IL-10 Levels Research Articles

Human-immunodeficiency virus infection associated with the impaired Th1 and pro-inflammatory cytokine response in latent tuberculosis-infected individuals: A comparative cross-sectional study

Tuberculosis (TB) and HIV co-infections are extensively overlapping, especially in developing countries. HIV infection is known as a major risk factor for the reactivation of latent TB into active TB. Although not fully understood and needs further study, HIV infection might enhance the reactivation of latent TB by breaching immune control mechanisms. We investigated the influence of HIV infection on the cytokine response of LTB-infected individuals. Heparinized venous blood was collected from 40 ART-naïve HIV-infected and 30 HIV-negative healthy controls for LTB screening, plasma collection, and PBMC isolation and stimulation. The level of cytokines in plasma and their production by PBMCs stimulated with purified protein derivative (PPD), staphylococcus enterotoxin B (SEB), or unstimulated PBMCs were analyzed using a cytometric bead array (CBA) assay. PPD-induced IL-2 by PBMCs was higher in LTB-infected groups compared with HIV-negative LTB-negative groups (p = 0.0015). When LTB-infected groups were co-infected with HIV (HIV+LTB+), the IL-2 (p < 0.0001) and IFN-gamma (p = 0.0144) production by PPD-stimulated PBMCs was reduced. The level of IL-2 (p = 0.0070), IL-6 (p = 0.0054), and TNF-alpha (p = 0.0045) in plasma were lower in HIV+LTB+ individuals compared with HIV-negative LTB-positive (HIV-LTB+) groups. Our findings suggested that HIV co-infection in LTB-positive individuals is associated with the diminished production of PPD-induced Th1 (IFN-gamma and IL-2) cytokines by PBMCs and in the plasma level of IL-2 and proinflammatory cytokines (IL-6 and TNF-alpha).

CircYTHDF1/miR-19b-3p/YTHDF1 axis contributes to pregnancy-induced hypertension development by enhancing vascular endothelial cell injury

ABSTRACT Objective The biological role of circ_0004858 (circYTHDF1) in pregnancy-induced hypertension (PIH) and the underlying mechanisms were unknown, and which were explored in this study. Methods ELISA was employed to detect the level of inflammatory cytokines and biochemical parameters; flow cytometry was employed to detect cell apoptosis; western blot and qRT-PCR were employed to examine expression level. Results The level of IL-1β, TNF-α, IL-6, TGF-β1, ET-1, and Ang-II were significantly elevated in the peripheral blood of PIH patients. The co-culture of HUVEC and CD4+ T cells isolated from the peripheral blood of PIH patients significantly elevated the apoptosis and expression level of NRF2/HO-1 but reduced the protein level of ferroptosis-related markers (GPX4, FSP, and CoQ10B) in HUVEC. Also, the expression of circYTHDF1 and YTHDF1 were markedly up-regulated in HUVEC co-cultured with CD4+ T cells isolated from PIH patients, but miR-19b-3p expression was markedly down-regulated, and the similar results were observed in Ang-II-treated HUVEC. Based on the predicted binding sites, the luciferase reporter assay confirmed the interaction between miR-19b-3p and circYTHDF1 or YTHDF1. The results of qRT-PCR and western blot further demonstrated that circYTHDF1 competitively bound to miR-19b-3p to up-regulate YTHDF1 in HUVEC. Functionally, deleting circYTHDF1markedly reduced ferroptosis and apoptosis in Ang-II-treated HUVEC, but both which were reversed by miR-19b-3p inhibitor, suggesting the involvement of circYTHDF1/miR-19b-3p/YTHDF1 axis in vascular endothelial cell injury in PIH. Conclusions This study may provide a novel insight into the pathogenesis of PIH as well as a new treatment strategy.

