Proinflammatory Cytokines In Patients Research Articles

Changes in the level of anti-inflammatory and pro-inflammatory cytokines in patients with external genital endometriosis (literature review)

Changes in the level of anti-inflammatory and pro-inflammatory cytokines in patients with external genital endometriosis (literature review)

Interleukin levels and depressive symptoms in psoriatic arthritis patients: insights from a case-control study on socio-demographic factors and disease perception.

In the course of psoriatic arthritis (PsA), depression occurs much more often than in the general population. Depression can be considered a poor prognostic factor. The aim of the study was to assess the relationships between the occurrence of depression and the levels of proinflammatory cytokines in patients with PsA. The study included 86 (47F/39M) patients with PsA. Only patients with high disease activity (DAPSA > 28) were enrolled in the study. The severity of depressive symptoms was assessed using the Beck Depression Inventory II (BDI-II) for all patients. Additionally, sociodemographic data were collected. All patients were also assessed for the levels of interleukins (IL): IL-1, IL-6, IL-17A, IL-23, and tumor necrosis factor alpha (TNF-α) using the enzyme-linked immunosorbent assay (ELISA) test. In the study group, depression (BDI-II ≥ 14) was diagnosed in 45 patients (52%). Patients with coexisting depression reported higher levels of pain and disease activity on the visual analogue scale compared to patients without depression (8.5 vs. 7.7, p < 0.001 and 9.3 vs. 8.4, p < 0.001, respectively). The mean levels of proinflammatory cytokines [pg/ml], IL-1 and IL-6, were also higher in the group of patients with depression (46.4 vs. 4.7, p < 0.001 and 10.5 vs. 4.9, p < 0.001, respectively). The coexistence of depression in the course of Psoriatic Arthritis (PsA) is associated with higher levels of IL-1 and IL-6. Depression has a negative impact on the perception of the underlying disease and is linked to reduced social and occupational activity.

CYTOKINE PROFILE RESPONSE IN PATIENTS WITH FRACTURES OF LONG BONES DURING COVID-19

Introduction: The immune system swiftly responds to the onslaught of trauma and the infectious agents it triggers. However, the mechanisms of action of the COVID-19 virus remain unidentified to date. Distinctive alterations that occur in the immune system of trauma victims with COVID-19, setting them apart from changes observed in other diseases. This underscores the specificity of traumatic disease within this patient with COVID-19.&#x0D; The study aims to assess the response of humoral immunity markers in patients with fractures of long bones and COVID-19 and to explore their role in early diagnosing infectious complications in this particular group of patients.&#x0D; Materials and methods: To accomplish the study objectives, we assembled a retrospective dataset comprising 289 cases of skeletal bone fractures treated at the Kyiv City Clinical Hospital of Emergency Medical Care from March, 2020 to February, 2021, meeting the inclusion criteria for the study. The entire dataset consisted of 289 cases of skeletal bone fractures, categorized into two groups: the main group and the control group.&#x0D; Results: On the first day of treatment, an increase in some pro-inflammatory cytokines (IL-6, IL-1β and IL-4) with a normal level of TNF-α, normal values of IFN-γ, IFN-α and a sharp decrease in the anti-inflammatory cytokine IL was observed among the patients of the main group -10. On the third day of the treatment, there was a significant increase in all pro-inflammatory cytokines (IL-6, IL-1β, IL-4 and TNF-α), both types of interferons, and an even sharper decrease in the anti-inflammatory cytokine IL-10. On the tenth day, the growth in the level of pro-inflammatory cytokines was noted, among which the level of TNF-α was the leader, a subnormal level of interferons and anti-inflammatory interleukin 10 was observed. Conclusions: The dynamics of pro-inflammatory cytokines in patients with long bone fractures against the background of COVID-19 tended to increase and had a maximum level on the third day of treatment. Anti-inflammatory cytokines demonstrate a tendency to depression and reache the reference value only on the 10th day of the study.

