Serum IL-18 Levels Research Articles

Predictive significance of interleukin-15 in urinary tract infections caused by beta-lactamase-producing Klebsiella pneumoniae

Klebsiella pneumoniae has been identified as one of the important pathogens involved in the pathogenesis of urinary tract infections (UTIs) in humans. This study sought to determine the prevalence of K. pneumoniae and its ability to produce extended-spectrum-β-lactamases (ESBLs) in patients with UTIs. Besides, the predictive significance of interleukin (IL)-15 in UTIs caused by ESBLs-producing K. pneumoniae (K-ESBLs) was also assessed.: During October 2020 – January 2021, a cross-sectional and case-control study was performed on 587 patients with UTIs. Serum level of IL-15 was assessed using an enzyme-linked immunosorbent assay kit. The prevalence of K. pneumonia was 15.8%. It was also found that 68.8% of the K. pneumonia isolates were K-ESBLs (64patients). IL-15 levels were significantly elevated in serum of UTI patients with K-ESBLs compared to 24 control subjects (29.4 ± 9.2 vs. 22.1 ± 5.1; p-value < 0.001). Receiver operating characteristic (ROC) curve analysis revealed that IL-15 occupied an area under the curve of 0.740 (95% Confidence Interval = 0.633–0.848; p-value < 0.001), and at cut-off value of 22 pg/mL, the sensitivity and specificity of IL-15 were 73.4 and 75.0%, respectively. When patients and controls were stratified by age groups, gender and diabetes, IL-15 serum levels showed no significant differences in each corresponding stratum. K-ESBLs accounted for a significant proportion of UTIs. Besides, IL-15 was proposed to have a significant predictive value in discriminating between UTI patients with K-ESBLs and controls.

IL-31 and IL-8 in Cutaneous T-Cell Lymphoma: Looking for Their Role in Itch.

The itch associated with cutaneous T-cell lymphoma (CTCL), including Mycosis Fungoides (MF) and Sézary syndrome (SS), is often severe and poorly responsive to treatment with antihistamines. Recent studies have highlighted the possible role of interleukins in nonhistaminergic itch. We investigated the role of IL-31 and IL-8 in CTCL, concerning disease severity and associated itch. Serum samples of 27 patients with CTCL (17 MF and 10 SS) and 29 controls (blood donors) were analyzed for interleukin- (IL-) 31 and IL-8; correlations with disease and itch severity were evaluated. IL-31 serum levels were higher in CTCL patients than in controls and higher in SS than in MF. Also, serum IL-31 levels were higher in patients with advanced disease compared to those with early disease, and they correlated positively with lactate dehydrogenase and beta 2-microglobulin levels, as well as with the Sézary cell count. Itch affected 67% of CTCL patients (MF: 47%; SS: 100%). Serum IL-31 levels were higher in itching patients than in controls and in patients without itching. There was no association between serum IL-8 and disease severity, nor with itching. Serum IL-8 levels correlated positively with peripheral blood leukocyte and neutrophil counts in CTCL patients. Our study suggests a role for IL-31 in CTCL-associated itch, especially in advanced disease and SS, offering a rational target for new therapeutic approaches. Increased serum IL-8 observed in some patients may be related to concomitant infections, and its role in exacerbating itch by recruiting neutrophils and promoting the release of neutrophil proteases deserves further investigation.

Predictive Ability of Serum IL-27 Level for Assessing Activity of Antineutrophil Cytoplasmic Antibody-Associated Vasculitis.