The Protective Effect of Esculentoside A on MPL/lpr Mice by Upregulating the Expression of CD19+IL-35+Breg Cells and Interleukin-35

Introduction: Esculentoside A (EsA) is one of the main components of the traditional Chinese medicine Phytolacca esculenta. The possible mechanism of action of EsA in the treatment of lupus nephritis (LN) was explored by observing the effects of EsA on CD19+ IL-35+regulatory B (IL-35+Breg) cells. Methods: Twenty-four MRL/lpr mice were randomly divided into control, EsA, and EsA+IL-12p35 antibody groups. Mice were administered the respective treatments intraperitoneally once a day for 4 weeks. The urine protein/creatinine ratio (UPCR) and blood creatinine (Cr) and IL-35, IL-10, and IL-17 expression levels were measured. Body and spleen weight were measured to calculate the splenic index (SI). Flow cytometry was performed to determine the proportion of CD19+ IL-35+ Breg cells in the spleen. Hematoxylin-eosin and PASM-Masson staining of renal tissues were performed, and the “Austin” acute index (AI) system for LN was determined. Results: The most severe conditions were seen in mice in the control group, with the highest UPCR, Cr, and IL-17 levels and SI and AI scores; the most severe renal histopathology, and the lowest proportion of CD19+ IL-35+ Breg cells and IL-35 and IL-10 levels. This was followed by the EsA+IL-12p35 antibody group. The EsA group had the lowest UPCR, Cr, and IL-17 levels and SI and AI scores; the mildest renal lesions; and the highest proportion CD19+ IL-35+ Breg cells and IL-35 and IL-10 levels. Conclusion: EsA delayed the progression of LN by promoting the proliferation of CD19+ IL-35+ Breg cells, upregulating the expression of IL-35, and decreasing the secretion of IL-17.

The effect of adipose-derived mesenchymal stem cells against high fructose diet induced liver dysfunction and dysbiosis.

High fructose diet (HFrD) has been approved to be involved in the pathogenesis of insulin resistance. Mesenchymal stem cells have a vital role in the treatment of various diseases including metabolic disturbances. We investigated the effect of Adipose-derived mesenchymal stem cells (ADMSCs) against HFrD-induced metabolic disorders and the molecular mechanisms for this effect. Rats were divided into 3 groups; control, HFrD, and combined HFrD with ADMSCs. We assessed liver functions, gut microbiota activity, oxidative stress, adiponectin, and IL10 levels. Also, we measured SREBP-1, IRS-1 expression using Western blot, and Malat1 expression using rt-PCR. ADMSCs antagonized metabolic abnormalities induced by HFrD in the form of improvement of liver functions and alleviation of oxidative stress. In addition, ADMSCs ameliorated gut microbiota activity besides the elevation of adiponectin and IL10 levels. ADMSCs attenuated insulin resistance through upregulation of IRS1 and downregulation of SREBP-1 and Malat1. ADMSCs can protect against HFrD-induced metabolic hazards.

Mechanism of the KIAA1429/KLF1/PD-L1 Axis in Regulating Immune Escape in Non-small Cell Lung Cancer.

Non-small cell lung cancer (NSCLC), accounting for approximately 80% of lung cancer cases, remains the leading cause of cancer-related mortality. Immune evasion is a critical challenge in NSCLC, contributing to poor treatment outcomes. This study investigates the role of KIAA1429 in immune evasion, aiming to identify novel therapeutic targets and provide a theoretical basis for NSCLC treatment. NSCLC cell lines were cultured to assess the expression of KIAA1429, KLF transcription factor (KLF1), and programmed cell death ligand 1 (PD-L1). Co-culture experiments were conducted with peripheral blood mononuclear cells (PBMCs) to evaluate cytotoxicity, CD8+T cell proportions, and levels of interferon-gamma (IFN-γ)/interleukin (IL)-10/IL-2. Additionally, N6-methyladenosine (m6A) modification in NSCLC cells, m6A enrichment on KLF1, and KLF1 mRNA stability were analyzed. Results showed increased expression of KIAA1429 and KLF1 in NSCLC cells. Knockdown of KIAA1429 inhibited NSCLC cell proliferation, enhanced PBMC cytotoxicity and CD8+T cell activation, increased IFN-γ and IL-2 levels, and decreased IL-10 levels. Mechanistically, KIAA1429 stabilized KLF1 mRNA level through m6A modification, promoting both KLF1 and PD-L1 expression. Overexpression of KLF1 or PD-L1 reversed the immune-modulating effects of KIAA1429 knockdown. In conclusion, KIAA1429 facilitates immune evasion in NSCLC by stabilizing KLF1 mRNA and upregulating PD-L1 expression.

Biomarkers to Differentiate Acute Chest Syndrome From Vaso-Occlusive Crisis in Children With Sickle Cell Disease.

