TNF-α In Patients Research Articles

Evaluation of TNF-α Concentration Level in Al-Najaf Hospitals Patients Infected with Hydatid Cysts

Human echinococcosis is a zoonotic disease caused by a species of medical importance, the Echinococcus granulosus , an etiological agent of cystic echinococcosis (CE). A radiological examination will be performed for these patients to diagnose Echinococcus granulosus parasite by find echinococcal cysts. All of these patients were involved in this study and during the period starting from October 2023 to the end of January 2024, from all ages of patient from both sex (Males and Females At Al-Sader Medical City, AL-Hakeem General Hospital, AL-Haidarya general Hospital and Al-Hayat Hospital. The mean level of TNF-α in patients is 163.27 pg/ml, which is significantly higher than the mean level of 38.58 pg/ml in controls (p-value < 0.001). The prevalence of hydatid disease in Al-Najaf Al-Ashraf in this study was 33%. Levels of the cytokines IL-6, TNF-α, IL-1ß, and IL-4 are more important in patients with Echinococcus granulosus under 40 years of age than in those over 40 years of age.

Expression of neutrophil extracellular trap-related proteins and its correlation with IL-17 and TNF-α in patients with oral lichen planus.

Neutrophil extracellular traps (NETs) are produced by polymorphonuclear neutrophils (PMNs) stimulated by interleukin-17 (IL-17) and tumor necrosis factor α (TNF-α). However, the level and role of NETs in oral lichen planus (OLP) remain poorly understood. This study aimed to investigate the expression of NETs in OLP and explore the correlation between NETs and the levels of IL-17 and TNF-α. The expression and distribution of NET-related proteins in tissue samples from each group were assessed using hematoxylin-eosin (HE) staining and immunofluorescence (IF). Additionally, the expression of NET-related proteins in peripheral blood samples from each group was evaluated using cell IF technique and fluorescence spectrophotometry. The relative formation level of NETs in each group was determined by fluorescence spectrophotometry via plasma co-culture. Furthermore, the levels of inflammatory cytokines IL-17 and TNF-α in plasma and culture supernatant were measured using enzyme-linked immunosorbent assay (ELISA). NET-related proteins were located in the subepithelial and lamina propria layers of OLP lesions. OLP had significantly higher expression of NET-related proteins in lesion tissues and peripheral blood compared to the healthy control (HC) group (p < 0.05). The rate of NETs formation in the erosive-stage OLP (EOLP) group was significantly higher than that in the HC group (p < 0.05), in contrast, no significant increase was observed in the non-erosive OLP (NEOLP) group (p > 0.05). Furthermore, the levels of IL-17 and TNF-α in the EOLP group were significantly elevated compared to those in the NEOLP group and HC group (p < 0.05), while the levels in the NEOLP group did not significantly differ from those in the HC group (p > 0.05). The rate of NETs formation showed a positive correlation with the levels of IL-17 and TNF-α in plasma. The expression of NET-related proteins was upregulated in OLP lesion tissues and peripheral blood. Elevated levels of IL-17 and TNF-α in peripheral blood plasma positively correlated with the rate of NETs formation, suggesting that IL-17 and TNF-α mediate the formation of NETs in OLP patients, and may thereby contribute to the development of OLP.

MicroRNA-296-5p Expression in COVID-19 Patients and its Relationship with Inflammatory Cytokines

Objectives: The cytokine storm, triggered by the activation of certain pro-inflammatory genes in the second phase of COVID-19, is associated with severe acute respiratory disorder. Evidence suggests that microRNAs (miR) and cytokine levels can play pivotal roles in host cell antiviral defense mechanisms. This study aimed to investigate the changes in IFN-γ inducible protein 10 (IP-10) and miR-296-5p expression, as well as their relationship with some inflammatory cytokines and biochemical variables in COVID-19 patients. Methods: This retrospective single-center study was conducted on 30 COVID-19 patients and 30 controls. The expression of miR-296-5p and IP-10 genes in peripheral blood mononuclear cells (PBMCs) was evaluated using real-time PCR. Serum levels of IL-6, TNF-α, and CRP were measured by ELISA. Results: Higher expression levels of miR-296-5p and IP-10 genes were observed in COVID-19 patients compared to controls (P=0.001). Furthermore, IP-10, IL-6, and TNF-α levels were significantly higher (PP&lt;0.01) in COVID-19 patients than in controls. The results also showed positive correlations between miR-296-5p expression and serum levels of IL-6, CRP, and TNF-α in patients with COVID-19. ROC curve analysis of miR[1]296-5p in COVID-19 patients showed an area under the curve of 0.830, 95% CI (0.658-0.815), P&lt;0.001, with an optimal cut-off point of 0.32965. Conclusion: Our results suggest a regulatory role for miR-296-5p in cytokine secretion in COVID-19. The results indicate that the expression of miR-296-5p and IP-10 genes in PBMCs might serve as convenient novel biomarkers for the prognosis of COVID-19.