The impact understanding of exosome therapy in COVID-19 and preparations for the future approaches in dealing with infectious diseases and inflammation

Cytokine storms, which result from an abrupt, acute surge in the circulating levels of different pro-inflammatory cytokines, are one of the complications associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. This study aimed to assess the effect of exosomes on the release of pro-inflammatory cytokines in patients with coronavirus disease 2019 (COVID-19) and compare it with a control group. The cytokines evaluated in this study were TNF-α, IL-6, IL-17, and IFN-γ. The study compared the levels of these pro-inflammatory cytokines in the peripheral blood mononuclear cells (PBMCs) of five COVID-19 patients in the intensive care unit, who were subjected to both inactivated SARS-CoV-2 and exosome therapy, with those of five healthy controls. The cytokine levels were quantified using the ELISA method. The collected data was analyzed in SPSS Version 26.0 and GraphPad Prism Version 9. According to the study findings, when PBMCs were exposed to inactivated SARS-CoV-2, pro-inflammatory cytokines increased in both patients and healthy controls. Notably, the cytokine levels were significantly elevated in the COVID-19 patients compared to the control group P-values were < 0.001, 0.001, 0.008, and 0.008 for TNF-α, IL-6, IL-17, and IFN-γ, respectively. Conversely, when both groups were exposed to exosomes, there was a marked reduction in the levels of pro-inflammatory cytokines. This suggests that exosome administration can effectively mitigate the hyperinflammation induced by COVID-19 by suppressing the production of pro-inflammatory cytokines in patients. These findings underscore the potential safety and efficacy of exosomes as a therapeutic strategy for COVID-19.

Increased expression of NLRP3 associated with elevated levels of HMGB1 in children with febrile seizures: a case–control study

BackgroundHigh mobility group box-1 (HMGB1) is an endogenous danger signal that mediates activation of the innate immune response including NLR pyrin domain containing 3 (NLRP3) inflammasome activation and proinflammatory cytokine release. Although HMGB1 and NLRP3 have been implicated in the pathophysiology of seizures, the correlation between HMGB1 and NLRP3 expression has not been determined in children with febrile seizures (FS). To explore the relationship between extra-cellular HMGB1 and NLRP3 in children with FS, we analyzed serum HMGB1, NLRP3, caspase-1, and proinflammatory cytokines in patients with FS.MethodsThirty children with FS and thirty age-matched febrile controls were included in this study. Blood was obtained from the children with FS within 1 h of the time of the seizure; subsequently, the serum contents of HMGB1, NLRP3, caspase-1, interleukin (IL)-1β, interleukin (IL)-6, and tumour necrosis factor-α (TNF-α) were determined by enzyme-linked immunosorbent assay. The Mann‒Whitney U test was used to compare serum cytokine levels between FS patients and controls. Spearman’s rank correlation coefficient was calculated to detect significant correlations between cytokine levels.ResultsSerum levels of HMGB1, NLRP3, caspase-1, IL-1β, IL-6, and TNF-α were significantly higher in FS patients than in febrile controls (p < 0.05). Serum levels of HMGB1 were significantly correlated with levels of NLRP3 and caspase-1 (both, p < 0.05). Serum levels of caspase-1 were significantly correlated with levels of IL-1β (p < 0.05). Serum levels of IL-1β were significantly correlated with levels of IL-6 and TNF-α (p < 0.05).ConclusionsHMGB1 is up-regulated in the peripheral serum of FS patients, which may be responsible, at least in part, for the increased expression of NLRP3 and Caspase-1. Increased expression of caspase-1 was significantly associated with elevated serum levels of IL-1β. Given that activated Caspase-1 directly regulates the expression of mature IL-1β and positively correlates with activation of the NLRP3 inflammasome, our data suggest that increased levels of peripheral HMGB1 possibly mediate IL-1β secretion through the activation of the NLRP3 inflammasome in children with FS. Thus, both HMGB1 and NLRP3 might be potential targets for preventing or limiting FS.

The Effects of Preoperative Epidural Steroid Injection on Pseudarthrosis Following Lumbar Fusion: A Retrospective Cohort Study.