Acute Chest Syndrome (ACS) is the leading cause of death in children with sickle cell disease (SCD) in the US-about half of the children who develop ACS present initially with pain. Here, we studied biomarkers to differentiate ACS from vaso-occlusive crises (VOC) in children with SCD who presented with pain to the emergency department (ED). We conducted a prospective cohort study of consecutive patients who presented to the ED with pain and were discharged with ACS or VOC between March, 2017 and February, 2020. We identified 7 patients with ACS and 19 patients with VOC. The two groups were comparable in age and sex. All patients with ACS had asthma versus 42% of the VOC group. The ACS group had lower weight and BMI z-scores. Patients with ACS compared to VOC had significantly higher respiratory rates, lower O2 saturation, and longer hospital stays. They also had higher white blood cell count, glucose level (> 99 mg/dL), anion gap (> 9 mEq/L), sPLA2 (> 7 pg/mL), IFN-γ (> 17.8 pg/mL), IL-10 (1.54 pg/mL), and IL-12 (> 0.5 pg/mL) levels. We identified biomarkers associated with ACS development in children with SCD presenting with pain that allow for earlier ACS interventions to reduce mortality and morbidity.

Amyloid beta-induced signalling in leptomeningeal cells and its impact on astrocyte response.

The pathological signature of Alzheimer's disease (AD) includes the accumulation of toxic protein aggregates, mainly consisting of amyloid beta (Aβ). Recent strides in fundamental research underscore the pivotal role of waste clearance mechanisms in the brain suggesting it may be an early indication of early onset AD. This study delves into the involvement of leptomeningeal cells (LMCs), crucial components forming integral barriers within the clearance system, in the context of AD. We examined the inflammatory cytokine responses of LMCs in the presence of Aβ, alongside assessments of LMC growth response, viability, oxidative stress, and changes in vimentin expression. The LMCs showed no changes in growth, viability, oxidative stress, or vimentin expression in the presence of Aβ, indicating that LMCs are less susceptible to Aβ damage compared to other CNS cells. However, LMCs exhibited a unique pro-inflammatory response to Aβ when compared to an LPS inflammatory control, showing an mRNA expression of pro-inflammatory cytokines such IL-6, IL-10 and IL-33 but no changes in IL-1α and IL-1β. Furthermore, LMCs influenced the astrocyte response to Aβ, as conditioned media from Aβ-treated LMCs was observed to downregulate somatic S100β in astrocytes. We also investigated whether the JAK/STAT3 pathway was involved in the Aβ response of the LMCs, as this pathway has been shown to be activated in astrocytes and neurons in the presence of Aβ. JAK/STAT3 activation was assessed through phosphorylated STAT3, revealing that JAK/STAT3 was not active in the cells when in the presence of Aβ. However, when JAK1 and JAK2 were inhibited, cytokine protein levels of IL7, IL10, IL15 and IL33 levels, which had shown alteration when LMCs were treated with Aβ, returned to base levels. This indicates that although JAK1/STAT3 and JAK2/STAT3 are not the direct pathway for Aβ response in LMCs, JAK1 and JAK2 may still play a role in regulating cytokine levels, potentially through indirect means or crosstalk. Overall, our findings reveal that LMCs are resilient to Aβ toxicity and suggest that JAK1/STAT3 and JAK2/STAT3 does not play a central role in the inflammatory response, providing new insights into the cellular mechanisms underlying AD.

Association of the humoral immune response with the inflammatory profile in Plasmodium vivax infections in pregnant women.

Plasmodium vivax infection, when it occurs during pregnancy, has often been associated with serious adverse pregnancy outcomes. However, immunological alterations in pregnancy and their consequences have been little explored. We characterized the humoral immune response in pregnant women exposed to malaria by P. vivax antigens and its association with the maternal inflammatory profile and poor pregnancy outcomes. An observational cohort study in the Brazilian Amazon was conducted between 2013 and 2015. After applying exclusion criteria, 242 mother-child pairs were included in the analysis. Data on maternal infection, gestational outcomes, and inflammatory factors were evaluated in the maternal peripheral plasma. In samples from the first infection, the presence of total IgG and its subclasses in plasma against PvMSP119 protein were also quantified. Previous exposure to malaria, observed by anti-total IgG antibodies to the PvMSP119 antigen, increased the inflammatory response to infection when the pregnant woman had malaria during pregnancy. IL-6 and IL-10 levels were positively correlated with parasitemia and with total IgG levels; but they were negatively correlated with the gestational age at delivery from Pv-infected woman. In multivariate linear regression analyses, IgG 1, 2 and 4 was negatively and positively associated with cytokines IL-6 and IL-10, respectively, in P. vivax-infection. An association between the humoral immune response and the peripheral inflammatory cytokine profile with the adverse outcomes in malaria in pregnancy by P. vivax was observed. Previous exposure to the parasite can influence the IL-6 and IL-10 response, which is associated with increased parasitemia, reduced maternal weight gain and premature delivery.

