with acute coronary syndrome on the degree of stenosis of the coronary arteries (9095%) and impaired myocardial contractility was established.

Predictive values of sST2 and IL-33 for heart failure in patients with acute myocardial infarction.

Timely prediction of the risk of heart failure in acute myocardial infarction patients is critical for better prognosis. This article aims to evaluate the predictive value of serum soluble growth stimulation expressed gene 2 (sST2) and interleukin-33 in patients with acute myocardial infarction complicated by heart failure. A total of 42 healthy controls and 144 acute myocardial infarction patients were recruited in the study. According to Killip cardiac function classification as the basis for concurrent heart failure, they were distributed into non-heart failure group (n = 76) and heart failure group (n = 68). ELISA was utilized to determine the serum sST2 and interleukin-33 levels, and the diagnostic efficiency was evaluated by receiver operating characteristics curve. sST2 and interleukin-33 levels in patients with acute myocardial infarction were significantly increased when compared with normal healthy controls, and were further enhanced in the heart failure group. With the increased Killip cardiac function classification, interleukin-33 and sST2 levels were gradually elevated. Multivariate analysis indicated that interleukin-33 and sST2 could be used as independent predictors for heart failure combined with acute myocardial infarction.

Lower levels of interleukin-35 in patients with prophase of liver failure are associated with progression to liver failure.

Cytokines play critical roles in the inflammatory processes underlying liver failure. The relevance of interleukin-35 (IL-35), an anti-inflammatory cytokine, in liver failure remains uncharacterized. This study was conducted to investigate whether the IL-35 level in patients with prophase of liver failure (PLF) is associated with prognosis and the possible mechanism of immune regulation for IL-35. This retrospective study enrolled 42 patients with PLF at the Department of Infection, First Affiliated Hospital of Soochow University between January 2016 and December 2018. Thirty patients with hepatitis and 30 healthy controls were also enrolled. We divide patients with prophase of liver failure into improvement group who recovered quickly (n=33) and deteriorate group who deteriorated to overt liver failure (n=9). Serum IL-35 level was measured by enzyme-linked immunosorbent assay (ELISA). The ratio of regulatory T cells to T-helper type-17 cells (Treg/Th17) in peripheral blood was determined by flow cytometry. Serum IL-35 level was higher in patients with PLF who showed subsequent improvement than in patients with PLF who showed deterioration to overt liver failure. The Treg/Th17 ratio was higher in patients with PLF who showed improvement than in patients with PLF who developed overt liver failure. The serum IL-35 level and Treg/Th17 ratio were positively correlated in patients with PLF. High serum IL-35 level is associated with better prognosis in patients with PLF.

The Prognostic Determinant of Interleukin-10 in Patients with Acute Ischemic Stroke: An Analysis from the Perspective of Disease Management.

Background In patients with ischemic stroke, the role of anti-inflammatory cytokine Interleukin-10 (IL-10) in predicting risk and outcomes is not very clear. This study is aimed at prospectively assessing the prognostic determinant value of IL-10 in patients with acute ischemic stroke in a cohort of Chinese people. Methods In a prospective cohort study, consecutive first-ever patients with acute ischemic stroke admitted to our hospital were included from October 2019 to October 2020. The serum level of IL-10 was measured at baseline. A structured follow-up telephone interview was performed on day 90 after admission. Logistic regression analyses were used to assess the prognostic value of IL-10 to predict the poor functional outcome (defined as a modified Rankin Scale score of 3 to 6) and mortality. Results The median age of the 236 enrolled patients was 65 years (interquartile range (IQR), 56-76), and 57.6% were male. There was a negative correlation between the National Institutes of Health Stroke Scale (NIHSS) score and IL-10 serum levels (r (Spearman) = −0.221, P = 0.001). Patients with elevated IL-10 levels (> the highest quartile = 5.24 pg/mL; n = 79) were at significantly lower risk of poor functional outcomes (odds ratio (OR), 0.35; 95% confidence interval (CI), 0.19 to 0.63; P < 0.001) and mortality (OR = 0.24; 95% CI = 0.11–0.52; P < 0.001) compared with patients with IL-10 levels in the lowest three quartiles. Conclusions Reduced serum levels of IL-10 were independently associated with both the clinical severity at admission and a poor functional prognosis in ischemic stroke patients, suggesting that the anti-inflammatory cytokine IL-10 was an important prognostic determinant.