Retrospective cohort study. The goal of this study is to evaluate the effects of preoperative lumbar epidural steroid injection on the rate of pseudarthrosis following lumbar spine fusion surgery. Epidural corticosteroids help to reduce nerve root edema and suppress proinflammatory cytokines in patients with radiculopathy. Corticosteroids may inhibit bone formation and reduce bone matrix synthesis rates. Thus, there is concern that corticosteroids may reduce lumbar fusion capability, potentially resulting in increased rates of symptomatic pseudarthrosis. We identified all patients who underwent 1-level or 2-level lumbar fusion surgery between 2018 and 2022. Patients were categorized into one of 3 groups: no preoperative epidural steroid injection (ESI) history (group 0), preoperative ESI within 90 days of surgery (group 1), or most recent ESI >90 days before surgery (group 2). The primary outcome of this study was pseudarthrosis. Binominal regression analyses were performed to determine the relationships between potential risk factors (sex, age, body mass index, smoking history, diabetes status, history of systemic steroid use, preoperative ESI, perioperative intravenous steroid administration, type of surgery, and postoperative ESI within 6mo) and the development of postoperative pseudarthrosis. A total of 446 patients were included in this study. Of those, 106 patients (23.7%) did not have a preoperative ESI (group 0), 132 patients (29.5%) had an ESI within 90 days of surgery (group 1), and 208 patients (46.6%) had their most recent ESI >90 days before surgery (group 2). The overall incidence of pseudarthrosis following lumbar fusion was 8.7% (39 of 446). Although the incidence of pseudarthrosis following ESI at any time point was higher than in our control cohort (group 0), this difference was not statistically significant. This study found no increased risk of postoperative pseudarthrosis in patients who underwent 1-level or 2-level lumbar fusions after preoperative ESI. Level III.

JNK Pathway-Associated Phosphatase Deficiency Facilitates Atherosclerotic Progression by Inducing T-Helper 1 and 17 Polarization and Inflammation in an ERK- and NF-κB Pathway-Dependent Manner.

JNK pathway-associated phosphatase (JKAP) regulates T cell-mediated immunity and inflammation, which are involved in atherosclerosis pathogenesis. This study investigated the effects of JKAP on T-helper (Th) cell polarization, inflammation, and atherosclerotic progression. Serum JKAP levels were measured in 30 patients with coronary heart disease (CHD) and 30 controls. CHD blood naïve CD4＋ T cells were acquired, followed by JKAP overexpression and knockdown with or without treatment with PD98059 (ERK inhibitor) or BAY-11-7082 (NF-κB inhibitor) in vitro. CD4＋ T-cell conditional JKAP ablation mice were established in vivo, followed by the construction of an atherosclerosis model. JKAP was reduced and negatively correlated with the Gensini score, CRP, Th1 cells, Th17 cells, and proinflammatory cytokines in patients with CHD. In vitro, JKAP overexpression suppressed Th1 and Th17 cell differentiation and proinflammatory cytokines, whereas JKAP knockdown exerted the opposite effect; however, JKAP modification did not affect Th2 cell differentiation. Interestingly, JKAP negatively regulated the ERK and NF-κB pathways; meanwhile, the PD98059 and BAY-11-7082 treatments repressed Th1 and Th17 cell differentiation, and attenuated the effect of JKAP knockdown on these indices. In vivo, conditional CD4＋ T-cell JKAP ablation increased Th1 and Th17 cell polarization in the spleen, lymph node, blood, and/or aortic root. Furthermore, CD4＋ T-cell conditional JKAP ablation exaggerated atherosclerotic lesions in the aorta, elevated CD4+ cell infiltration and proinflammatory cytokines in the aortic root, and activated the ERK and NF-κB pathways in the aortic root. JKAP ablation facilitates atherosclerosis progression by promoting Th1 and 17 polarization and inflammation through regulation of the ERK and NF-κB pathways.

Cryoablation triggers type I interferon-dependent antitumor immunity and potentiates immunotherapy efficacy in lung cancer

BackgroundCryoablation is a minimally invasive option for patients with medically inoperable non-small cell lung cancer (NSCLC) and can trigger abscopal immune-regulatory effects. However, it remains unclear how cryoablation affects the...