Exosomes derived from platelet-rich plasma present a novel potential in repairing knee articular cartilage defect combined with cyclic peptide-modified β-TCP scaffold

BackgroundThe aim of this study was to investigate the therapeutic effects and mechanisms of PRP-exos combined with cyclic peptide-modified β-TCP scaffold in the treatment of rabbit knee cartilage defect.MethodsPRP-exos were extracted and characterized by TEM, NTA and WB. The therapeutic effects were evaluated by ICRS score, HE staining, Immunohistochemistry, qRT-PCR and ELISA. The repair mechanism of PRP-exos was estimated and predicted by miRNA sequencing analysis and protein–protein interaction network analysis.ResultsThe results showed that PRP-exos had a reasonable size distribution and exhibited typical exosome morphology. The combination of PRP-exos and cyclic peptide-modified β-TCP scaffold improved ICRS score and the expression level of COL-2, RUNX2, and SOX9. Moreover, this combination therapy reduced the level of MMP-3, TNF-α, IL-1β, and IL-6, while increasing the level of TIMP-1. In PRP-exos miRNA sequencing analysis, the total number of known miRNAs aligned across all samples was 252, and a total of 91 differentially expressed miRNAs were detected. The results of KEGG enrichment analysis and the protein–protein interaction network analysis indicated that the PI3K/AKT signaling pathway could impact the function of chondrocytes by regulating key transcription factors to repair cartilage defect.ConclusionPRP-exos combined with cyclic peptide-modified β-TCP scaffold effectively promoted cartilage repair and improved chondrocyte function in rabbit knee cartilage defect. Based on the analysis and prediction of PRP-exos miRNAs sequencing, PI3K/AKT signaling pathway may contribute to the therapeutic effect. These findings provide experimental evidence for the application of PRP-exos in the treatment of cartilage defect.

The gut microbiota is essential for Trichinella spiralis-Evoked suppression of colitis.

Inflammatory bowel disease (IBD) increases the risk of colorectal cancer, and it has the potential to diminish the quality of life. Clinical and experimental evidence demonstrate protective aspects of parasitic helminth infection against IBD. However, studies on the inhibition of inflammation by helminth infection have overlooked a key determinant of health: the gut microbiota. Although infection with helminths induces alterations in the host microbiota composition, the potential influence and mechanism of helminth infections induced changes in the gut microbiota on the development of IBD has not yet been elucidated. In this study, we analyzed the intersection of helminth Trichinella spiralis and gut bacteria in the regulation of colitis and related mechanisms. T. spiralis infected mice were treated with antibiotics or cohoused with wild type mice, then challenged with dextran sodium sulfate (DSS)-colitis and disease severity, immune responses and goblet cells assessed. Gut bacteria composition was assessed by 16S rRNA sequencing and short-chain fatty acids (SCFAs) were measured. We found that protection against disease by infection with T. spiralis was abrogated by antibiotic treatment, and cohousing with T. spiralis- infected mice suppressed DSS-colitis in wild type mice. Bacterial community profiling revealed an increase in the abundance of the bacterial genus Muribaculum and unclassified_Muribaculaceae in mice with T. spiralis infection or mice cohoused with T. spiralis- infected mice. Metabolomic analysis demonstrated significantly increased propionic acid in feces from T. spiralis- infected mice. Data also showed that the gut microbiome modulated by T. spiralis exhibited enhanced goblet cell differentiation and elevated IL-10 levels in mice. These findings identify the gut microbiome as a critical component of the anti- colitic effect of T. spiralis and gives beneficial insights into the processes by which helminth alleviates colitis.