Gene polymorphism and serum levels of interleukin-18 in patients with coronary artery disease and type 2 diabetes mellitus

Background Circulating concentrations of interleukin-18 (IL-18) were shown to be correlated with the vascular events in patients with coronary artery disease (CAD). Objectives To assess the serum levels of IL-18 and its gene polymorphism in CAD and diabetic patients and correlate these findings with clinical, echocardiographic, laboratory, and coronary angiographic findings. Patients and methods This cross-sectional observational study included 180 patients, who were divided according to presence or absence of CAD and type 2 diabetes mellitus into four groups: group I (41 patients), nondiabetic patients without CAD; group II (51 patients), nondiabetic patients with CAD; group III (40 patients), diabetic patients without CAD; and group IV (48 patients), diabetic patients with CAD. Serum levels of IL-18 and its genotyping distributions were measured in all groups and correlated with the angiographic coronary scoring systems. Results Serum IL-18 level was higher significantly in patients with CAD (groups II and IV) than in patients without CAD (groups I and III) (P Conclusion IL-18 is a novel and independent risk factor for CAD, and it is associated with its extent and severity. IL-18 gene polymorphism at 137 G/C site could be a risk factor for development of CAD, presumably by increasing serum IL-18 levels. Individuals carrying the G allele and the G/G genotype of IL-18 have an increased risk to develop CAD.

ROLE OF MACROPHAGE MIGRATION INHIBITORY FACTOR, CLUSTER OF DIFFERENTIATION 19 AND INTERLEUKIN 23 IN INDIVIDUALS INFECTED WITH Salmonella typhi

Salmonella enterica serovar typhi (S.typhi) is one of the most important gram negative bacteria that cause enteric fever and stimulate the immune response in infected patients. This study aimed to compare the humoral and cellular immune responses in patients infected with S.typhi. For this, the concentration of three immunological markers viz., Macrophage migration inhibitory factor (MIF), Cluster of Differentiation 19 (CD19), and Interleukin 23 (IL-23) were measured by the Enzyme-Linked Immunosorbent Assay in the serum of 54 S.typhi infected patients, and 31 healthy individuals. The results demonstrated a significant increase (P =&lt;0.05) in the serum concentration of MIF in patients infected with acute infection of S. typhi compared with healthy individuals but there were no significant differences in chronic infection. While there was a significant increase (P =&lt;0.05) in serum concentration of CD19 and IL-23 in patients infected with acute and chronic infection of S.typhi as compared with healthy individuals. In conclusion, macrophage migration inhibitory factor plays a vital role in patients infected with acute infection of S. typhi and has no synergism with T-cell and B-cell in acute and chronic infection.

Celastrol Regulates the Secretion of Interleukin-17 in Patients with Sympathetic Ophthalmia Through Signal Transducer and Activator of Transcription 3.

Purpose: The excessive secretion of interleukin (IL)-17 contributes to the pathological process of sympathetic ophthalmia (SO). Celastrol is a naturally active product and exhibits an immunosuppressive effect. However, whether the supplementation of celastrol relieves SO remains unclear. Methods: The peripheral blood mononuclear cells (PBMCs) were extracted from the venous blood samples of 20 SO patients and 20 healthy controls, followed by stimulating with various concentrations of celastrol. The levels of IL-23 and IL-17 were measured by enzyme-linked immunosorbent assay and real-time polymerase chain reaction assay. The activation of the signal transducer and activator of transcription 3 (STAT3) in PBMCs of SO patients was detected by Western blot. Results: The levels of IL-23 and IL-17 in PBMCs isolated from SO patients were significantly increased compared with those in PBMCs isolated from healthy controls. Celastrol treatment inhibited the production of both IL-23 and IL-17 in PBMCs of SO patients in a dose-dependent manner. In PBMCs isolated from SO patients and healthy controls, the administration of recombinant human IL-23 (rIL-23) enhanced the production of IL-17, which was then suppressed by co-stimulation with celastrol. Also, celastrol treatment reduced rIL-23-induced phosphorylation of STAT3 in PBMCs isolated from SO patients. Conclusions: Celastrol can reduce the production of IL-17 in PBMCs of SO patients. The mechanism may be related to the reduction of IL-23 secretion, which in turn inhibits the phosphorylation of STAT3.