INCREASED LEVELS OF PROINFLAMMATORY CYTOKINES IN BLOOD PLASMA IN PATIENTS WITH CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION

HighlightsIL-8 and MCP-1 have a significant role in the CTEPH pathogenesis, which indicates the importance of nonspecific immunity in the formation and progression of CTEPH. The coupling between cytokines and hemodynamic parameters, cardiac structural changes and plasma biochemical parameters were determined. AbstractBackground. Chronic thromboembolic pulmonary hypertension (CTEPH) pathogenesis is complex and not fully understood. Particular attention to the microvascular damage genesis in CTEPH is given to aseptic inflammation, which in turn could be mediated through various molecular mechanisms. According to the conflicting and incomplete data on changes in the profile of factors controlling inflammation in CTEPH, research in this field would identify new therapeutic targets for the prevention and treatment of CTEPH.Aim. To study the profile of plasma proinflammatory cytokines in patients with chronic thromboembolic pulmonary hypertension (CTEPH) and evaluate the coupling of these cytokines with the main morphofunctional and laboratory values of the disease severity.Methods. 34 patients with CTEPH were included in this study. To characterize the group, the following methods were used: echocardiographic examination, catheterization of the right cardiac chambers. Biomarkers of heart failure, systemic inflammation, as well as erythropoiesis and iron metabolism were assessed in all patients. The control group included 10 donors. To study the proinflammatory cytokine profile in plasma, interleukins (IL) 6, 8, 18, monocyte chemoattractant protein-1 (MCP-1) and matrix metalloproteinase 9 were determined using standard enzyme-linked immunosorbent assay (ELISA) kits.Results. Hemodynamic and morphofunctional changes in the pulmonary circulation specific to pulmonary hypertension were determined with catheterization of the right cardiac chambers and echocardiography. During plasma proinflammatory cytokines analysis, a significant increase in the level of IL-8 (p = 0.030) and MCP-1 (p = 0.031) in CTEPH group compared to the control group was observed. No significant differences for other analyzed markers were found. In the elaboration of the correlation analysis, moderate inverse coupling between proinflammatory markers and hemodynamic parameters characterizing the CTEPH severity were revealed, as well as positive correlations with parameters of remodeling of the right cardiac chambers and iron metabolism.Conclusion. The increased levels of IL-8 and MCP-1 in patients with CTEPH identified in the present study indicate a significant role of nonspecific immunity in the formation and progression of CTEPH. The coupling between cytokines and hemodynamic parameters, structural cardiac changes and plasma biochemical parameters were determined. Based on the obtained data, it is possible to develop new medicinal substances, targeting towards proinflammatory cytokines, their receptors and signaling pathways.

Altered levels of cytokine, T- and B-lymphocytes, and PD-1 expression rates in drug-naïve schizophrenia patients with acute phase

Many studies have investigated the changes of immune cells and proinflammatory cytokines in patients with acute schizophrenia, but few studies have investigated the functional phenotypes of immune cells and the expression rate of programmed cell death protein 1 (PD-1)/ programmed cell death-Ligand 1 (PD-L1). The aim of this study was to investigate the extent of immune cells activation, PD-1/PD-L1 expressions, and altered cytokine levels in drug-naïve schizophrenia patients with acute-phase. 23 drug-naïve schizophrenia patients in acute-phase and 23 healthy individuals were enrolled in this study as experimental and control groups, separately. Socio-demographic information including gender, age, duration of illness, and smoking status was collected for each subject. Beckman DXFLEX triple laser thirteen-color flow cytometer and self-contained software CytoFLEX flow cytometric analysis software were used to detect the expressions of PD-1/PD-L1 on CD4+/CD8+ T lymphocytes, B lymphocytes, monocytes and NK cells. BD Bioscience was used to examine the levels of cytokines including interferon (IFN)-γ, tumor necrosis factor (TNF)-α, Interleukin (IL)-2, IL-4, IL-6, and IL-10. Drug-naïve schizophrenia patients in acute-phase had higher levels of peripheral blood CD4+ T lymphocytes and B lymphocytes, higher PD-1 expression in B lymphocytes, and lower levels of CD8+ T lymphocytes. In addition, IL-6 levels of peripheral blood were higher in schizophrenia patients (all P < 0.05). Significant immune stress was present in schizophrenia patients with acute-phase.

