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Background Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation, hyperpigmentation, scarring, and psychological impact. Aim The purpose of this study was to investigate the significance of two genetic variants in the promoter region of the tumor necrosis factor‐alpha (TNF‐α) gene and their association with insulin resistance (IR) in acne patients. To understand how these variants contribute to AV and its associated IR. Subjects and methods An analytical cross‐sectional study with a case‐control design and research evaluation was carried out on 87 AV patients and 73 healthy volunteers. The medical histories of both groups were obtained, as well as the severity and duration of inflammation among acne sufferers, as well as demographic data. Biochemical analysis was performed on both sets of participants, including fasting blood glucose levels, insulin levels while fasting, IR, and serum TNF‐α. PCR‐RFLP analysis identified −863 G > A (rs1800630) and −308 G > A (rs1800629) variations, and real‐time PCR analysis evaluated TNF‐α gene expression in both patients and healthy people. Results Acne patients exhibited significantly higher levels of IR, fasting glucose, fasting insulin, serum TNF‐α, and TNF‐α folding change, when compared to healthy controls. The co‐dominant model for −863 G > A and −308 G > A variants exhibited significant variations between the two groups. Severe acne patients who had the A/A genotype for −308 variants exhibited higher levels of IR, serum TNF‐α, and TNF‐α folding change. Highly significant positive linear correlation between IR, serum TNF‐α, and TNF‐α folding change in severe AV. Conclusion There is a correlation between AV, especially severe acne, and the −863 G > A and −308 G > A polymorphism, which influences TNF‐α gene expression and serum TNF‐α levels.

Rheumatoid arthritis (RA) is a severely disabling chronic autoimmune disorder that leads to progressive inflammation of the joints and surrounding tissues. TNF-α, a potent proinflammatory cytokine, plays a pivotal role in the pathogenesis of RA. The endogenous formation of TNF-α may be influenced by TNF-α promoter polymorphisms. Hence, the present study was designed to explore any possible association between genetic polymorphism of TNF-α -308 G/A, messenger RNA (mRNA) expression, serum levels of TNF-α, and inflammatory markers in North Indian RA patients. A total of 214 controls and 187 RA patients were recruited according to the revised American College of Rheumatology 2010 criteria. TNF-α -308 G/A genetic polymorphism within promoter region was analyzed by using PCR-RFLP. Levels of inflammatory markers and serum TNF-α were estimated by ELISA. The mRNA expression of TNF-α gene was measured by quantitative real-time PCR. Higher levels of autoantibodies (RF and anti-CCP) were present in RA patients as compared to controls. We found a positive and significant correlation of circulating TNF-α levels with RF ( r  = 0.18), anti-CCP ( r  = 0.16), and mRNA expression of TNF-α gene ( r  = 0.57) in RA patients. The mRNA expression levels of TNF-α was 4.5-fold higher in patients with RA as compared to controls. The heterozygous mutant variants (G/A) and homozygous mutant variants (A/A) were found to be significantly associated with RA as compared to control (OR = 1.52 and 3.02, respectively). Our observations illustrated a significant association of allele -308 A TNF-α with progression of RA. Significant and positive correlation of TNF-α levels with mRNA expression and inflammatory marker levels suggests that serum TNF-α may be a susceptibility marker for RA.

BackgroundInflammation is suggested to play a role in the development of non-motor Parkinson’s disease (PD) symptoms. We aimed to investigate the association between serum tumor necrosis factor-alpha (TNF-α) levels and cognition in PD patients. Thirty patients with PD and 30 healthy controls were included. Evaluation and staging of PD were done using Unified PD Rating Scale. Cognitive assessment was done using Addenbrooke’s Cognitive Examination (ACE-III) and trail making B tests. Measurement of serum levels of TNF-α was done.ResultsPatients had significantly worser cognitive scores than controls except for language subclass of ACE score. Mean serum TNF-α level was significantly greater in PD patients as compared to controls. TNF-α serum level was significantly negatively correlated with ACE visuospatial function. Sensitivity and specificity of TNF-α to detect cognitive dysfunction in PD using ACE III and trail making B tests were (73.1, 75%), (57.1, 56.2%), respectively, whereas sensitivity and specificity of TNF-α to detect severity of PD using H&Y staging in PD were 50%.ConclusionPatients with PD frequently have cognitive impairment. Elevated serum TNF-α levels in patients with PD, and association of this cytokine to visuospatial impairment, implicate this pro-inflammatory cytokine in the neurobiology of cognitive impairment in PD.