Features of changes in nonspecific factors of immunological reactivity in obesity

Introduction. The study of pathogenetic factors of obesity is an urgent task of modern medicine. The formation of obesity is characterized by changes in the activity of individual mechanisms of innate immunity. At the same time, the values of laboratory indicators that characterize them are often within the current boundaries of the reference values of laboratory indicators of the immunity of a healthy person. This complicates the pathogenetic assessment of the mechanisms of nonspecific immunological reactivity in obesity and determines the need for further study of the characteristics of nonspecific immune defense factors in this pathology.Aim. To identify the features of changes in cellular and humoral factors of nonspecific immunological reactivity in obesity.Materials and methods. A single-center cross-sectional, one-time controlled study was conducted with the participation of 118 people, of which 87 people were obese patients (BMI 37.2 [34.1; 42.05] kg/m2), 31 people had normal body weight (BMI 21.9 [ 20.2; 23.5] kg/m2) and were included in the control group. All patients underwent a study of lipid profile (total cholesterol, high-density lipoproteins, low-density lipoproteins, very low-density lipoproteins, triglycerides), carbohydrate metabolism (glucose, insulin, glycated hemoglobin), C-reactive protein, indicators of cellular and humoral factors of nonspecific immunity (leukogram, cytokine profile, C3-C4 complement components).Results. An increase in the total number of leukocytes was revealed, due to neutrophil granulocytes against the background of the development of a disproportion between the percentage and absolute value of the number of lymphocytes and monocytes, the concentration of C3 and C4 complement components, C-reactive protein, as well as an increase in the level of IL-6, which confirms the presence of low-grade chronic inflammation in obese patients. Statistically significant correlations of immunological parameters with anthropometric data, indicators of carbohydrate and lipid metabolism were revealed.Conclusion. The results of the study indicate that obesity causes activation of certain cellular and humoral mechanisms of nonspecific immune defense involved in the formation of the inflammatory process. Confirmation of the presence of a latent inflammatory process in obesity is an increase in the level of leukocytes and their individual cellular forms, C-reactive protein, C3 and C4 complement components, IL-6. A feature of the changes is the presence of fluctuations in the values of the studied indicators within the current boundaries of the reference values of laboratory indicators, which makes it difficult to timely diagnose chronic inflammation in obesity

Vanillic acid ameliorates diethyl phthalate and bisphenol S-induced oxidative stress and neuroinflammation in the hippocampus of experimental rats.

Long-term adverse effects on human health are caused by exogenous compounds that alter the functions of biological systems, especially neuroendocrine disruptors like diethyl phthalate (DEP) and bisphenol S (BPS). Although vanillic acid (VA) has pertinent neuropharmacological characteristics, its effect against DEP + BPS-induced neurotoxicity has not been explored. This study proposed that VA may offer protection against the neurotoxicity caused by DEP + BPS. Thirty male Wistar rats were randomly distributed across five groups: a control group receiving DMSO, a group exposed to a mixture of BPS and DEP, two BPS + DEP-exposed groups treated with VA at doses of 25 mg/kg or 50 mg/kg, and a nonexposed group treated with 50 mg VA/kg. After 21 days, the hippocampal tissues were processed for biochemical analyses. Our results indicate that exposure to DEP + BPS upregulated neurosignaling mediators (NTPDase, ADA, MAO-A, and Ca2+), inhibited others (AChE and Ca2+/Mg2+-ATPase), decreased hippocampus antioxidants (GSH, GPx, CAT, and SOD), and elevated markers of oxidative stress/damage (NO, H2O2, MDA, and AOPP). AR, BAX, TNF-α, BAK1, and IL-1β expressions were upregulated, while IL-10 and BDNF expressions were downregulated. NF-κB and caspase-3/9 pathways were also upregulated. Co-treatment with vanillic acid remarkably precluded these neurotoxic outcomes by improving neurosignaling, augmenting antioxidant status, abrogating oxidative damage, inflammation (TNF-α, IL-1β), and apoptosis (BAX, BAK1, caspase-3/9). Vanillic acid also restored IL-10 and BDNF levels, thereby exhibiting neuroprotective effects, corroborated by histological examinations. We posit vanillic acid as a safe and effective therapeutic agent against neurotoxicity occasioned by exposure to neuroendocrine disruptors.

F-Box and WD repeat domain containing 7 induces infectious osteomyelitis by regulating MYB stability and ubiquitination.