Bupropion Associated Immunomodulatory Effects on Peripheral Cytokines in Male with Major Depressive Disorder

Background: Experimental and clinical studies have reported increased levels of pro-inflammatory cytokines in patients with major depressive disorder (MDD), suggesting that immune system dysregulation may contribute to MDD pathophysiology. Aim: Due to the lack of knowledge about the immune potential of antidepressants, this study investigated the immunomodulatory effects of bupropion, a norepinephrine–dopamine reuptake inhibitor. Methods: This study involved 18 patients with MDD treated with bupropion (150 mg/d) for 4 weeks and 23 healthy volunteers. All participants underwent multiplex bead-based cytokine assessment before and after bupropion treatment to quantify the following cytokines: interleukin (IL)-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-17, interferon-γ, tumor necrosis factor-α, granulocyte colony-stimulating factor, granulocyte-macrophage CSF, monocyte chemotactic protein-1, and macrophage inflammatory protein-1β. Results: Four-week treatment with bupropion significantly increased the levels of IL-1β (P = 0.011), IL-4 (P = 0.019), IL-5 (P = 0.019), IL-7 (P = 0.021), and IL-8 (P = 0.023) compared to the control group. Furthermore, the percentage change in most cytokines, including anti-inflammatory cytokines such as IL-4, IL-5, IL-10, and IL-13, was significantly increased after bupropion treatment. Conclusion: The promoted synthesis of anti-inflammatory cytokines to surpass the pro-inflammatory cytokines may be a crucial step in the treatment of MDD patients with bupropion.

Immunogenetics of Schizophrenia in the Light of Modern Genome-Wide Association Studies

Background: Immunological and genetic studies of schizophrenia form two areas of biological psychiatry in which significant progress has been made in recent years related to understanding the role of both neuroinflammation and genetic vulnerability in the development of this disease. However, data to explain the complicity of these two factors in the etiology and pathogenesis of schizophrenia are still insufficient. The aim of the review is to assess the degree of interaction between genetic predisposition and neuroinflammation in the pathogenetic mechanisms of schizophrenia based on the currently available information on genes associated with the immune system according to genome-wide association analysis (GWAS), as well as models that involve the interaction of immunological and genetic factors, including taking into account environmental adversities. Material and method: using keywords “genome-wide association study, Mendelian randomization, regulatory regions, maternal immunity activation, synaptic pruning, microglia” both in international and domestic databases the scientific publications selected. Conclusions: recent studies have identified genomic regions that contain genes involved in the functioning of the immune system. Particular attention is paid to the MHC region, and one of the most important achievements in its study is the establishment of the role of the complement gene (component C4A) in the formation of synapses and their abnormal elimination. Other genes, both inside and outside the major histocompatibility complex (MHC) region, are of interest, and their functions in the brain and their involvement in the pathogenesis of schizophrenia have yet to be elucidated. The establishment of causal relationships between GWAS data for schizophrenia and immunological indicators of inflammation using the Mendelian randomization (MR method) indicates that the increase in the level of pro-inflammatory cytokines in patients with schizophrenia is an intrinsic symptom of the disease, and is not a consequence of the course of the pathological process. Adverse environmental factors play an important role in the interaction of genetic variants associated with schizophrenia and microglial activation, which leads to synaptic disorders.

Cardiovascular evaluation and endothelial dysfunction in Cushing syndrome following remission: a prospective study.

Cushing syndrome (CS) is a well-known risk factor for cardiovascular morbidities. We aimed to evaluate endothelial and cardiovascular functions, endothelial mediators and pro-inflammatory cytokines in patients with CS before and after remission. Adult patients with newly diagnosed endogenous CS were included. Metabolic [body mass index (BMI), glucose, and lipid values] and cardiovascular evaluation studies [24-h ambulatory blood pressure monitoring, carotid intima-media thickness (CIMT), flow-mediated dilation (FMD), and echocardiography] were performed, and endothelial mediators [asymmetric dimethyl arginine (ADMA) and endothelin-1 (ET-1)] and pro-inflammatory cytokines [interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α)] were measured. Control group was matched in terms of age, gender, and BMIs. Twenty-five patients, mean age 40.60 ± 14.04years, completed the study. Compared to controls (n = 20) mean arterial pressure (MAP) and CIMT were higher (p < 0.005 and p = 0.012, respectively), and FMD (p < 0.001) and mitral E/A ratio (p = 0.007) lower in the patients during active disease. Baseline serum ADMA, ET-1, and IL-1β were similar between the groups, while TNF-α was lower in the patients (p = 0.030). All patients were in complete remission 1 year following surgery. BMI, LDL cholesterol, serum total cholesterol, fasting plasma glucose, MAPs, and CIMT significantly decreased (p < 0.005), while there was no improvement in FMD (p = 0.11) following remission. There was no significant change in ADMA, IL-1β, and TNF-α levels, but ET-1 increased (p = 0.011). Remission in CS improves some cardiovascular parameters. ADMA and ET-1 are not reliable markers for endothelial dysfunction in CS. Metabolic improvements may not directly reflect on serum concentrations of TNF-α and IL-1β following remission of CS.