Regulation of the PD-1/PD-L1 Axis and NK Cell Dysfunction by Exosomal miR-552-5p in Gastric Cancer

ObjectiveNK cells play a vital role in tumor immune resistance. Various factors affect NK cell activity. While NK cell dysfunction has been observed in numerous malignancies, the underlying mechanisms in gastric cancer remain unclear.MethodFlow cytometry was used to identify the phenotypic distribution and expression of activated receptors on NK cells. ELISA was used to determine the expression of cytokines. We examined the expression of NK cell-related genes and explored their association with survival and prognosis. Additionally, we conducted PCR detection of miR-552-5p expression levels in plasma exosomes of patients and investigated its correlation with phenotypic distribution and activated receptors. We used flow cytometry and ELISA to verify the role of miR-552-5p in NK cell dysfunction. Furthermore, we investigated the potential role of PD-1/PD-L1 in regulating NK cell dysfunction in patients’ cells.ResultsWe observed a significant decrease in the percentage of NKG2D and NKp30 and IFN-γ and TNF-α in patients than in healthy volunteers. Patients with low levels of CD56, CD16, NKG2D, and NKP46 exhibited poorer survival prognoses. Moreover, increased expression levels of plasma exosomal miR-552-5p in patients were negatively associated with NK cell phenotypic distribution and activated receptor expression. MiR-552-5p downregulated the secretion of perforin, granzyme, and IFN-γ as well as the expression of NKp30, NKp46, and NKG2D. Additionally, it suppressed the cytotoxicity of NK cells. The inhibitory effect of miR-552-5p, on NK cell function was reversed when anti-PD-L1 antibodies were used.ConclusionExosomal miR-552-5p targets the PD-1/PD-L1 axis, leading to impaired NK cell function.

Effect of Statins on Serum Levels of TNF-alpha and Interleukin-6 in Patients with Kidney Disease: A Meta-analysis of Randomized Clinical Trials.

Some clinical trials have indicated the beneficial effects of statins in patients with kidney disease, while others have reported no positive effect of statins in these patients. We conducted this meta-analysis to identify the effects of statins on serum levels of interleukin-6 (IL-6) and Tumor Necrosis Factor Alpha (TNF-α) in patients with kidney disease. A systematic literature search was performed using PubMed, Scopus, and Web of Science databases to identify all studies published from inception to August, 2022. The major outcome variable was the Weighted Mean Difference (WMD). Eligible studies were stratified based on target population, intervention duration, dosage and type of statins, and solubility of statins. Meta-analysis performed on seven publications (8 studies), including 213 patients with kidney disease and 188 control individuals, indicated that the concentration of IL-6 was marginally decreased in patients with kidney disease following statin therapy disease (WMD = -1.15 pg/mL; 95% CI = -2.33 to 0.04, P = 0.05, I2 = 68.5%). The findings of subgroup analysis based on the dosage of statins showed that neither highintensity nor moderate/low-intensity statin treatment could significantly influence the serum level of IL-6. Lipophilic statins were more effective than hydrophilic statins, and they marginally decreased the levels of IL-6 (WMD = -1.21 pg/mL; 95% CI = -2.43 to 0, P = 0.05, I2 = 55.7%). Meta-analysis of four publications (five studies) with 157 patients with kidney disease and 132 control subjects showed that statins reduced the serum levels of TNF-α in patients with kidney disease when compared with control individuals (WMD= -2.66 pg/mL; 95% CI = -4.26 to -1.06, P < 0.001, I2 = 63%). Statins only marginally decreased the concentration of IL-6 in patients with kidney disease, but neither high-intensity nor moderate/low-intensity statin treatment could significantly influence the level of IL-6. However, statins reduced serum levels of TNF-α in patients with kidney disease.