Serum interleukin- (IL-) 27 level has been reported to increase in patients with several autoimmune diseases; however, its significance in patients with antineutrophil cytoplasmic antibody- (ANCA-) associated vasculitis (AAV) is unknown. In this study, we investigated the associations between serum IL-27, laboratory features, and activity of AAV and evaluate the predictive ability of serum IL-27 level for disease activity. This study included 77 AAV patients, and we collected clinical and laboratory data at blood sampling. Inflammation-related variables included white blood cell, neutrophil, lymphocyte and platelet counts, serum albumin, erythrocyte sedimentation rate, and C-reactive protein levels. Serum IL-27 and IL-18 levels were measured from stored sera using Human Magnetic Luminex® assay. High disease activity of AAV was defined as the highest tertile of Birmingham vasculitis activity score (BVAS) (≥11). The mean age of the enrolled patients was 59.9 years, and 38 (49.4%) were diagnosed as microscopic polyangiitis. In the multivariable analysis, serum albumin (β = −0.419) and serum IL-27 level (β = 0.221) were significantly associated with BVAS. Furthermore, patients with renal manifestation exhibited higher serum IL-27 (mean 308.7 pg/mL vs. 105.8 pg/mL) and IL-18 levels (mean 376.7 pg/mL vs. 270.4 pg/mL) than those without. On applying the optimal cut-off of serum IL-27 level for predicting high activity, AAV patients with serum IL − 27 level ≥ 300.8 pg/mL had a significantly higher risk for having high disease activity than those with serum IL − 27 level < 300.8 pg/mL (relative risk 3.380, 95% confidence interval 1.223, 9.345, P = 0.016). These results suggest that serum IL-27 level is associated with the cross-sectional activity and the presence of renal manifestation and could be used to predict high disease activity in patients with AAV.

Elevated Serum Interleukin-23 Levels in Patients with Oral and Cutaneous Lichen Planus.

Lichen planus is considered a chronic inflammatory disease which affects different sites, such as the skin, mucous membranes, hair, and nails. Based on the evidence, a complex cytokine network plays a crucial role in lichen planus pathogenesis. The study was aimed at assessing the serum IL-23 levels in the patients with cutaneous and oral lichen planus compared to healthy controls. Method. The study included 30 cutaneous lichen planus patients, 20 oral lichen planus patients, and 33 control subjects. Five milliliters of peripheral blood was obtained from each patient, and the serum was separated. IL-23 levels were determined using the ELISA kit, and the data were analyzed using the Mann–Whitney test. Results. IL-23 levels in the patient serum with oral lichen planus (P value ≤ 0.001) were significantly higher than in controls. Furthermore, there were significant differences in IL-23 serum levels in the patients with cutaneous lichen planus compared to the healthy controls (P value ≤ 0.001). Moreover, IL-23 serum levels were statistically different between patients with cutaneous lichen planus and patients with oral lichen planus (P value ≤ 0.001). Based on the mean concentration of interleukin-23, IL-23 levels were higher in the patients with oral lichen planus than in the patients with cutaneous lichen planus. Conclusions. Elevated serum IL-23 levels in the patients with oral lichen planus may indicate that IL-23 plays a crucial role in the pathogenesis of oral lichen planus. However, more research is needed with a larger sample size.

Correlation between serum IL-23 and serum total IgE levels in allergic rhinitis patients

Background: Allergic rhinitis (AR) is an immunoglobulin E (IgE) mediated inflammatory chronic disorder of the nasal mucosa caused by contact to allergens which affects a significant percentage of population. Th17 cells might be involved in the acute phase of the allergic reaction. Th17 cells are regulated by IL-23, which is a member of the IL-12 cytokine family. IL-23 was suggested to be a pivotal cytokine involved in the pathogenesis of AR and may become a novel target in the treatment of AR. Objective: Here we investigate the role of serum IL-23 and its correlation with serum total IgE level in AR. Methodology: This case control study included the investigation of 48subjects. Blood samples were collected for measuring serum IL-23 and total IgE levels by ELISA. Results: positive correlation was found between IL-23 and total IgE serum level in AR patients. Conclusion: Positive correlation was found between serum IL-23 and serum total IgE levels in allergic rhinitis patients.

The Clinical Significance of Serum IL-33 and sST2 Alterations in the Post-Stroke Depression