Vitiligo is a chronic acquired pigmentary disorder of the skin; it results from immunological distruction of functioning melanocytes. The cytokine TNF-α plays a central role in the initiation of melanocyte apoptosis in vitiligo. Single nucleotide polymorphism (SNP) in the promoter region of the gene coding for serum TNF-α may affect its production. The aim of this study is to assess serum TNF-α as a risk factor for generalized vitiligo among Iraqi patients and to rule out that polymorphism at the position affects serum TNF-α. This case-control study was conducted at Sulaymaniyah Dermatology Teaching Center (SDTC), Iraq. Serum concentration of TNF-α was measured using enzyme linked immunosorbent assay (ELISA) technique in 80 patients with generalized vitiligo and 40 clinically healthy controls. The amplification refractory mutation system polymerase chain reaction (ARMS-PCR) technique was used for detection of TNF gene polymorphism. TNF-α level correlated with TNF- gene polymorphism. Serum concentration and TNF gene polymorphism have been analyzed in correlation with demographic features and clinical characteristics of patients with generalized vitiligo. Statistically significant elevation of serum TNF-α seen in patients compared to a control group ( -value 0.01). Significantly higher TNF-α level ( -value 0.01) found among patients with active generalized vitiligo. Elevated serum levels of TNF-α were significantly associated with both TNFA1 (TNF ) allele ( value 0.04) and TNFA2 (TNF A) allele ( -value 0.03). TNF-α polymorphism was not affected by demographic features and clinical characteristics of patients with generalized vitiligo. TNF-α in the serum is a risk factor for generalized vitiligo among Iraqi patients. Patients with active vitiligo have a higher serum TNF-α level. No difference was found between serum level of TNF-α with TNF-α polymorphism at position (TNF ). This involves substituting G allele for the A allele.

BackgroundMultiple sclerosis (MS) is an inflammatory demyelinating disorder that affects the central nervous system (CNS) of females more than males. The objective of the current study was to assess serum level of prolactin (PRL) and tumor necrosis factor alpha (TNFα) in patients with relapsing remitting multiple sclerosis (RRMS) and to explore their role in disease activity.Subjects and methodsFifty females were included in this study, 40 patients with RRMS were evaluated during relapse and remission and 10 age-matched healthy subjects who served as controls. All patients were subjected to neurological evaluation including Expanded Disability Status Scale (EDSS), brain, and spine magnetic resonance image (MRI); serum PRL and TNFα levels were measured for all patients (during relapse and remission) and controls.ResultsMedian serum PRL level was significantly higher in MS patients during relapse than remission and control subjects (P = 0.041). TNFα level was significantly higher in MS patients in relapse than remission (P = 0.026) as well as the healthy controls (P = 0.001). The area under the receiver operating characteristic curve (AUROC) was analyzed for prediction of MS relapse, AUROC of serum TNFα was 0.811 and that of serum PRL was 0.678. Both serum PRL and TNFα were positively correlated in MS patients in relapse with each other (r = 0.672, P < 0.001) and also with age, EDSS, number of relapses, and MRI lesion number (P value = 0.001).ConclusionElevated serum PRL and TNFα levels are associated with relapse in MS patients. Moreover, they are positively correlated with EDSS, disease duration, and MRI lesion number.