Osteomyelitis is a bone inflammation initiated by invading pathogens. Macrophages and inflammation play essential roles in osteomyelitis. F-Box and WD repeat domain containing 7 (Fbxw7) is a tumour suppressor and E3 ubiquitin ligase. In the present study, the potential roles of Fbxw7 in osteomyelitis were explored. The mRNA level of Fbxw7 was measured in bone marrow cells from patients with osteomyelitis and Staphylococcus aureus (S. aureus)-infected macrophages. The conditional knockout mice with Fbxw7 deficiency in myeloid cells were generated. The expression of interleukin (IL)-6, IL-23a and nitric oxide synthase 2 (Nos2) was measured in S. aureus-infected Fbxw7-deficient bone marrow-derived macrophages (BMDMs). The body weight loss, bacterial burden, bone loss and formation and serum level of IL-6, IL-23 and TNF-α were measured in S. aureus-infected Fbxw7 conditional KO mice. The interacting partners of Fbxw7 were predicted using STRING and the interaction were tested. Elevated expression of Fbxw7 was observed in bone marrow cells from patients with osteomyelitis and in S. aureus-infected macrophages. The expression of IL-6, IL-23a and Nos2 was remarkably suppressed in S. aureus-infected Fbxw7-deficient BMDMs. Fbxw7 conditional knockout mice had less body weight loss, higher bacterial burden, less bone loss and formation and decreased serum level of cytokines. Fbxw7 interacted with MYB. S. aureus-infected Fbxw7-deficient BMDMs had higher level of MYB and less ubiquitination of MYB. Fbxw7 promotes osteomyelitis symptoms by regulating ubiquitination and stability of MYB.

Glutathione inhibits lung cancer development by reducing interleukin-6 expression and reversing the Warburg effect

Reduced glutathione (GSH) is widely used as an antioxidant in clinical practice, but whether GSH affects the development of early lung cancer remains unclear. Herein, we investigated the mechanism underlying the anticancer effect of GSH in patients with pulmonary nodules. Thirty patients with pulmonary nodules were treated with GSH intravenously for 10 days at a dose of 1.8 g/d, followed by oral administration of the drug at a dose of 0.4 g three times daily for 6 months. The results showed that GSH treatment promoted nodule absorption and reduced the IL-6 level in the peripheral blood of the patients. GSH reduced IL-6 expression in inflammatory BEAS-2B and lung cancer cells and inhibited the proliferation of lung cancer cell lines in vitro. In addition, GSH reduced IL-6 expression by decreasing ROS via down-regulating PI3K/AKT/FoxO pathways. Finally, GSH reversed the Warburg effect, restored mitochondrial function, and reduced the IL-6 expression via PI3K/AKT/FoxO pathways. The in vivo experiment confirmed that GSH inhibited lung cancer growth, improved mitochondrial function, and reduced the IL-6 expression by regulating key enzymes via the PI3K/AKT/FoxO pathway. In conclusion, we uncovered that GSH exerts an unprecedentedly potent anti-cancer effect to prevent the transformation of lung nodules to lung cancer by improving the mitochondrial function and suppressing inflammation via PI3K/AKT/FoxO pathway. This investigation innovatively positions GSH as a potentially safe and efficacious old drug with new uses, inhibiting inflammation and early lung cancer. The use of the drug offers a promising preventive strategy when administered during the early stages of lung cancer.

Association Between Prostatitis and Some Biochemical Markers in Patients of the AL-Najaf Province, Iraq

One of the most common clinical conditions in men is prostate disease, especially prostatitis, which causes various symptoms, that negatively affect patient life. Our current study investigated the relationship between prostatitis and IL-6, zinc, and ESR levels for patients who visited AL-Sader Medical City in the province of AL-Najaf, between March and November 2023. our study included 90 samples of people infected with prostatitis and 30 samples of healthy people between the ages of (20-40) years. The level of IL-6 was calculated using the ELISA technique, The level of zinc as an antioxidant asses by using the spectrophotometer and ESR was measured by using the Westergren technique to determine the inflammation case in patients and compared with the healthy group. The results showed an increase in the level of IL-6 in patients with prostatitis compared with a healthy group (908.72±140.19,214.16±85.56) pg/ml respectively. but showed a decrease in the level of Zinc in prostatitis patients compared with the healthy group (38.93±10.92U/ml, 89.36±9.61U/ml) respectively. Also showed an elevated level of ESR, where according to (48.41±13.49 ) mm/hour in patients group compared with a healthy group (14.60±4.14) mm/ hour. The data was analyzed by SPSS program version 23, where the factor effect was considered significant when p<0.05. we conclude from our current study the significant relationship between IL-6, Zinc levels, and prostatitis, as well as the role of the ESR test as an indicator of prostatitis