The Effect of High-Intensity Interval Exercise on Short-Term Glycaemic Control, Serum Level of Key Mediator in Hypoxia and Pro-Inflammatory Cytokines in Patients with Type 1 Diabetes-An Exploratory Case Study.

Type 1 diabetes (T1D) is associated with hyperglycaemia-induced hypoxia and inflammation. This study assessed the effects of a single bout of high-intensity interval exercise (HIIE) on glycaemia (BG) and serum level of pro-inflammatory cytokines, and an essential mediator of adaptive response to hypoxia in T1D patients. The macronutrient intake was also evaluated. Nine patients suffering from T1D for about 12 years and nine healthy individuals (CG) were enrolled and completed one session of HIIE at the intensity of 120% lactate threshold with a duration of 4 × 5 min intermittent with 5 min rests after each bout of exercise. Capillary and venous blood were withdrawn at rest, immediately after and at 24 h post-HIIE for analysis of BG, hypoxia-inducible factor alpha (HIF-1α), tumour necrosis factor alpha (TNF-α) and vascular-endothelial growth factor (VEGF). Pre-exercise BG was significantly higher in the T1D patients compared to the CG (p = 0.043). HIIE led to a significant decline in T1D patients' BG (p = 0.027) and a tendency for a lower BG at 24 h post-HIIE vs. pre-HIIE. HIF-1α was significantly elevated in the T1D patients compared to CG and there was a trend for HIF-1α to decline, and for VEGF and TNF-α to increase in response to HIIE in the T1D group. Both groups consumed more and less than the recommended amounts of protein and fat, respectively. In the T1D group, a tendency for a higher digestible carbohydrate intake and more frequent hyperglycaemic episodes on the day after HIIE were observed. HIIE was effective in reducing T1D patients' glycaemia and improving short-term glycaemic control. HIIE has the potential to improve adaptive response to hypoxia by elevating the serum level of VEGF. Patients' diet and level of physical activity should be screened on a regular basis, and they should be educated on the glycaemic effects of digestible carbohydrates.

Retracted: Effects of Periodontal Treatment on Levels of Proinflammatory Cytokines in Patients with Chronic Periodontitis: A Meta-Analysis.

[This retracts the article DOI: 10.1155/2022/9349598.].

Evaluation Thrombocytosis in CKD Stage V Patient on Hemodialysis Treatment : Case Report

Chronic kidney disease (CKD), also known as renal failure, primarily affects people with a history of hypertension and diabetes. In this medical condition, the rate of filtration or kidney function can decrease over the course of a month or a year. Several studies have found an increase in pro-inflammatory cytokines in patients with CKD. Platelet dysfunction and hyperreactivity have been linked to chronic inflammation. When the platelet count exceeds 450,000/l, thrombocytosis occurs. It is also referred to as thrombocythemia. Reactive thrombocytosis accounts for 80-90% of all thrombocytosis events, with inflammation being one of the most common causes. We report a 67-year-old man presenting to the hospital with fever and weakness. The patient had a history of CKD stage V and currently was rceiving hemodialysis treatment. Laboratory finding showed patient had thrombocytosis. Further examination is required to determine the cause of thrombocytosis in CKD patient.