IntroductionThis study was to test whether the serum levels of IL-33 and sST2 are correlated with the development of depression after acute ischemic stroke.MethodsPatients diagnosed with acute ischemic stroke were selected. This study took the 24-item Hamilton Depression Rating Scale (HAMD) (score ≥20) as the diagnostic criteria for depression. On the 21st day after admission, patients who met the depression diagnostic criteria were included in the depression group, and patients who failed to meet the diagnostic criteria were included in the non-depression group. The serum levels of IL-33, sST2 and hsCRP were measured by enzyme-linked immunosorbent assay (ELISA).ResultsOn 1st day after stroke, compared with the non-depression group, there was no significant difference in the serum IL-33, sST2 and hsCRP levels in the depression group; on 21st day after stroke, compared with the non-depression group, the serum IL-33 and hsCRP levels were significantly increased, while the sST2 level was significantly decreased in the depression group. Correlation analysis showed that IL-33 was positively correlated with the depression quantitative score and hsCRP, while sST2 was negatively correlated with the depression quantitative score and hsCRP. Regression analysis showed that IL-33 and sST2 were independent risk factors for the depression after acute ischemic stroke.DiscussionThe abnormal alterations of serum IL-33 and sST2 levels in the stroke patients may serve as one of the risk factors for the occurrence and exacerbation of the depression, and its mechanism may be related to the promotion of inflammatory factor production in vivo.

Relationship of Serum Cytokine Profile to Steroid Resistance in Demyelinating Neurologic Illnesses

Background and Purpose: Corticosteroids form main stay of treatment of autoimmune neurological diseases. Immunotherapy with Intravenous Immunoglobulin, Plasmapheresis, biological agents like Rituximab, Infliximab, etanarcept are also used for treatment of patients who are resistant to steroid treatment and in severe cases. This study was aimed to elicit the relationship between serum cytokine levels and steroid resistance which is important for early commencement of other medications. Methods: The serum samples of patients who presented with autoimmune neurological diseases were collected and cytokine levels were estimated. The cytokine profile of patients who responded well to steroid treatment was compared with that of steroid nonresponders. Results: The steroid unresponsive group had significantly higher serum Interferon gamma and IL-13 levels than steroid unresponsive group. Conclusion: when patients present with high serum levels of IL-13 and Interferon Gamma they should be considered for prompt escalation of immunomodulatory therapy.

Serum interleukin-33 level may serve as a new marker for psoriasis diagnosis

Background Psoriasis is a Th1/Th17 disease resulting from a dysregulated interplay between keratinocytes and immune cells, leading to skin hyperproliferation. Increased levels of interleukin (IL)-33 were reported in various Th1/Th17-driven autoimmune diseases, such as rheumatoid arthritis and inflammatory bowel disease, with correlation to disease severity. Increased levels of IL-33 have been reported in lesional skin of psoriatic patients. The authors hypothesized that keratinocyte-released IL-33 might play a role in psoriasis pathogenesis; thus, inhibiting IL-33 activity might be a breaking new therapeutic strategy in its treatment. Patients and methods Serum IL-33 levels were measured by an enzyme-linked immunosorbent assay for 30 patients with active psoriasis (group A), 30 patient with stable psoriasis (group B), and 30 healthy age-matched and sex-matched controls (group C). Results Serum IL-33 showed statistically significant higher mean value among patients with psoriasis compared with the control group. The level of IL-33 in active psoriasis was significantly higher than in inactive psoriasis. Moreover, there was a statistically significant correlation between IL-33 and psoriasis area and severity index (PASI) score. Receiver operating characteristics curve detected the validity of serum IL-33 in differentiating patients with psoriasis from controls. At the cutoff point of IL-33 as 22.72 pg//ml, psoriasis could be predicted with 96.67% sensitivity and 93.33% specificity. Serum IL-33 was a statistically significant predictor of PASI score, with 63.5% of PASI scores predicted by serum IL-33. Conclusion Serum IL-33 may represent a new marker for psoriasis diagnosis as well as a predictor of the disease severity.

Serum IL-35 is decreased in overweight patients with rheumatoid arthritis: its correlation with Th1/Th2/Th17-related cytokines

BackgroundObesity is correlated with worse drug responses and high disease activity in patients with rheumatoid arthritis (RA). Interleukin (IL)-35 is a novel anti-inflammatory cytokine that mainly produced by regulatory T (Treg). This study was performed to analyze whether IL-35 was correlated with obesity in RA and investigate the correlation between other Th1/Th2/Th17-related cytokines and obesity in RA.ResultsThe serum IL-35 level was analyzed in RA (n = 81) and healthy donors (n = 53) by ELISA assay, and was compared between three groups (body mass index (BMI) < 18.5,≥18.5 to 25, > 25). Serum cytokines including IL-2, IL-4, IL-10, IL-17, INF-γ, TNF-α levels were measured using Flowcytometry assay. Clinical information was extracted from medical records. Serum IL-35 level in overweight patients were significantly decreased than those in lean patients. Furthermore, Th1/Th2/Th17-related cytokines from overweight patients with RA showed the characteristic immunological features. Serum IL-6, IL-17 and TNF-α levels were positively correlated with BMI. However, serum IL-2, IL-4, IL-10 and IFN-γ concentrations were not correlated with BMI.ConclusionsQuantitative changes in serum IL-35 level were characteristic in overweight patients with RA. These findings indicate that IL-35 plays an important role in the development of RA and may prove to be a potential biomarker of active RA.