Association between tumor necrosis factor-α gene polymorphism and interleukin-6 level with mortality of neonatal sepsis

Sepsis is a systemic infection that significantly causes morbidity and mortality among neonates, which is associated with immature immune response. Variations in the tumor necrosis factor-alpha gene (TNF-α) -308G/A may be linked to neonatal sepsis mortality by modulating interleukins (ILs) involved in the immune response cascade, such as IL-6. The aim of this study was to investigate the association between TNF-α -308G/A gene variation and IL-6 level with mortality of neonatal sepsis. A cohort of 30 neonates diagnosed with clinical sepsis was recruited. Blood culture was performed for all patients and serum IL-6 levels were examined 24 hours after suspected sepsis. Genetic analysis of TNF-α single nucleotide polymorphisms (SNP) -308G/A was conducted using polymerase chain reaction and DNA sequencing. The association was assessed based on bivariate logistic regression. We found that 12 (40%) of 30 patients had blood culture-proven sepsis. Genotype of TNF-α -308G/A stratified of the patients was 56.7% for GA and 43.3% for GG. There were no AA variations found in this study. There was no significant association between the TNF-α -308 G/A genotype and mortality in neonatal sepsis (p=0.211). Similarly, the allelic model of TNF-α -308 gene had no association with mortality (p=0.325). Additionally, there was no association between serum IL-6 level and mortality in neonatal sepsis (p=0.253). In conclusion, SNP of TNF-α -308 gene and IL-6 level are not associated with mortality in neonatal sepsis.

Levels of IL-6 and IL-8 in complicated versus uncomplicated urinary tract infection

Background: Urinary tract infections (UTIs) are one of the world's most frequent infectious diseases, affecting 150 million people each year and resulting in severe morbidity and high medical expenditures. UTIs can be clinically defined as uncomplicated UTIs (uUTIs) or complicated UTIs (cUTIs) to differentiate infections of benign origin from those with a higher risk of recurrence or progression to severe pathology. The aim of this study was to evaluate interleukin-6 (IL-6) and IL-8 as potential biomarkers in differentiating complicated and uncomplicated Methods: Ninety samples of urine were collected. There were 43 samples from healthy controls and 47 samples from UTI patients, those who have been clinically diagnosed with UTIs by the urologist. The serum IL-6 and IL-8 were measured using an enzyme-linked immunosorbent assay and commercially available kits. Results: The levels of both IL-6 and IL-8 were significantly higher in UTI patient then in control subjects (p=0.001, p=0.001). A significant difference was observed in the mean of level IL-6 between culture positive UTI patients and culture negative UTI patients (p=0.014). In addition, the type of bacterial growth, a significant difference was observed in the mean of serum IL-6 and IL-8 level in UTI caused by gram negative bacteria in comparison with UTI caused by gram positive bacteria. Conclusion: High levels of IL-6 are associated with the growth of gram-negative bacteria, and this indicates that gram-negative bacteria could induce stronger inflammatory responses than gram-positive bacteria. IL-8 levels are higher in UTIs caused by gram-negative bacteria. This result further supported the evidence that gram-negative bacteria are potent inducers of inflammatory responses.

Serum IL-6 as a Potential Biomarker of Metabolic Status in Schizophrenia Patients and Its Correlation with Psychotic Symptoms

