OBJECTIVE:This study aimed to evaluate the relationship between interleukin (IL)-38, IL-41, and allergic rhinitis (AR). METHODS:Forty outpatients with AR and 40 healthy controls (HC) were recruited. Data such as the sex and age of the participants were collected. IgE levels were detected and 15 allergens were tested in patients with AR. Blood was collected from the participants and serum IL-38, IL-41, IL-17 and IgE levels were measured using an enzyme-linked immunosorbent assay. RESULTS:Serum IL-38 and IL-41 levels in patients with AR were significantly lower than in HC (both P < .05), and serum levels of IL-17 and IgE in patients with AR were significantly higher than in HC (P < .0001 and P < .05). The levels of IL-38 and IL-41 levels in AR patients were significantly negatively correlated with IL-17 levels (r = -0.4813, P = .0017 and r = -0.4385, P = .0047, respectively); however, there was no significant correlation with IgE levels (r = -0.02976, P = .8554 and r = -0.1688, P = .2977, respectively). According to the analysis of the receiver operating characteristic curve, the area under the curve (AUC) for IL-38 was 0.6544 (P = .0175), and the AUC for IL-38 and IL-41 combined with IL-17 were 0.7919 (P < .0001) and 0.7585 (P < .0001), respectively. CONCLUSIONS:The decreased serum levels of IL-38 and IL-41 in outpatients with AR suggest that IL-38 and IL-41 may serve as potential indicators for the diagnosis of AR.

Interleukin (IL)-41, a newly identified cytokine also categorized as an adipokine, was previously known by several names, including Metrnl, Cometin, and Subfatin. IL-41 is ubiquitously expressed throughout the body, with particularly high concentrations in the skin, mucosa, and white adipose tissue. This review consolidates current knowledge on IL-41, emphasizing its dual roles in metabolic regulation, such as glucose homeostasis and adipose tissue browning, as well as immune modulation. Evidence suggests its protective functions in various contexts, including inflammatory injuries, allergic diseases, and cardiometabolic disorders. We examine its potential signaling pathways and associations with diverse diseases, and outline unresolved questions and future research directions. The collective findings highlight the significant potential of IL-41 as a novel biomarker and therapeutic target for inflammation and immune-related diseases.

BackgroundCutaneous warts are common HPV-induced lesions with limited treatments for recalcitrant cases. Fatty-acid metabolism (FAM) maintains epidermal homeostasis, but whether papillomavirus infection actively suppresses FAM programs and whether restoring FAM-related regulators can modulate keratinocyte dysfunction remain unclear.MethodsWe established a murine MmuPV1 wart model and performed bulk RNA-seq. FAM-related DEGs were identified via network analysis and machine learning. Immune infiltration was assessed by CIBERSORT. In vitro validation used HPV16 E6/E7-transfected HaCaT cells.ResultsTranscriptome analysis revealed significant suppression of FAM pathways in wart lesions. Four key FAM-related differentially expressed genes (Nr1h3, Dgat1, Scd1, and Fabp4) were identified from RNA-seq-based bioinformatic analyses and further supported by in vitro E6/E7-related expression assays. In vitro, HPV16 E6/E7 expression reduced these genes in HaCaT keratinocytes. NR1H3 overexpression partially attenuated E6/E7-induced proliferation and differentiation abnormalities, lipid-droplet accumulation, and IL-6/CCL2 secretion, with partial restoration of ABCA1 expression and inhibition of NF-kB activation.ConclusionsPapillomavirus infection is associated with coordinated suppression of FAM-related programs. NR1H3, Dgat1, Scd1, and Fabp4 represent candidate metabolic regulatory nodes; their therapeutic relevance requires further in vivo validation.

BackgroundInterleukin (IL)-38 has been recently identified as an anti-inflammatory cytokine. Polymyositis (PM) and dermatomyositis (DM) are two prevalent clinical inflammatory myopathies. This study aims to investigate the serum concentrations of IL-38 in patients with PM/DM and their association with these conditions.MethodsSerum IL-38 levels were quantified using the enzyme-linked immunosorbent assay method in a cohort of 117 subjects, comprising 77 patients with myositis (8 with PM and 69 with DM) and 40 healthy controls. A comprehensive assessment of preliminary clinical characteristics was conducted for each participant through physical examination and review of medical records. The diagnostic utility of IL-38 in PM/DM was evaluated using the receiver operating characteristic curve.ResultsThe findings revealed that serum IL-38 concentrations were significantly elevated in patients with PM/DM compared to the control group, irrespective of the presence of interstitial lung disease. No significant difference was observed between the PM and DM groups. Furthermore, IL-38 demonstrated a positive correlation with the visual analogue scale, lactate dehydrogenase (LDH), and other inflammatory markers. Finally, IL-38, either independently or in conjunction with LDH, exhibits significant diagnostic potential.ConclusionThe study’s findings reveal that patients with PM/DM who present elevated serum levels of IL-38 also show a positive correlation with LDH levels. This suggests IL-38 may participate in modulating inflammatory immune responses in PM/DM and could serve as a potential candidate indicator for these conditions.