High Serum Level of Interleukin-15 Predicts Poor Prognosis in Adult Standard-Risk Acute Lymphoblastic Leukaemia

BackgroundInterleukin-15 (IL-15) is a proinflammatory cytokine involved in the proliferation, survival and activation of acute lymphoblastic leukaemia (ALL). However, the prognostic significance of serum IL-15 level in adult patients with standard-risk ALL has not been well established.MethodsSerum IL-15 level was measured using enzyme-linked immunosorbent assay in 130 adult patients diagnosed with standard-risk ALL.ResultsThe optimal cut-off value for IL-15 in predicting patient survival is 4.82 pg/mL, with an area under the curve value of 0.808 (P < 0.001). The early complete response (CR) on day 14 in in low IL-15 group is 65.3%, which is significantly higher than that in high IL-15 group (39.7%, P= 0.003). Patients in the low IL-15 group exhibited significantly higher survival rate compared with those in the high IL-15 group [5-year event-free survival (EFS) rate: 62.2% vs. 23.3%, P < 0.001; 5-year overall survival (OS) rate: 64.1% vs. 27.7 %, P= 0.001]. Multivariate analysis revealed that serum IL-15 level > 4.82 pg/mL, late CR and older age are adverse factors for EFS and OS.ConclusionsSerum IL-15 level at diagnosis is a novel, effective predictor of prognosis in adults with standard-risk ALL. [Display omitted] DisclosuresNo relevant conflicts of interest to declare.

Association of interleukin-18 genotypes (-607C > A) and (-137 G > C) with the hepatitis B virus disease progression to hepatocellular carcinoma.

Chronic infection with HBV has been reported to be associated with the development of HCC. The inflammation mounted by cytokine-mediated immune system plays an important role in the pathogenesis of HBV-associated HCC. IL-18 is a pro-inflammatory cytokine whose role in the development of HBV-associated chronic to malignant disease state has not been much studied. The present study was conceived to determine the role of genetic polymorphisms in IL-18, serum levels of IL-18, and expression level of its signal transducers in the HBV disease progression. A total of 403 subjects were enrolled for this study including 102 healthy subjects and 301 patients with HBV infection in different diseased categories. Polymorphism was determined using PCR-RFLP. Genotypic distributions between the groups were compared using odd's ratio and 95% CI were calculated to express the relative risk. Circulating IL-18 levels were determined by ELISA. Expression levels of pSTAT-1 and pNFƙB was determined by western blotting. In case of IL-18(- 607C > A), the heterozygous genotype (CA) was found to be a protective factor while in case of IL-18(- 137G > C) the heterozygous genotype (GC) acted as a risk factor for disease progression from HBV to HCC. Moreover, serum IL-18 levels were significantly increased during HBV disease progression to HCC as compared to controls. Also the levels of activated signal transducers (pSTAT-1 and pNF-κB) of IL-18 in stimulated PBMCs were significantly increased during HBV to HCC disease progression. These findings suggest that IL-18 has the potential to act as a biomarker of HBV-related disease progression to HCC.

Evaluation of serum interleukin-6 (IL-6), IL-13, and IL-17 levels and computed tomography finding in interstitial lung disease associated with connective tissue disease patients.