Objectives: This study aimed to investigate the serum IL-6 level in schizophrenia patients, considering disease chronicity and metabolic status, and to examine its correlation with psychotic symptom scores. The present study also evaluated the diagnostic value of serum IL-6 as a peripheral biomarker for assessing the metabolic health of schizophrenia patients. Methods: Serum IL-6 levels were measured using enzyme-linked immunosorbent assay (ELISA) in 92 schizophrenia patients [44 First Episode Drug Naive (FEDN), 48 chronic schizophrenia (CSZ) patients] and 32 healthy controls. Patients were also stratified into high-risk and no-risk cohorts based on their metabolic status. Psychotic symptoms were assessed with the Positive and Negative Syndrome Scale (PANSS). Findings: Serum IL-6 levels were significantly higher in schizophrenia patients compared to healthy controls (p<0.001), with no difference between FEDN and CSZ patients (p=0.475). Elevated IL-6 levels were observed in patients in high-risk group compared to those in no-risk group (p<0.001). There was a positive correlation between serum IL-6 levels and BMI (r=0.557, p<0.001), G score (r=0.244, p=0.01), and total PANSS score (r=0.228, p=0.02). Similar associations were found in CSZ patients. The ROC curve analysis showed that serum IL-6 has strong diagnostic potential for distinguishing schizophrenia patients in the high-risk group from those in the no-risk group (AUC=0.875, 95% CI: 0.781-0.969, p<0.001), suggesting its value as a biomarker. Novelty: This study highlights the stable role of serum IL-6 in schizophrenia patients regardless of disease chronicity. The findings suggest that serum IL-6 levels were significantly associated with disease severity as measured by PANSS and metabolic health of schizophrenia patients, providing new insights into its prognostic and diagnostic utility. Early identification and targeted management of high-risk groups can improve patient outcomes and quality of life. Keywords: Schizophrenia, IL-6, FEDN, Chronic, PANSS, Metabolic status, Biomarker

Evaluating peripheral blood lymphocyte subset composition and lipopolysaccharide-induced cytokine secretory activity in mononuclear leukocyte cultures from patients with febrile and meningeal forms of tick-borne encephalitis

Introduction.Multiple studies on immune response in patients with various clinical forms of tick-borne encephalitis (TBE) have shown conflicting results. The study aim was to estimate the changes in peripheral blood lymphocyte subset counts and activity of spontaneous and lipopolysaccharide (LPS)-stimulated cytokine production in the mononuclear leukocyte cultures in patients with febrile and meningeal acute TBE.Materials and methods.Groups 1 and 2 included 16 and 12 patients with febrile and meningeal acute TBE, respectively. The control group included 13 healthy donors. Hemogram and T-lymphocyte, T-helper cell, T-cytotoxic and NK cell counts were analyzed by flow cytometry at week 1 of the disease as well as the spontaneous and LPS-stimulated secretion levels of TNFα, IL-1β, IL-6, IL-10, IL-8, and MCP-1 were assessed by ELISA in the supernatants of mononuclear cell cultures twice: during hospitalization and two weeks later. Statistical analysis was performed by the Mann–Whitney U-test, and Wilcoxon test.Results.Group 2 demonstrated significant decrease in spontaneous and/or LPS-stimulated levels of proinflammatory cytokines IL-1β, IL-6, MCP-1, and TNFα, but showed higher IL-8 level as compared with Group 1. In addition, spontaneous and/or LPS-induced levels of IL-6 and TNFαin Group 2 did not significantly differ from the controls, which presumably also indicated the suppression of their production. In contrast, spontaneous and/or LPS-induced levels of IL-1β, IL-6, MCP-1, and TNFαin Group 1 were higher than in the controls. The spontaneous IL-10 level in the patients from both groups were higher than in the controls. Peripheral blood lymphocyte and T-cytotoxic T-lymphocyte counts in both groups of TBE patients were lower than in the controls. There was significant increase in neutrophil counts, decrease in NK cell count in Group 2 as compared to the patients with a milder febrile form.Conclusion.Meningeal acute TBE patients was presumably associated with inadequate immune response with NK cell deficiency, T-cell dysfunction, increased neutrophil count in the peripheral blood and impaired pro-inflammatory cytokine production related to innate immune response.

The role of epithelial alarmins and Th2 cytokines in the inflammatory response in allergic rhinitis

Allergic rhinitis (AR) occupies a leading position among the causes of morbidity throughout the world, to date, it has been diagnosed in 400 million people. In the formation and progression of AR, a significant role is assigned to cytokines associated with the second type of immune response, in particular, IL-4, IL-5, IL-9, IL-13, IL-25, IL-33, thymic stromal lymphopoietin (TSLP). This literature review provides information on the influence of the listed mediators on the structural cells of the nasal cavity and blood immune cells (T- and B-lymphocytes, eosinophils, macrophages, dendritic cells), and discusses their association with the manifestation of AR symptoms and the severity of the disease. The results of studies aimed at establishing the level of IL-4, IL-5, IL-9, IL-13, IL-25, IL-33 and TSLP in biological fluids (blood serum, nasal lavage) and their expression in nasal epithelial cells in patients with AR compared to healthy people are assessed.