Dynamics of serum levels of TNF-α in a longitudinal follow-up study in 98 patients with juvenile idiopathic arthritis treated with anti-TNF-α biological drugs

ObjectiveTo determine the dynamics of serum levels of TNF-α in patients with juvenile idiopathic arthritis (JIA) treated with anti-TNF-α biological drugs and investigate their association with the disease activity.MethodsWe conducted a single-centre, observational cohort study in 98 patients with JIA (30 boys, 68 girls, mean age 11.3 years) treated with anti-TNF-α biological drugs. Clinical examinations and laboratory assessments of serum levels of TNF-α were performed before starting therapy with biological drug and at 6-month intervals afterwards up to 2.5 years.ResultsThe analysis of serum levels of TNF-α in relation to the disease activity states showed the highest mean serum levels of TNF-α in patients on etanercept who had low disease activity states and in patients on adalimumab who had inactive disease. The correlation analysis in patients with JIA treated with etanercept or adalimumab showed a weak negative correlation between the serum levels of TNF-α and JADAS10 scores (p = 0.007), (r = − 0.177).ConclusionThe assessment of serum levels of TNF-α in children with JIA during treatment with etanercept or adalimumab is not a reliable biomarker of disease activity or immunological remission. Longitudinal measurement of TNF-α has no added clinical value in patients with JIA treated with anti-TNF-α biological drugs.Key Points• There is limited evidence regarding the effect of anti-TNF therapy on serum concentrations of TNF-α in patients with juvenile idiopathic arthritis• Our study showed an increase in the serum level of TNF-α after the initiation of therapy with either etanercept or adalimumab, which was more significant in patients with inactive or low disease activity• Serum TNF-α is most likely not biologically active during therapy with TNF-α inhibitors and therefore not a reliable biomarker of disease activity or immunological remission in patients with juvenile idiopathic arthritis

Discriminatory performance of the pulpal inflammatory biomarkers; Interleukin-8 and TNF-α in patients with symptoms indicative of reversible and irreversible pulpitis: A diagnostic accuracy study.

The success of vital pulp treatment (VPT) procedures is dependent on an accurate diagnosis of the pulpal inflammatory condition. Compared with current subjective pulpal diagnostic tests, inflammatory molecular biomarkers involved in the pathogenesis of pulpitis represent potential objective indicators of the degree of pulpal inflammation. Therefore, the aim of this study was to quantify level of inflammatory biomarkers - Interleukin 8 (IL-8) and TNF-α in patients diagnosed with reversible pulpitis (RP), irreversible pulpitis (IR) and normal pulp (NP) and investigate their diagnostic accuracy in differentiating between healthy and inflamed conditions. This prospective, cross-sectional study enrolled 72 patients aged 14-53 years with extremely deep carious lesions after establishing a clinical diagnosis of RP (n = 42), symptomatic IR (n = 22) and NP (n = 8). 50 μL of pulpal blood sample was collected from all the patients using a micropipette after pulpal exposure. The level of IL-8 and TNF-α was assessed in pg/mL using enzyme-linked immunosorbent assays. Mann-Whitney U test was applied to establish the association between IL-8/TNF-α level and degree of pulp inflammation. Receiver operating curve (ROC) analysis was carried out to calculate area under the curve (AUC) for RP versus IR. Cut-off values were established using Youden's index. IL-8 and TNF-α levels differed significantly between RP and IR groups (p ≤ .001). The median value of IL-8 in RP and IP groups was 259.8 pg/mL [187.5-310.0] and 1357.8 pg/mL [1036.7-2177.6] respectively. The AUC-ROC curve for RP versus IR was 0.997 with 95.5% sensitivity and 99.76% specificity. The median value of TNF-α in RP and IR groups was 75.4 pg/mL [62.7-95.8] and 157.6 pg/mL [94.1-347.3]. The AUC-ROC curve for TNF-α was 0.812 with a sensitivity and specificity of 59.1% and 92.1%, respectively. IL-8 and TNF-α levels were below detection levels for all NP samples. This study showed that pulpal blood could provide an excellent medium for establishing pulpal diagnosis under extremely deep carious lesions. The selected cytokines, IL-8 and TNF-α, demonstrated excellent discriminatory performance for reversible and irreversible pulpitis. Future studies should correlate the IL-8/TNF-α levels with VPT treatment outcomes.