Background Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic lung disease that has increasingly been associated with dysregulated mitochondrial quality control and dynamics. However, the molecular mechanisms underlying these alterations remain incompletely understood. This study aimed to systematically identify and validate candidate biomarkers related to mitochondrial dynamics in IPF and to characterize their cell-type specificity and putative regulatory relationships. Methods We integrated bulk transcriptomic datasets from the Gene Expression Omnibus (GEO), single-cell RNA sequencing (scRNA-seq) data, and literature-derived mitochondrial dynamics gene sets. Candidate genes were identified through differential expression analysis and consensus clustering, followed by functional enrichment and protein-protein interaction (PPI) network analyses. A total of 101 machine-learning model combinations-including random forest, LASSO, and support vector machine-were constructed to select optimal feature genes. Diagnostic performance was assessed using receiver operating characteristic (ROC) analysis and further evaluated with artificial neural network (ANN) modeling. Additional analyses included chromosomal localization, immune infiltration profiling, multilayer regulatory network construction (transcription factors, lncRNAs, circRNAs), molecular docking prediction, and single-cell expression and pseudotime trajectory analysis. Key biomarkers were further evaluated by RT-qPCR in an independent clinical cohort. Results Integrated multi-omics and machine-learning analyses identified CD247, IL7R, and RETN as candidate biomarkers related to mitochondrial dynamics-associated pathways in IPF. Across independent transcriptomic datasets, RETN was upregulated, whereas CD247 and IL7R were downregulated, and each showed diagnostic value (single-gene AUC > 0.7). The ANN model based on these genes achieved encouraging discriminative performance (training AUC = 0.91; validation AUC = 0.82), and expression differences were confirmed by RT-qPCR in a modest independent cohort. Enrichment analyses indicated convergence on spliceosome-related pathways, and regulatory-network analysis highlighted interactions involving transcription factors and non-coding RNAs, including circRNA CDR1as. Molecular docking suggested putative interactions with selected compounds. Single-cell analyses suggested that dysregulation was most evident in monocyte-associated compartments in one publicly available scRNA-seq dataset, and pseudotime analysis indicated dynamic expression patterns, with early transient increases in CD247 and IL7R and progressive elevation of RETN. Conclusion Through multi-omics integration and machine-learning approaches, we identified and preliminarily validated CD247, IL7R, and RETN as candidate biomarkers related to mitochondrial dynamics-associated pathways in IPF. These findings provide transcriptomic and cell-type-specific evidence suggesting potential immune-mitochondrial associations in IPF and may inform future biomarker validation and mechanistic hypothesis generation.

Background Interleukin (IL)-41 is a novel cytokine, also known as Metrnl, and its role in ankylosing spondylitis (AS) remains unknown. The aim of this study is to measure the serum IL-41 levels in AS patients and their correlation with other clinical indicators.Methods This study recruited 106 participants, including 32 active AS patients, 32 inactive AS patients, and 42 healthy controls (HC). Basic information and clinical indicators of participants were obtained through physical examination and blood sample testing. Enzyme-linked immunosorbent assay was used to detect IL-41 levels.Results Patients with active and inactive AS had significantly higher serum IL-41 levels than HC. Moreover, correlation analysis showed that IL-41 in active AS was positively correlated with lymphocyte percentage; IL-41 in inactivated AS is negatively correlated with alkaline phosphatase and creatinine. IL-41 as an independent protective factor for AS had good value for the diagnosis of AS.Conclusion This study indicates that serum IL-41 levels are elevated in both active and inactive AS patients, suggesting that IL-41 may be a novel biomarker for AS.