MicroRNA-345-3p is a potential biomarker and ameliorates rheumatoid arthritis by reducing the release of proinflammatory cytokines

ObjectivesThe study was to explore the influence of microRNA (miR)-345-3p on proinflammatory cytokines in patients with rheumatoid arthritis (RA).MethodsA total of 32 RA patients and 32 healthy patients were enrolled. Proinflammatory factors in patients’ serum were detected by ELISA, and miR-345-3p was detected by RT-qPCR. The correlation between miR-345-3p expression and proinflammatory factors in RA patients was analyzed. The diagnostic value of miR-345-3p and proinflammatory factors in RA patients was analyzed by receiver operating curve diagnosis. The predictive value of miR-345-3p levels and proinflammatory factors in RA patients was analyzed by multivariate Cox regression. HFLS-RA and HFLS cells were cultured, in which miR-345-3p and proinflammatory cytokines were detected by RT-qPCR. Cell proliferation and apoptosis were determined by CCK-8 and flow cytometry, respectively.ResultsMiR-345-3p was lowly expressed in the serum of RA patients. MiR-345-3p and proinflammatory factors were of diagnostic and predictive values in RA. Elevated miR-345-3p restrained the production of proinflammatory factors of HFLS-RA cells, improved cell proliferation, and reduced apoptosis.ConclusionMiR-345-3p is a potential biomarker and ameliorates RA by reducing the release of proinflammatory cytokines.

Pro-inflammatory cytokines in patients with low back pain: A comparative study

Introduction and objectivesThere are controversial results regarding the value of serum IL-8 and TNFα in patients with non-specific low back pain.This study aimed to compare pro-inflammatory cytokines between patients with non-specific back pain and pain-free controls. Materials and methodsWe conducted a case–control study including 106 participants: 46 patients with chronic non-specific low back pain (G1) and 60 pain-free controls (G0). The interleukin (IL-)6, IL-8, IL-17, IL-23, IL-22, and Tumor necrosis factor α (TNFα) were measured. We collected demographic and clinical data, including age, gender, low back pain duration and radicular pain. The pain degree was assessed using the Visual Analogic Scale. ResultsThe mean age was 43.17±8.7 years in G1. Radicular pain was found in 37 cases with a Visual Analogic Scale of 3.03±2.5mm. The magnetic resonance imaging was performed in (G1), showing disk herniation and degenerative disk disease in 54.3% (n=25) and 45.7% of cases (n=21), respectively. The IL-8 was higher in G1 (18.84±44.64 versus 4.34±1.23pg/mL, p:0.033). IL-8 levels correlated with TNFα (0.942, p<10–3), IL-6 (0.490, p=0.011) and Visual Analogic ScaleRadicular-pain (r:0.297, p:0.047).IL-17 was higher in patients with restricted lumbar spine mobility (9.64±20.77 versus 1.19±2.54pg/mL, p:0.014). ConclusionsOur results provide evidence that IL-8 and TNFα play a role in low back pain and radicular pain due to disk degeneration or herniation. These findings could potentially be used by future studies to develop new non-specific low back pain therapeutic strategies.