Seipin is involved in oxygen-glucose deprivation/reoxygenation induced neuroinflammation by regulating the TLR3/TRAF3/NF-κB pathway

Seipin plays a crucial role in lipid metabolism and is involved in neurological disorders. However, the function and mechanism of action of seipin in acute ischemic stroke have not yet been elucidated. Here, we aimed to investigate the effect of seipin on neuroinflammation induced by oxygen-glucose deprivation/reoxygenation (OGD/R) and further explore the molecular mechanism by functional experiments. Our results revealed a significant decrease in seipin mRNA levels, accompanied by enhanced expression of TNF-α in patients with AIS, and a significant negative correlation between seipin and TNF-α was observed. Additionally, there was a negative correlation between seipin levels and the National Institutes of Health Stroke Scale (NIHSS) score. Furthermore, seipin levels were also decreased in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and OGD/R-treated BV2 cells. RNA sequencing analysis showed that seipin knockdown altered the Toll-like receptor 3 (TLR3) signaling pathway. It was further confirmed in vitro that seipin knockdown caused significantly increased secretion of inflammatory factors including TNF-α, interleukin (IL)-1β, and interferon (IFN)-β. Meanwhile, seipin knockdown activated the Tlr3 signal pathway while this effect could be reversed by Tlr3 inhibitor in OGD/R treated BV2 cells. Furthermore, neuroinflammation induced by OGD/R was significantly reduced by seipin overexpression. Overall, our study demonstrate that seipin deficiency aggravates neuroinflammation by activating the TLR3/TRAF3/NF-κB signaling pathway after OGD/R stimuli, and suggest that seipin may be a potential therapeutic target for AIS.

Significant improvements in the olfactory sensitivity of bipolar I disorder patients during euthymia versus manic episodes: a longitudinal study.

Research has indicated that individuals diagnosed with bipolar disorder (BD) might experience alterations in their olfaction or levels of serum tumor necrosis factor-α (TNF-α), but no studies have investigated olfactory function and serum TNF-α in BD patients simultaneously. Moreover, there is a lack of existing research that compares the longitudinal olfactory function between individuals with manic and euthymic BD I. Patients with manic BD I (BDM, n=44) and healthy controls (HCs, n=32) were evaluated symptoms (measured via the Young Manic Rating Scale, YRMS), social function (measured via the Global Assessment Function, GAF), serum TNF-α, and olfactory function (via the Sniffin' Sticks test) including olfactory sensitivity (OS) and olfactory identification (OI). The BDM patients were followed up to the remission period and re-evaluated again. We compared OS, OI and serum TNF-α in manic and euthymic patients with BD I and HCs. We examined the correlation between olfactory function and symptoms, social function, and serum TNF-α in patients with BD I. The BDM patients exhibited significantly lower OS and OI compared to the HCs (Z = -2.235, P = 0.025; t = -6.005, P < 0.001), while a positive correlation was observed between OS and GAF score (r = 0.313, P = 0.039). The OS in the BD I remission group (n=25) exhibited significantly superior performance compared to the BDM group (t = -4.056, P < 0.001), and the same as that in the HCs (P = 0.503). The change in OS showed a positive correlation with the decrease in YMRS score (r = 0.445, P = 0.026), and a negative correlation with the course of disease (r = -0.594, P = 0.002). The TNF-α in BD I patients was significantly lower compared to HCs (P < 0.001), and not significantly correlated with olfactory function (all P > 0.05). The findings suggest that OS and OI are impaired in BDM patients, and the impaired OS in those patients can be recovered in the remission stage. OI may serve as a potential characteristic marker of BD. OS might be useful as an index for BDM treatment efficacy and prognosis.

Diagnostic and prognostic significance of miR-486-5p in patients who underwent minimally invasive surgery for lumbar spinal stenosis.

This study aimed to investigate the expression and clinical value of microRNA miR-486-5p in diagnosing lumbar spinal stenosis (LSS) patients and predicting the clinical outcomes after minimally invasive spinal surgery (MISS) in LSS patients, and the correlation of miR-486-5p with inflammatory responses in LSS patients. This study included 52 LSS patients, 46 patients with lumbar intervertebral disk herniation (LDH) and 42 healthy controls. Reverse transcription quantitative PCR was used to detect miR-486-5p expression. The ability of miR-486-5p to discriminate between different groups was evaluated by receiver-operating characteristic analysis. The visual analogue scale (VAS), Oswestry Disability Index (ODI) and Japanese Orthopaedic Association (JOA) scores at 6months postoperatively were used to reflect the clinical outcomes of LSS patients. Enzyme-linked immunosorbent assay was used to measure the levels of inflammatory factor [interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α)]. The correlation of miR-486-5p with continuous variables in LSS patients was evaluated by the Pearson correlation coefficient. Expression of serum miR-486-5p was upregulated in LSS patients and had high diagnostic value to screen LSS patients. In addition, serum miR-486-5p could predict the 6-month clinical outcomes after MISS therapy in LSS patients. Moreover, serum miR-486-5p was found to be positively correlated with the levels of IL-1β and TNF-α in patients with LSS. miR-486-5p, increased in LSS patients, can function as an indicator to diagnose LSS and a predictive indicator for the clinical outcomes after MISS therapy in LSS patients. In addition, miR-486-5p may regulate LSS progression by modulating inflammatory responses.