Interstitial lung disease (ILD) is one of the most severe complications which is associated with connective tissue disease (CTD) and causes to morbidity and mortality. So, we aimed to determine serum levels of interleukin-6 (IL-6), IL-13, and IL-17, to investigate whether these cytokines are related to CTD-ILD, and to find their possible contribution to determining the prognosis of the disease. A total of 150 participants, 80 patients diagnosed with CTD-ILD (mean age, 58.21 ± 12.36) and 70 healthy controls (mean age, 57.07 ± 9.60) were recruited from the rheumatology department between January 2016 and June 2019 in the study. High-resolution computed tomography (HRCT) findings were scored as similarly to previous studies. Serum IL-6, IL 13, and IL-17 levels were measured by ELISA test kits. The levels of IL-6, IL-13, and IL-17 in CTD patients were significantly higher than the healthy individuals (p < 001), but the HRCT score's relation were not determined. IL-6 was associated with disease duration and disease activity scores of DAS28, ESDAII, and dSSc. There was a significant relation between dSSc, HCRT fibrosis, and total score.CRP, hemoglobin, and platelets were associated with the HRCT inflammation pattern. At the study, it has been observed that serum IL-13, IL-6 and IL-17 levels are increased in patients with CTD-ILD. Besides, IL-6 was associated with disease activity scores of DAS28, ESDAII, and dSSc. Also, HRCT fibrosis score is associated with dSSc. Further and comprehensive studies are needed to understand better the complex intersection of lung disease with systemic autoimmunity. Key Points • Serum IL-13, IL-6, and IL-17 levels are increased in patients with CTD-ILD. • IL-6 was associated with disease activity scores of DAS28, ESDAII, and diffuse skin involvement. • HRCT fibrosis score is associated with diffuse skin involvement in patients with SSc-ILD. • HRCT inflammation score is associated with PAH.

Study of the correlation between the noncanonical pathway of pyroptosis and idiopathic inflammatory myopathy

BackgroundThe pathogenesis of idiopathic inflammatory myopathy (IIM) is complex and unclear. The purpose of this study was to investigate whether the noncanonical pathway of pyroptosis is involved in the pathogenesis of IIM, and the intervention effect of drugs glyburide and bright blue G (BBG). MethodsAfter the drug intervention, we detected the expression of the caspase-4, caspase-5, caspase-11, GSDMD, pannexin-1, NLRP3 and P2X7R proteins in skeletal muscle tissues from the six groups using Western blotting. We detected the expression of the caspase-11, GSDMD, pannexin-1, NLRP3 and P2X7R mRNAs in skeletal muscle tissues from the six groups using RT-qPCR and detected the serum IL-18 and IL-1β levels in the six groups using ELISAs. ResultLower expression levels of the P2X7R and NLRP3 proteins were observed in the EAM + BBG group than in the EAM1 group (P < 0.05). The expression of NLRP3 in the EAM + glyburide group was lower than in the EAM2 group (P < 0.05). Lower expression levels of the P2X7R and NLRP3 mRNAs were detected in the EAM + BBG group than in the EAM1 group (P < 0.05). NLRP3 was expressed at lower levels in the EAM + glyburide group than in the EAM2 group (P < 0.05). Lower serum IL-1β levels were detected in the EAM + BBG group than in the EAM1 group (P < 0.05), and serum IL-1β and IL-18 levels in the EAM + glyburide group were lower than those in the EAM2 group (P < 0.05). ConclusionOur results suggest that the noncanonical pathway of pyroptosis may be involved in the pathogenesis of IIM, and glyburide and BBG exert certain intervention effects on its pathogenesis.

CD3+CD4+gp130+ T Cells Are Associated With Worse Disease Activity in Systemic Lupus Erythematosus Patients.