Diagnostic value of IL-17 in neurointoxication with mercury

It is known that sufficient changes are observed in cellular and humoral links of immune system upon chronic exposure vapors of metallic mercury. In previous studies, upon development and in the course of the chronic mercury intoxication (CMI) we revealed pronounced regular changes of inflammatory mediators (IL-1, IL-2, IL-4, IL-6, IL-8, IL-10, TNFα), and showed an important role of autoimmune reactions affecting nervous tissue proteins. Over last 20 years, an increased interest was shown for interleukin 17 (IL-17) and its role in a number of inflammatory and autoimmune diseases. However, there is no data on its role in neurointoxication with mercury. Considering that IL-17 has proinflammatory activity and stimulates production of the individual cytokines, the goal of our work at the next stage of research, was to identify quantitative changes of serum IL-17 in patients with mercury neurointoxication of various severity, aiming to substantiate additional criteria for early and effective diagnosis of the disease.The study was performed in males chronically exposed to metallic mercury vapors with early signs of neurointoxication (n = 37), individuals diagnosed with CMI (n = 40), and “conditionally healthy” men (n = 34). Proper diagnosis confirmed by history of working contacts with a harmful industrial factor, and absence of comorbid pathologies served as inclusion criteria. Statistical processing of the results was carried out using the STATISTICA 6.0 application package (StatSoft, USA). The study has revealed a statistically significant increase in serum IL-17 concentrations, both in the patients with early signs of neurointoxication with metallic mercury vapors, and individuals with CMI, when compared with the comparison group, thus indicating its activation, and being consistent with results of several workers who showed an IL-17 increase in immunoinflammatory diseases. Correlation analysis has shown an association between IL-17 and inflammatory mediators, i.e., the patients with early signs of neurointoxication had an increased production of IL-17 accompanied by an increase in anti-inflammatory IL-10, whereas the CMI patients with an increase in IL-17 concentration showed a decrease in pro-inflammatory TNFα, thus confirming its role in immunopathogenesis of mercury neurointoxication. Further study of IL-17 involvement in the initiation and maintenance of chronic inflammation will not only contribute to better understanding of the disease origin, but also, most importantly, implication of novel, more effective treatments.

Sleep moderates the effect of positive affect on circulating interleukin-6 in patients with temporomandibular disorder

Temporomandibular disorders (TMD) are idiopathic orofacial pain conditions. Inflammation—particularly elevated circulating levels of interleukin-6 (IL-6)—is associated with pain symptoms. Prior work in healthy samples has shown that trait positive affect (PA) is associated with lower IL-6, but that poor sleep attenuates PA and elevates IL-6. Although poor sleep has been associated with increased IL-6 in chronic pain, the effects of trait PA on IL-6 and potential moderation by sleep are not known. We thus investigated the effect of PA on circulating IL-6 and moderation of that effect by sleep, in 118 women with TMD and at least subclinical insomnia. Participants completed the insomnia severity index at baseline and subsequently completed a 14-day daily diary assessing sleep continuity, PA and negative affect. Sleep continuity was objectively assessed with wrist actigraphy over the same period. Both diary and actigraphy data were aggregated by computing person means. IL-6 was measured via blood samples obtained at 5 intervals prior to (i.e., resting), during and following an evoked pain testing session involving painful mechanical, heat and cold stimuli. PA did not predict resting or pain-evoked IL-6. However, multiple measures of sleep interacted with PA in the prediction of resting IL-6. Specifically, diary total sleep time (TST; b = -0.002, p = .003) and insomnia severity (b = .02, p = .03) moderated the effect of PA on resting IL-6, such that higher PA predicted lower resting IL-6 only when insomnia severity was lower or TST was higher. Remaining measures of sleep continuity were not significant moderators. Lower self-reported TST and higher insomnia severity eroded the salutary effects of PA on resting IL-6, underscoring sleep as a key intervention target in TMD. Modulation of positive affect's effect on IL-6 could be a pathway through which poor sleep impacts TMD-related outcomes. 3R01DE019731-05S1.

Assessment of Serum Level of Interleukin-17 in Patients with Vitiligo

Vitiligo is a multifactorial disorder related to both genetic and non-genetic factors. The pathogenesis of vitiligo is associated with the melanocytes destruction that may result from immune and inflammatory mediators. The autoimmune theory is the most important theory about the pathogenesis of vitiligo. The aims of the study are the evaluation and assessment of serum levels of IL17 in vitiligo patients to reveal their possible role in pathogenesis of vitiligo and to correlate their levels with the severity of the disease. Patients and Methods: In this study, thirty patients (15 male and 15 females) were included in the present study and 30 apparently healthy, age and sex matched individuals were included as a control group. Patients were recruited from the outpatient clinic of Benha University Hospitals from Dermatology, Venereology and Andrology Department. All patients were subjected to full history, full dermatological and general examination. Measurement of serum levels of IL-17 using the commercially available ELISA kit. Results: The present study revealed significant increase in serum levels of IL-17 in patients than controls. Conclusion: Vitiligo is associated with increased serum level in IL-17 indicating that IL-17 may play a significant role in the pathogenesis of vitiligo.

The Effectiveness of Acceptance and Commitment Therapy on Distress Tolerance, Pain Perception and Interleukin-12 in patients with Multiple Sclerosis

The Effectiveness of Acceptance and Commitment Therapy on Distress Tolerance, Pain Perception and Interleukin-12 in patients with Multiple Sclerosis

Immunoglobulin E and Serum Interleukin-4 in Patients with Alopecia Areata and Its Correlation to the Severity of the Disease

Immunoglobulin E and Serum Interleukin-4 in Patients with Alopecia Areata and Its Correlation to the Severity of the Disease