THE SEVERITY OF VASCULAR INFLAMMATION AND ITS RELATIONSHIP WITH CLINICAL AND FUNCTIONAL FEATURES IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE WITHOUT CONCOMITANT CARDIOVASCULAR PATHOLOGY

The Russian Federation is one of the countries with a high prevalence of chronic obstructive pulmonary disease (COPD). In the last decade, the list of families of chemical regulators of vascular inflammation in COPD has been supplemented with information about growth factors, whose participation in the processes of regulation of vascular function seems significant. The study of the role of angiogenesis factors in patients with isolated COPD disease is insufficient at this stage and needs to be clarified. Objective. To study was to identify diagnostic and prognostic criteria for the severity of vascular inflammation and to assess its relationship with clinical and functional features in patients with COPD without concomitant cardiovascular pathology in comparison with the clinical phenotype of the disease. Material and methods. 96 patients with COPD were examined, the median age was 61 years. In addition to standard clinical, functional and laboratory research methods, the severity of vascular inflammation was assessed in all examined patients with the determination of quantitative indicators of human platelet growth AA factor and tumor necrosis factor-α (TNFα) by quantitative solid-phase enzyme immunoassay Results. In all patients with isolated COPD, regardless of the risk of developing the underlying disease, an increase in the level of platelet growth AA factor and TNFα was noted. The level of platelet growth AA factor and TNFα in patients with COPD, regardless of the risk of exacerbation, was correlated with the functional state of the lungs, clinical phenotype and severity of clinical manifestations of the disease. The value of platelet growth AA factor above 317 ng/ml in patients with COPD may be an early marker of endothelial dysfunction and a predictor of the development of hemostatic disorders and concomitant cardiovascular pathology.

TNF-α Levels Are Increased in Patients with Subjective Cognitive Impairment and Are Negatively Correlated with β Amyloid-42.

The role of tumor necrosis factor-α (TNF-α) in Alzheimer's disease (AD) has recently become a topic of debate. TNF-α levels increase in the blood of patients with AD, and amyloid beta (Aβ) plaques contain TNF-α deposits. The therapeutic efficacy of blocking TNF-α in patients with AD remains controversial as it is mostly based on preclinical studies. Thus, whether and how TNF-α contributes to amyloidogenic processes in AD is still an open question to be addressed. We analyzed plasma TNF-α and Aβ42 levels in patients with subjective cognitive impairment (SCI), mild cognitive impairment (MCI), and AD, and in healthy volunteers (HLT). In addition, we performed correlation analysis to evaluate whether changes in plasma TNF-α levels correlate with cognitive decline, Aβ42 levels, age, and BMI, which are all factors considered to contribute to or predispose individuals to AD. We found that TNF-α and Aβ42 plasma levels were higher in patients with AD than in HLT individuals. High TNF-α levels were also observed in patients with SCI, in whom TNF-α and Aβ42 levels were negatively correlated. Notably, TNF-α did not affect the amyloidogenic pathway in human microglial cultures exposed to 48 h of incubation, although it did trigger neuroinflammatory processes. These results imply that high TNF-α levels are more likely to be a clinical condition linked to AD than are direct contributors. Nonetheless, elevated levels of TNF-α in early-stage patients, like those with SCI and MCI, may provide a distinguishing feature for identifying clinical profiles that are at risk of having a poorer outcome in AD and could benefit from tailored therapies.

THE SEVERITY OF VASCULAR INFLAMMATION AND ITS RELATIONSHIP WITH CLINICAL AND FUNCTIONAL FEATURES IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE WITHOUT CONCOMITANT CARDIOVASCULAR PATHOLOGY