The receptors for IL-35, IL-12Rβ2 and gp130, have been implicated in the inflammatory pathophysiology of autoimmune diseases. In this study, we set out to investigate the serum IL-35 levels and the surface levels of IL-12Rβ2 and gp130 in CD3+CD4+, CD3+CD4─ and CD3─CD4─ lymphocyte subpopulations in systemic lupus erythematosus (SLE) patients (n=50) versus healthy controls (n=50). The potential T cell subsets associated with gp130 transcript (i.e. IL6ST) expression in CD4+ T cells of SLE patients was also examined in publicly-available gene expression profiling (GEP) datasets. Here, we report that serum IL-35 levels were significantly higher in SLE patients than healthy controls (p=0.038) but it was not associated with SLEDAI-2K scores. The proportions of IL-12Rβ2+ and gp130+ cells in SLE patients did not differ significantly with those of healthy controls in all lymphocyte subpopulations investigated. Essentially, higher SLEDAI-2K scores were positively correlated with increased proportion of gp130+ cells, but not IL-12Rβ2+ cells, on CD3+CD4+ T cells (r=0.425, p=0.002, q=0.016). Gene Set Enrichment Analysis (GSEA) of a GEP dataset of CD4+ T cells isolated from SLE patients (n=8; GSE4588) showed that IL6ST expression was positively associated with genes upregulated in CD4+ T cells vs myeloid or B cells (q<0.001). In an independent GEP dataset of CD4+ T cells isolated from SLE patients (n=9; GSE1057), IL6ST expression was induced upon anti-CD3 stimulation, and that Treg, TCM and CCR7+ T cells gene sets were significantly enriched (q<0.05) by genes highly correlated with IL6ST expression (n=92 genes; r>0.75 with IL6ST expression) upon anti-CD3 stimulation in these SLE patients. In conclusion, gp130 signaling in CD3+CD4+ T cell subsets may contribute to increased disease activity in SLE patients, and it represents a promising therapeutic target for inhibition in the disease.

Epithelial expression and role of secreted STC1 on asthma airway hyperresponsiveness through calcium channel modulation

Asthma is characterized by airway hyperresponsiveness (AHR), inflammation, and airway remodeling. Airway hyperresponsiveness results from enhanced airway smooth muscle (ASM) contraction potentially under the control of an epithelium-derived relaxing factor (EpDRF). However, relatively rare is known about EpDRF. We aimed to elucidate the role of epithelium-derived stanniocalcin-1 (STC1) on AHR and ASM contraction. Stanniocalcin-1 levels in the serum of asthmatic patients and healthy volunteers and in bronchoalveolar lavage fluid (BALF) from ovalbumin (OVA)-challenged mice were measured by ELISA. The effects of exogenous STC1 on AHR and on inflammation were examined in mice. IL-13 modulation of STC1 mRNA and protein levels was studied in human bronchial epithelial cell lines (16HBE). The function of STC1 on Ca2+ influx and ASM contraction was examined ex vivo. Serum STC1 was decreased in asthma (n=93) compared with healthy volunteers (1071±30.4 vs 1414±75.1pg/ml, p<0.0001, n=23) and correlated with asthma control (p=0.0270), lung function (FEV1, p=0.0130), and serum IL-13 levels (p=0.0009). Treatment of ten asthmatic subjects with inhaled corticosteroids/long-acting beta2-agonists (ICS/LABA) for 1year enhanced STC1 expression which correlated with improved asthma control (p=0.022). STC1 was mainly expressed in bronchial epithelium and intranasal administration of recombinant human STC1 (rhSTC1) reduced AHR and inflammation in mice. IL-13 suppressed STC1 release from 16HBE, whereas rhSTC1 blocked store-operated Ca2+ entry (SOCE) by suppressing stromal interaction molecule 1 (STIM1) and further inhibited ASM cell contractility by suppressing Ca2+ -dependent myosin light chain (MLC) phosphorylation. Our data indicate that STC1 deficiency in asthmatic airways promotes STIM1 hyperactivity, enhanced ASM contraction, and AHR. STC1 may be a candidate EpDRF.

Detection of Interleukin-2 and Interleukin-31 among Patients with Uremic Pruritus

Uremic pruritus is a form of chronic itching that affects patients with advanced end-stage renal disease. Itis one of the most common symptoms in patients with end-stage renal disease, with approximately 60–90percent of patients on hemodialysis (HD) experiencing it. The study aims to assess the role of interleukin-31and Interleukin-2 in the pathogenesis of uremic pruritus among hemodialysis patients attending the EbnSina Dialysis Center in Diyala, and Correlation between Interleukin 31 and Interleukin-2 with severityof uremic pruritus. A study was performed from 1 Sep 2020 to 20 Jan 2021 in Ebn Sina Dialysis center,Diyala Governorate. the study was conducted on 150 patients with CKD divided to two groups, 75 patientswith uremic pruritus and 75 patients without uremic pruritus, the control groups was 26 healthy persons.Itch intensity was scored by VAS as mild, moderate and severe. Serum IL-31 levels and serum IL-2 levelswere determined by the enzyme-linked immunosorbent assay methodology. The various characteristics pfpruritus was assessed using an interview questionnaire. MS excel package and SPSS 20 software was usedfor analysis. Among 226 HD patient excluded under 20 age and hepatitis C and Hepatitis B HD patients,33.8% had uremic pruritus. The patients with pruritus had higher serum IL-31 levels and IL-2 than thosewithout uremic pruritus and control groups, it was statically significant. As well as the IL-31 and IL-2showed no significant differences among patients with mild, moderate, and severe itch. IL-31 and IL-2 playimportant role in the pathogenesis of uremic pruritus. Further studies to confirm the role of cytokines in thepathogenesis of UP.