Diabetic foot ulcer (DFU) is among the many complications of diabetes and it takes a very long period of time to heal. It can lead to the amputation of the lower limb, thereby resulting to death or in most cases, a bad quality of life. The aim and objective of this study is to assess the effect of bitter melon leaves extracts on serum TNF-α levels and improvement of diabetic foot ulcers. The study technique used here is the randomized, double-blinded, placebo-controlled trial. Thirty patients suffering from DFU participated in the trial and according to PEDIS scores were divided into two groups, of which 15 patients were in the treatment group and administered with bitter melon leaves extract at a dose of 6 g/day and the remaining 15 patients were in the control group and were given placebo. This intervention was done for 4 weeks and the examination of serum TNF-α levels was carried out at baseline and at the end of treatment. The readings of the healing process for diabetic foot ulcers with PEDIS scores were also taken at baseline, weeks 2, 3 and 4. Data were analyzed using the paired t-test and the independent t test. After 4 weeks of treatment, there was a decrease in baseline serum TNF-α levels in the treatment and control groups (29.5 ± 8.6 pg/ml, P = 0.0001 and 202.5 ± 610.2 pg/ml, P = 0.001). There was no effect on serum TNF-α levels (P = 0.28). There was a decrease in PEDIS degrees from baseline, week 2, 3 and 4 in the treatment and control groups (2.7±0.5; 2.7±0.5; 2.7±0.6; 1.9±0.6 and 2.6±0.5; 2.6±0.5; 2.5±0.6; 2.2±0.8). However there was no effect on diabetic foot ulcer improvement both groups in week 2 (P = 0.46), week 3 (P = 0.57) and week 4 (P = 0.29). Bitter melon leaves extracts is proven to have no effect on the serum TNF-α levels and improvement of diabetic foot ulcers.

Purpose: To examine whether associations exist between chronic insomnia disorder (CID) and overlooked inflammatory factors (Serum amyloid protein A [SAA]), tumor necrosis factor [TNF]-[alpha], granulocyte-macrophage colony-stimulating factor [GM-CSF], and regulated on activation and normal T cell expressed and presumably secreted [RANTES]). Patients and Methods: A total of 65 CID patients and 39 sex- and age-matched good sleeper (GS) controls participated in this study. They completed a baseline survey to collect data on demographics, and were elevated sleep and mood by Pittsburgh Sleep Quality Index (PSQI), Athens Insomnia Scale (AIS), 17-item Hamilton Depression Rating Scale (HAMD17) and 14-item Hamilton Anxiety Rating Scale (HAMA-14), respectively. The blood samples were collected and tested the serum levels of SAA, TNF-[alpha], GM-CSF and RANTES. Results: The CID group had higher serum levels of SAA, TNF-[alpha], and GM-CSF and a lower level of RANTES than the GS group. In the Spearman correlation analysis, SAA and GMCSF positively correlated with the PSQI and AIS scores. After controlling for sex, HAMD17 score, and HAMA-14 score, the partial correlation analysis showed that GM-CSF was positively correlated with PSQI score. Further stepwise linear regression analyses showed that GM-CSF was positively associated with the PSQI and AIS scores, while RANTES was negatively associated with them, and SAA was positively associated with just the AIS score. Conclusion: The serum levels of inflammatory mediators (SAA, TNF-[alpha], and GM-CSF) were significantly elevated and the level of RANTES was significantly decreased in CID patients and, to some extent, the changes are related to the severity of insomnia. These findings may help us to improve interventions to prevent the biological consequences of CID by inhibiting inflammation, thereby promoting health. Keywords: chronic insomnia disorder, serum amyloid protein A; tumor necrosis factor (TNF)-[alpha], granulocyte-macrophage colony-stimulating factor, regulated on activation and normal T cell expressed and presumably secreted

Although it has been reported that the MHC class I molecule, HLA-B51, is a risk factor for Behçet's disease (BD), contribution of the tumor necrosis factor (TNF) genes, which are located in the vicinity of the HLA-B locus, to the genetic susceptibility for BD has yet to be elucidated. The purpose of this study was to analyze the effect of TNF-alpha promoter polymorphisms at positions -308, -238 and -376 on the susceptibility, severity and clinical features of BD. The TNF-alpha gene sequences from 107 patients with BD and 102 healthy subjects were amplified by the polymerase chain reaction. Sequence analysis of the TNF-alpha gene locus, which contains promoter polymorphisms at positions -376, -308, and -238, was performed with a DNA sequencing kit on automated sequencer. The patients were classified according to disease severity and clinical features. Serum TNF-alpha level in the study groups was measured by sandwich enzyme immunoassay. In patients with BD the frequencies of TNF-alpha -308 (19.4% vs 18.4%), -238 (3.7% vs 5.9%), and -376 (0.9% vs 2.9%) gene polymorphisms were not found to be significantly different from those in healthy subjects. The TNF-alpha gene polymorphisms did not show any association with disease severity or clinical features. Serum TNF-alpha level was significantly higher in patients with BD than in healthy controls (3.10 +/- 1.45 pg/ml vs 2.43 +/- 1.94 pg/ml, P < 0.01). Serum TNF-alpha level was not found to be significantly associated with disease severity, activity, clinical findings and TNF-alpha genotypes. The results of this study suggest that the TNF-alpha gene polymorphisms are unlikely to play an important role in the pathogenesis and severity of BD.