The Russian Federation is one of the countries with a high prevalence of chronic obstructive pulmonary disease (COPD). In the last decade, the list of families of chemical regulators of vascular inflammation in COPD has been supplemented with information about growth factors, whose participation in the processes of regulation of vascular function seems significant. The study of the role of angiogenesis factors in patients with isolated COPD disease is insufficient at this stage and needs to be clarified. Objective. To study was to identify diagnostic and prognostic criteria for the severity of vascular inflammation and to assess its relationship with clinical and functional features in patients with COPD without concomitant cardiovascular pathology in comparison with the clinical phenotype of the disease. Material and methods. 96 patients with COPD were examined, the median age was 61 years. In addition to standard clinical, functional and laboratory research methods, the severity of vascular inflammation was assessed in all examined patients with the determination of quantitative indicators of human platelet growth AA factor and tumor necrosis factor-α (TNFα) by quantitative solid-phase enzyme immunoassay Results. In all patients with isolated COPD, regardless of the risk of developing the underlying disease, an increase in the level of platelet growth AA factor and TNFα was noted. The level of platelet growth AA factor and TNFα in patients with COPD, regardless of the risk of exacerbation, was correlated with the functional state of the lungs, clinical phenotype and severity of clinical manifestations of the disease. The value of platelet growth AA factor above 317 ng/ml in patients with COPD may be an early marker of endothelial dysfunction and a predictor of the development of hemostatic disorders and concomitant cardiovascular pathology.

The Levels of Serum Leptin and TNF-α in Patients with Alcoholic Liver Disease in the Alcoholic Indian Population

ABSTRACT Alcoholic liver disease, resulting from chronic alcohol use, includes conditions like fatty liver, alcoholic hepatitis, and cirrhosis. This study assessed TNF-α and leptin levels in 45 alcoholic liver disease patients, explored their relationship, and examined the rs1137101 polymorphism in the leptin receptor gene. Participants (mean age 40.13 ± 10.36) had consumed alcohol for an average of 15.31 ± 9.49 years at a daily intake of 253.33 ± 118.25 mL. TNF-α increased with age, while no age-leptin correlation was observed. TNF-α and leptin showed a negative correlation. The study identified a 48% minor allele G frequency for rs1137101. The findings highlight a significant correlation between TNF-α and leptin levels in alcoholic liver disease, suggesting potential roles as inflammatory mediators. More prospective studies are needed to enhance our understanding of these factors and improve disease management, potentially reducing morbidity and mortality rates.

Serum neopterin, YKL-40, IL-6, and TNF-α in patients with obstructive sleep apnea

Objective: Obstructive Sleep Apnea (OSA) is characterized by recurrent episodes of complete or partial upper airway obstruction during sleep. The role of locally increased inflammation in the upper respiratory tract is known in the pathogenesis of OSA. This study aimed to examine the role of some inflammatory markers in OSA. Materials and Methods: Adult patients who underwent diagnostic polysomnography (PSG) for the first time, were evaluated in this prospective study. Serum levels of neopterin, human cartilage glycoprotein 39 (YKL-40), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were examined in the study group. Results: The study included 165 adult patients. Individuals of 56 who were did not have OSA were taken as the control group. Patients diagnosed with OSA (n=109) were included in the study and divided into two groups mild-moderate and severe based on the OSA apnea-hypopnea index (AHI). The study groups were divided into 3 cathegories: AHI &lt;5 (control) Group 1, AHI 5-15 (mild), and AHI 15-30 (moderate) Group 2, AHI&gt;30 (severe) Group 3. Individuals of 165 who completed the study [Group 1 (n=56), Group 2 (n=69), Group 3 (n=40)] were included in the statistical evaluation. There was a significant difference between the groups in terms of neopterin, YKL-40, and IL-6 values (p&lt;0.05). The median value of IL-6 and neopterin measured in the severe group was significantly higher than the value measured in the control and mild-moderate groups (p&lt;0.001). The mean value of YKL-40 measured in the severe group was significantly higher than the value measured in the control group (p=0.012). No significant difference was observed in TNF-α serum levels of groups. Conclusion: Serum levels of neopterin, YKL-40, and IL-6 were found to be elevated in OSA patients (especially in the severe group).

EBV Impact in Peripheral Macrophages' Polarization Cytokines in Pediatric Patients.

Macrophages are exceptionally flexible cells. The presence of inflammatory cytokines such as IFN-γ and TNF-α results in an M1 (CD68) activation, while cytokines such as IL-10 or TGF-β induce the M2 (CD163) activation. Our aim was to study the behavior of peripheral cytokines involved in macrophage polarization and relate them with tissue findings to further comprehend the role of macrophages in EBV pediatric infection. We studied cytokine expression in tonsils and peripheral blood samples of children in different stages of infection. Peripheral cytokines were compared with macrophage polarization markers and viral protein expression in tonsils. Only IL-10 showed a negative correlation between compartments, exclusively in patients undergoing viral reactivation (R). Higher expressions of peripheral IL-1β, IL-23, and IL-12p40 in R children were observed. Lower expressions of local and peripheral TNF-α in patients with broader expressions of latent and lytic viral proteins were demonstrated. In healthy carrier (HC) patients, IL-23 positively correlated with CD163, and IP-10 positively correlated with CD68. Our results indicated that EBV might modulate antigen expression in the presence of TNF-α and influence peripheral cytokine expression differently in each stage of infection. Moreover, peripheral cytokines might have a particular role in macrophage polarization in HC.