Enhanced serum interferon-lambda 1/interleukin-29 levels in patients with psoriasis vulgaris

BackgroundInterferon (IFN)-λ1, also named Interleukin (IL)-29, is a new member of the Type III IFN or IFN-λ family. IL-29 plays an important role in the pathogenesis of many types of autoimmune and inflammatory diseases. ObjectiveTo study the role of IL-29 in the pathogenesis of psoriasis vulgaris. MethodsThe authors detected the serum levels of IL-29 in forty-one patients with psoriasis vulgaris, twenty-three patients with atopic dermatitis and thirty-eight age and gender-matched controls by sandwich Enzyme-Linked Immunosorbent Assay (ELISA). The effects of IL-29 on the expression of cytokines, such as IL-6, IL-17, IL-8, IL-4, IL10, Interferon (IFN-γ) and Tumor Necrosis Factor-α (TNF-α), in PBMCs and HaCat cells were determined by real-time quantitative PCR. ResultsOur data indicated that serum IL-29 levels were significantly elevated in patients with psoriasis vulgaris when compared with atopic dermatitis patients and the control group. Moreover, Serum levels of IL-29 were closely associated with the severity of psoriasis vulgaris. Furthermore, IL-29 up-regulated the mRNA expression levels of IL-6, IL-17 and TNF-α in PBMCs from psoriasis vulgaris patients. In addition, IL-29 enhanced the IL-6 and IL-8 expression from the HaCat cells. ConclusionThis study provides the first observations on the association of IL-29 and psoriasis vulgaris and showed elevated IL-29 serum levels. The authors suggest that IL-29 may play a role in the pathogenesis of psoriasis vulgaris.

Supraphysiological estradiol promotes human T follicular helper cell differentiation and favours humoural immunity during in vitro fertilization.

During pregnancy, humoural immunity is essential for protection against many extracellular pathogens; however, autoimmune diseases may be induced or aggravated. T follicular helper (Tfh) cells contribute to humoural immunity. The aim of this study was to test whether Tfh cell function can be manipulated via hormones. Seventy‐four women who underwent in vitro fertilization were recruited and divided into four groups: menstrual period (MP), controlled ovarian hyperstimulation (COH), embryo transfer (ET) and pregnant after embryo transfer (P). A flow cytometry analysis was performed to identify Tfh cells in peripheral blood mononuclear cells (PBMCs). Bioinformatics analysis revealed a possible pathway between Tfh and B cells. Enzyme‐linked immunosorbent assays were used to detect interleukin (IL)‐21 and IL‐6. The quantitative polymerase chain reaction was performed to quantify BCL‐6, BACH2, XBP‐1, IRF‐4 and G protein‐coupled (GP)ER‐1 mRNA expression. Compared with the MP group, the COH, ET and P groups showed more Tfh and B cells, as well as higher IL‐21, IL‐6, BCL‐6 and BACH2 expression. Furthermore, Tfh cell frequency in PBMCs, as well as serum IL‐21 and IL‐6 levels, were all positively correlated with serum estradiol (E2) levels; the B cell percentage also correlated positively with Tfh cells in PBMCs. Combined with the bioinformatics analysis, XBP‐1, IRF‐4 and GPER‐1 expression was related to E2 levels, both in vivo and in vitro. We speculate that E2 augments Tfh cells and favours humoural immunity. This study indicates that Tfh cell regulation may be a novel target in maintaining the maternal‐foetal immune balance.

Decreased Levels of Serum IL-34 Associated with Cognitive Impairment in Vascular Dementia.