Pro-inflammatory cytokines in patients with low back pain: A comparative study

There are controversial results regarding the value of serum IL-8 and TNFα in patients with non-specific low back pain. This study aimed to compare pro-inflammatory cytokines between patients with non-specific back pain and pain-free controls. We conducted a case–control study including 106 participants: 46 patients with chronic non-specific low back pain (G1) and 60 pain-free controls (G0). The interleukin (IL-)6, IL-8, IL-17, IL-23, IL-22, and Tumor necrosis factor α (TNFα) were measured. We collected demographic and clinical data, including age, gender, low back pain duration and radicular pain. The pain degree was assessed using the Visual Analogic Scale. The mean age was 43.17 ± 8.7 years in G1. Radicular pain was found in 37 cases with a Visual Analogic Scale of 3.03 ± 2.5 mm. The magnetic resonance imaging was performed in (G1), showing disk herniation and degenerative disk disease in 54.3% ( n = 25) and 45.7% of cases ( n = 21), respectively. The IL-8 was higher in G1 (18.84 ± 44.64 versus 4.34 ± 1.23 pg/mL, p :0.033). IL-8 levels correlated with TNFα (0.942, p < 10–3), IL-6 (0.490, p = 0.011) and Visual Analogic Scale Radicular-pain ( r :0.297, p :0.047). IL-17 was higher in patients with restricted lumbar spine mobility (9.64 ± 20.77 versus 1.19 ± 2.54 pg/mL, p :0.014). Our results provide evidence that IL-8 and TNFα play a role in low back pain and radicular pain due to disk degeneration or herniation. These findings could potentially be used by future studies to develop new non-specific low back pain therapeutic strategies. Existen resultados controvertidos en cuanto al valor de la interleucina (IL) 8 y el factor de necrosis tumoral α (TNFα) séricos en pacientes con lumbalgia inespecífica. Este estudio tuvo como objetivo comparar las citoquinas proinflamatorias entre pacientes con dolor de espalda inespecífico y controles sin dolor. Realizamos un estudio de casos y controles que incluyó a 106 participantes: 46 pacientes con dolor lumbar crónico inespecífico (G1) y 60 controles sin dolor (G0). Se midieron las IL-6, IL-8, IL-17, IL-23, IL-22 y el TNFα. Recopilamos datos demográficos y clínicos, incluidos la edad, el sexo, la duración del dolor lumbar y el dolor radicular. El grado de dolor se evaluó mediante la escala analógica visual. La edad media fue de 43,17 ± 8,7 años en G1. Se encontró dolor radicular en 37 casos con una escala analógica visual de 3,03 ± 2,5 mm. La resonancia magnética se realizó en G1, mostrando hernia discal y enfermedad discal degenerativa en el 54,3% (n = 25) y el 45,7% de los casos (n = 21), respectivamente. La IL-8 fue mayor en G1 (18,84 ± 44,64 versus 4,34 ± 1,23 pg/ml, p = 0,033). Los niveles de IL-8 se correlacionaron con TNFα (0,942, p < 10 −3 ), IL-6 (0,490, p = 0,011) y escala visual analógica dolor radicular (r = 0,297, p = 0,047). IL-17 fue mayor en pacientes con movilidad restringida de la columna lumbar (9,64 ± 20,77 versus 1,19 ± 2,54 pg/ml, p = 0,014). Nuestros resultados proporcionan evidencia de que la IL-8 y el TNFα juegan un papel en el dolor lumbar y en el dolor radicular debido a la degeneración o a hernia discal. Estos hallazgos podrían potencialmente ser utilizados por estudios futuros para desarrollar nuevas estrategias terapéuticas no específicas para el dolor lumbar.

Blocking activation of CD4−CD8− T cells modulates their cytotoxic potential and decreases the expression of inflammatory and chemotactic receptors

CD4−CD8− (double negative – DN) T cells represent a small fraction of circulating T lymphocytes but are a major source of pro-inflammatory cytokines in patients with infectious diseases, including chronic Chagas cardiomyopathy (CCC), one of the deadliest cardiopathies known. Chagas disease is caused by an infection with the protozoan parasite Trypanosoma cruzi and can lead to either an asymptomatic form or a high-mortality cardiac disease. While circulating DN T cells represent a major inflammatory cytokine-expressing cell population in Chagas disease, their potential to be recruited to the heart and to perform cytotoxicity has not been determined. Our previous studies showed that blocking DN T cell activation decreases the expression of IFN-gamma, a cytokine involved in the severity of CCC. Here, studying a well-characterized cohort of Chagas patients with CCC or the asymptomatic form of Chagas disease (indeterminate form, IND), we evaluated the expression of cytotoxic molecules, cytokine and chemokine receptors in γδ+ and αβ+ DN T cells by multiparameter flow cytometry, and investigated whether blocking the activation of DN T cells influences the expression of these molecules. We observed that DN T cells from CCC display a higher expression of granzyme A, perforin, inflammatory molecules, and inflammatory chemokine receptors than cells from IND. Messenger RNA coding for these molecules is also upregulated in the heart of CCC patients. Importantly, blocking the activation of DN T cells from CCC modulates their cytotoxic potential and the expression of inflammatory and of chemokine receptors, suggesting that targeting DN T cell activation may be a valid strategy to reduce recruitment to the heart, inflammation, cytotoxicity and, thereby diminish CCC progression and severity.