Role of TNF-α in patients with omicron coronavirus: A cross-sectional study

Abstract Background: Severe acute respiratory syndrome coronavirus (SARS-CoV-2) omicron variant has spread through the world and has caused a global pandemic. In order to make an accurate diagnosis of the disease’s severity, several immunological and biomarkers (tumor necrosis factor alpha (TNF-α), D-dimer, serum ferritin, glutamate oxaloacetate transaminase, glutamate pyruvate transaminase (GPT), and lactate dehydrogenase (LDH)) are evaluated immediately. Objectives: The current study aimed to determine the concentration of TNF-α level in the omicron coronavirus patients, and to determine the correlation of TNF-α with some biomarkers [TNF-α, D-dimer, serum ferritin, glutamic-oxaloacetic transaminase (GOT), GPT, and LDH]. Materials and Methods: Sixty patients (40 males and 20 females), with the age ranging from 23 to 71 years from the intensive care unit of a tertiary hospital in Babylon Iraq, were included in the current investigation. The period of study was between October and December 2021. Included criteria omicron coronaviruses patients with positive “Real-Time Polymerase Chain Reaction (RT-PCR)” results while the excluded criteria omicron coronaviruses patients with positive “RT-PCR” results were reviewed. Then the positive patient divided by using saturation oxygen (SPO2) into three groups (mild, moderate, and severe groups). Sex, age, and SPO2 were recorded, and biomarkers (GOT, GPT, and LDH) were measured in all patients using a bio-based device (ACCENT-200 ALAT KIT). The D-dimer and serum ferritin for all patients were done by VIDS instrument. Results: In this sample, the ages ranged from 23 to 71, with a mean of 60.32 ± 13.39. TNF-α concentrations were found to be significantly greater in the severe patient group compared to the mild patient group and the moderate patient group (P = 0.06). Severe patients had greater GPT and GOT concentrations than mild and moderate patients. There was a positive and statistically significant association between TNF-α and D-dimer in the mild group (r = 0.734**, P = 0.000). Neither TNF-α nor serum ferritin levels were correlated with liver function tests. Conclusion: Among omicron coronavirus patients, GOPT, GPT, and LDH were all elevated in the severe group, whereas there was no statistically significant difference between the mild and moderate groups (mild, moderate, and severe group). TNF-α levels were not associated with liver function tests in this research.

Plasma tumour necrosis factor-alpha-related proteins in prognosis of heart failure with pulmonary hypertension.

Patients with heart failure (HF) exhibit poor prognosis, which is further deteriorated by pulmonary hypertension (PH), with negative impact on morbidity and mortality. As PH due to left HF (LHF-PH) is among the most common causes of PH, there is an urge according to the 2021 European Society of Cardiology HF guidelines to find new biomarkers that aid in prognostication of this patient cohort. Given the role of tumour necrosis factor-alpha (TNF-α) in HF progression, we aimed to investigate the prognostic value of plasma proteins related to TNF-α in patients with LHF-PH, in relation to haemodynamic changes following heart transplantation (HT). Twenty TNF-α-related plasma proteins were analysed using proximity extension assay in healthy controls (n=20) and patients with LHF-PH (n=67), before and 1year after HT (n=19). Plasma levels were compared between the groups, and the prognostic values were determined using Kaplan-Meier and Cox regression analyses. Plasma levels of lymphotoxin-beta receptor (LTBR), TNF receptor superfamily member 6B (TNFRSF6B), and TNF-related apoptosis-inducing ligand receptors 1 and 2 (TRAIL-R1 and TRAIL-R2, respectively) were higher in LHF-PH pre-HT vs. controls (P<0.0001), as well as higher in pre-HT vs. post-HT (P<0.001). The elevated pre-HT levels of LTBR, TNFRSF6B, TRAIL-R1, and TRAIL-R2 decreased towards the levels of healthy controls after HT. Higher preoperative levels of LTBR, TNFRSF6B, TRAIL-R1, and TRAIL-R2 in LHF-PH were associated with worse survival rates (P<0.002). In multivariate Cox regression models, each adjusted for age and sex, LTBR, TNFRSF6B, TRAIL-R1, and TRAIL-R2 predicted mortality (P<0.002) [hazard ratio (95% confidence interval): 1.12 (1.04-1.19), 1.01 (1.004-1.02), 1.28 (1.14-1.42), and 1.03 (1.02-1.04), respectively]. Elevated pre-HT plasma levels of the TNF-α-related proteins LTBR, TNFRSF6B, TRAIL-R1, and TRAIL-R2 in LHF-PH decreased 1year after HT, displaying a normalization pattern towards the levels of the healthy controls. These proteins were also prognostic, where higher levels were associated with worse survival rates in LHF-PH, providing new insight in their potential role as prognostic biomarkers. Larger studies are warranted to validate our findings and to investigate their possible pathobiological mechanisms in LHF-PH.