Objective Interleukin- (IL-) 34 is a new type of cytokine with neuroprotective effects discovered in recent years. However, the relationship between IL-34 and vascular dementia (VaD) has not yet been elucidated. The purpose of this study is to determine whether IL-34 is involved in cognitive impairment of VaD. Methods From January 2017 to December 2020, 84 VaD patients and 60 healthy controls who attended Qingpu Branch of Zhongshan Hospital were prospectively included in the study. Once included in the study, demographic features of all research subjects are collected. They include age, gender, education, white blood cells (WBC), neutrophil, lymphocyte, systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose (FBG), triglycerides (TG), and total cholesterol (TC). Meanwhile, the Montreal Cognitive Assessment (MoCA) scale was used to assess the cognitive function of participants. The serum IL-34 level was determined by enzyme-linked immunosorbent assay (ELISA). Results There was no significant difference between the demographic features of VaD patients and healthy controls (p > 0.05). However, the serum IL-34 levels of VaD patients and healthy controls are 27.6 ± 3.9 pg/ml and 41.8 ± 6.0 pg/ml, respectively, and there is a significant statistical difference between them (p < 0.001). The results of bivariate correlation analysis showed that serum IL-34 levels were significantly positively correlated with MoCA scores (r = 0.371, p = 0.023). Further regression analysis showed that IL-34 was still correlated with MoCA after adjusting for demographic features (β = 0.276, p = 0038). Conclusions Serum IL-34 levels in VaD patients were significantly reduced, which may be an independent predictor of cognitive impairment in VaD patients.

POS0433 CAN INTERLEUKIN 33 (IL-33) BE CONSIDERED A VALUABLE BIOMARKER IN THE EARLY STAGES OF SYSTEMIC SCLEROSIS? ANALYSIS OF A MONOCENTRIC COHORT

Background:The ScS approach has changed considerably in recent years especially concerning the very early diagnosis of the disease (VEDOSS) at the time when the patient is still in an undifferentiated form (UCTD) at risk of developing SSc (1, 2). Of great value are different clinical, instrumental and laboratory findings, such as specific autoantibodies and Nailfold VideoCapillaroscopy (NVC), able to identify those cases progressing into overt SSc. IL-33 cytokine is known to exert pro-fibrotic effects through its membrane receptor ST2 on immune cells and myofibroblasts and recent studies suggest that it can be released following endothelial cell activation at the onset of SSc (3, 4).Objectives:Our aim has been to evaluate IL-33 serum levels in a monocentric cohort of VEDOSS patients, looking for the possible association with clinical phenotype and disease progression, focusing on the microvascular capillaroscopic changes.Methods:Fourty-seven VEDOSS patients underwent a complete clinical, instrumental and laboratory evaluation, including NVC and specific SSc autoantibodies. At baseline serum IL-33 levels were measured using an ELISA assay. In 32 of them we also had a second serum sample at a follow-up time of at least 24 months (range 24 to 96 months).Results:During the follow-up time, 17 patients were subsequently reclassified as having ScS whereas 30 remained VEDOSS. The “progressor” subjects positively correlated with the presence of anti-Topoisomerase I antibodies (p&gt;0,004). IL-33 concentrations had a median value of 427.2 pg/ml (IQR 967.9 pg/ml) at baseline and of 130.4 pg/ml (IQR 399 pg/ml) at the follow up, showing a statistically significant difference independently from the progression of the disease (p=0.03). Besides significantly higher levels were detected in those patients with more severe NVC changes, defined as “active” pattern (p&lt;0.05). Among the 47 VEDOSS patients, 12 started some kind of vascular therapy. In these patients serum IL-33 concentrations significantly lowered during the follow-up respect to those without any treatment (p&lt;0.03)Conclusion:The analysis of our data confirms previous report (5) on higher IL-33 serum levels in the very early stages of UCTD patients at risk for SSc, regardless of their progression in established SSc, although related to more severe microvascular NVC involvement. The lowering of IL-33 serum levels that we detected in the follow up of our patients, may be linked to the well-known endothelial changes during the progression of the SSc and seems also to be partially affected by treatments. Investigation on a greater number of patients are needed to better understand our findings.