The possible role of serum interleukin 4 (IL-4) and tumor necrosis factor alpha (TNF- α) in pathogenesis of the reflux symptoms in children with primary acid gastroesophageal reflux (GER) and acid GER secondary to cow's milk allergy (CMA). Out of 264 children, 76 (28.8%) patients with primary GER and 62 (23.5%) patients with GER secondary to CMA (pH – monitoring) serum IL-4 and TNF- α concentrations were assessed before treatment, 1 and 2 years after the initiation of the periodically administered pharmacotherapy. Children with primary GER had mean IL-4 concentrations 0.17 ± 0.06 pg/ml before treatment, 0.08 ± 0.07 pg/ ml after 1-year and 0.07 ± 0.06 pg/ml after 2-years of treatment. The mean IL-4 concentrations were 1.07 ± 0.24, 0.5 ± 0.22 and 0.44 ± 0.19 pg/ml respectively in children with GER secondary to CMA. The mean serum TNF- α concentrations was 3.62 ± 1.30 pg/ml before treatment, 2.16 ± 1,35 pg/ ml after 1 year and 1.65 ± 1.16 pg/ml after 2 years of treatment in children with primary GER. In group with GER secondary to CMA mean serum TNF- α concentrations were 4.95 ± 1.88, 2.53 ± 0.80 and 2.02 ± 0.78 pg/ml respectively. Statistical analysis of the concentration of both cytokines showed their differentiation between them and in the study groups. The highest mean serum IL-4 and TNF-α concentrations were observed in children with GER secondary to CMA and in children in control group (with cow's milk allergy and/or other food allergy diagnosed – CMA/FA) before the treatment administration.

The present study was designed to investigate the hypothesis that selective loss of peripheral blood CD45RO+ T lymphocytes in patients with chronic idiopathic neutropenia of adults (CINA), previously reported from our laboratory, may be due to enhanced extravasation into the tissues. Serum levels of endothelial cell-derived soluble cell adhesion molecules (sELAM, sICAM and sVCAM), usually used as indicators of endothelial cell activation, were measured in 73 CINA patients and 32 healthy volunteers using a micro-ELISA method. We found that patients had markedly elevated concentrations of all three soluble cell adhesion molecules studied compared to the controls, and serum levels of sELAM, sICAM and, more importantly, sVCAM correlated inversely with the numbers of both CD4+/CD45RO+ and CD8+/CD45RO+ T cell subsets. Using a micro-ELISA method, we also measured serum levels of two endothelial cell activators, interleukin (IL)-1beta and TNF-alpha, and found that CINA patients had significantly higher cytokine concentrations than control subjects. Serum levels of IL-1beta and TNF-alpha correlated positively with the values of all three soluble cell adhesion molecules and inversely with the numbers of CD4+/CD45RO+ and CD8+/CD45RO+ T cell subsets. Moreover, we measured serum levels of the chemokine RANTES by a micro-ELISA technique and found that CINA patients also had elevated concentrations of the molecule compared to controls. Serum RANTES correlated positively with IL-1beta, TNF-alpha, sICAM, sVCAM and sELAM and inversely with the numbers of both CD4+/CD45RO+ and CD8+/CD45RO+ T cell subsets. These findings strongly suggest that CINA patients have an activated endothelium to which CD45RA+ and CD45RO+ T cells tether and roll, but firm adhesion and transendothelial migration are restricted to CD45RO+ T cell subsets, as endothelial VCAM-1 interacts with the vascular leukocyte adhesion molecule-4 (VLA-4) constitutively expressed on CD45RO+ but not on CD45RA+ T cells. Subsequent subendothelial and tissue migration of CD45RO+ T cells may be facilitated by the chemokine RANTES, which acts mainly on CD45RO+ T cells. We concluded that selective loss of peripheral blood CD45RO+ T lymphocytes in CINA patients is probably due, at least in part, to enhanced extravasation of both CD4+/CD45RO+ and CD8+/CD45RO+ T cell subsets into the tissues.