Immunological disorders in patients with mammary gland pathology in infertility associated with anovulation

The objective: to study the state of the immune system in women with pathology of the mammary glands and infertility, and on the background of menstrual cycle disorders.Materials and methods. The research was performed in two stages. The first (1) stage included examination of women with infertility associated with anovulation who had breast pathology. These patients were divided into three groups: 1.1 group – 44 patients with diffuse fibrocystic breast disease (FBD), 1.2 group – 4 patients with fibroadenoma of the mammary glands, 1.3 group (control one) – 37 patients without pathological changes in the mammary glands.During the second (2) stage of the study, 110 women were examined: 2.1 group – 52 patients with regular menstruations and luteal phase insufficiency (LPI) and 2.2 group – 58 patients with anovulatory cycles.During two research stages, the immune status (CD3, CD4, CD8, immunoregulatory index (CD4/CD8), CD72, CD16, circulating immune complexes) and cytokine profile (IL-1, IL-2, IL-6, TNF-α, INF) in venous blood were determined. Differences were considered statistically significant at p&lt;0.05.Results. A significant increase in the CD8 index was found in the group of patients with normal mammary glands (34.7±6.9 pg/ml; p&lt;0.05) and with a diffuse form of FBD (35.13±6.9 pg/ml; p&lt;0.05) versus its normal level in the group of patients with fibroadenoma (26.5±15.9 pg/ml; p&gt;0.05).During the analysis of the CD16 level, it was determined its significantly increased to 18.8±3.1 pg/ml (р&lt;0.05) in patients with LPI and regular menstrual cycle and to 26.3±4.8 pg/ml (р&lt; 0.05) – in patients with anovulation without LPI, the difference between the groups was significant. The level of CD16 was significantly higher in anovulatory menstrual cycle disorder without LPI compared to patients with menstrual cycle disorder and LPI.The concentration of TNF-α in patients with a regular menstrual cycle (998.1±166.3 pg/ml; p&lt;0.05) and with an anovulatory cycle without LPI (1029.3±187.1 pg/ml; p&lt;0.05) was significantly higher compared to normal values (778.5±64.0 pg/ml). The level of IL-2 was significantly lower than normal indices. Thus, in the group of women with LPI, this indicator was 17.13±2.85 pg/ml (р&lt;0.05), and by anovulation without LPI – 16.84±3.07 pg/ml (р&lt;0.05) versus normal parameter 22.29±0.81 pg/ml.Conclusions. In patients with diseases of the mammary glands and infertility associated with anovulation without LPI, a significant decrease in the activity of T2-helpers (IL-2) and an increase in the activity of T1-helpers (TNF-α) were determined in cases of anovulation without LPI compared with cases of luteal phase insufficiency.

Assessment of Salivary TNF-α Level in Patients with Different Severities of Periodontitis

Aim of the study: To assess the salivary levels of TNF-α in patients with different severities (stages I-IV) of periodontitis in comparison to healthy control.&#x0D; Materials and methods: 171 individuals both men and women were inducted into this study. There were five groups established for them: clinically healthy periodontium control group (19 subjects), Stage I periodontitis (38 subjects), Stage II periodontitis group (38 subjects), Stage III periodontitis (38 subjects), and, Stage IV (38 subjects). The clinical periodontal parameters were examined after collecting whole unstimulated salivary samples from all individuals. TNF-α levels in saliva samples were estimated using the enzyme-linked immunosorbent assay (ELISA) method.&#x0D; Results: The results revealed the mean level of salivary TNF-α was the highest in the stage IV periodontitis group (200.634±50.232), followed by stage III periodontitis group (159.315±36.473), then stage II periodontitis group (128.054±32.651), then stage I (102.798±21.685), and then the control group (51.454±10.446) in which their salivary levels were the lowest with significant differences among the groups (p&lt; 0.01).&#x0D; Conclusion: it may be suggested that TNF-α is related to periodontitis. Also, their salivary levels may have diagnostic potential.