Background Ankylosing spondylitis (AS) is a chronic autoimmune disease that primarily affects the axial joints. Immune cells play a key role in the pathogenesis of AS. This study integrated bioinformatics methods with experimental validation to explore the role of natural killer (NK) cells in AS.Methods Two microarray datasets, GSE25101 and GSE73754, were selected, and the scRNA-seq data were obtained from GSE194315 and Liu’s research. Differentially expressed genes (DEGs) and functional enrichment analysis were performed respectively. Weighted gene co-expression network analysis (WGCNA) was conducted to identify key modules of co-expressed genes and genes involved in NK cell function. The diagnostic value of the identified key genes was evaluated using ROC curves, logistic regression analysis, and a nomogram. Real-time PCR (RT-PCR) was used to quantified the expression of genes. Statistical analysis was conducted using the R software package, and a p-value of less than 0.05 was considered statistically significant.Results Pathways enrichment analysis revealed the involvement of NK cell-mediated immune pathways and regulation of the innate immune response, indicating the crucial role of innate immunity, especially NK cells, in AS pathogenesis. The construction of a co-expression network revealed that the MElightyellow module was most relevant to the NK cell-mediated immune pathway. IL2RB, CD247, PLEKHF1, EOMES, S1PR5, FGFBP2 from the MElightyellow module were identified as key genes involved in NK cell-mediated immune response and served as potential diagnostic biomarkers for AS, with moderate to high diagnostic values based on AUC values. Further analysis using scRNA-seq profiling revealed the higher expression level of IL2RB, CD247, PLEKHF1, S1PR5, FGFBP2 in NK cells compared to that in other cell types. CD247, PLEKHF1, EOMES, S1PR5, and FGFBP2 were reduced expressed in AS patients as compare to control group verified by scRNA-seq data, CD247, EOMES, FGFBP2, IL2RB and S1PR5 were reduced expressed verified by RT-PCR, and PLEKHF1, S1PR5, and FGFBP2 was upregulated after TNF-α blocker therapy.Conclusion The study revealed the potential role of NK cells and identified IL2RB, CD247, PLEKHF1, EOMES, S1PR5, and FGFBP2 as key genes associated with NK cells in the pathogenesis of AS.

BACKGROUND:Polymyositis (PM) and dermatomyositis (DM) are two common subtypes of idiopathic inflammatory myopathies (IIM). The concentration of serum interleukin (IL)-41 in patients with PM/DM has not been reported. This study aims to investigate the levels of IL-41 in the serum of individuals diagnosed with PM/DM. METHODS:A total of 118 participants were enrolled in the study, comprising 80 patients with PM/DM and 38 healthy controls (HC). Comprehensive clinical data for each participant were collected through physical examinations and detailed clinical histories. The levels of IL-41 were quantified using the enzyme-linked immunosorbent assay (ELISA). Spearman's correlation analysis was employed to examine the relationship between IL-41 levels and various clinical parameters. The diagnostic potential of IL-41 was assessed using the receiver operating characteristic (ROC) curve. RESULTS:Serum IL-41 levels were significantly elevated in PM/DM patients with interstitial lung disease (ILD) compared to HC [1001.03 (572.95, 1604.83) pg/mL vs 361.03 (302.24, 541.06) pg/mL, P < 0.0001]. Furthermore, a significant difference was also observed in serum IL-41 levels between PM/DM patients without ILD and HC [561.81 (407.94, 827.34) pg/mL vs 361.03 (302.24, 541.06) pg/mL, P = 0.0139]. IL-41 exhibits substantial diagnostic potential for PM/DM, and its combination with lactate dehydrogenase enhances diagnostic efficacy. Moreover, IL-41 acts as an independent risk factor for the onset of PM/DM. CONCLUSIONS:This study revealed that serum IL-41 levels are elevated in patients with PM/DM, suggesting that IL-41 could serve as a novel biomarker for the identification of these conditions.

OBJECTIVE:The aim was to investigate the mediating role of inflammatory biomarkers in the causal effect of body composition on glycaemic traits and type 2 diabetes. METHODS:A retrospective observational study and a Mendelian randomization (MR) study were used. Observational analyses were performed using data from 4717 Chinese children and adolescents aged 6-18 years who underwent dual-energy X-ray absorptiometry for body composition. MR analyses were based on summary statistics from UK Biobank, deCODE2021, Meta-Analysis of Glucose and Insulin-Related Traits Consortium (MAGIC) and other large consortiums. Inflammatory biomarkers included leptin, adiponectin, osteocalcin, fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH). RESULTS:In a retrospective observational study, increased fat mass had a positive effect on homeostasis model assessment of insulin resistance (HOMA-IR) and homeostasis model assessment of pancreatic beta cell function (HOMA-β) through FGF23, whereas fat-free mass produced the opposite effects. PTH and osteocalcin played significant roles in the association of fat mass and fat-free mass with fasting glucose, fasting insulin and HOMA-IR (all p < 0.05). Mediation MR results indicated that childhood body mass index affected glycaemic traits through leptin and adiponectin. There existed a causal effect of fat-free mass on type 2 diabetes via FGF23 (indirect effect: OR [odds ratio]: 1.14 [95% CI, confidence interval: 1.01-1.28]) and adiponectin (OR: 0.85 [95% CI: 0.77-0.93]). Leptin mediated the causal association of fat mass (indirect effect: β: -0.05 [95% CI: -0.07, -0.02]) and fat-free mass (β: 0.03 [95% CI: 0.01, 0.04]) with fasting glucose. CONCLUSIONS:Our findings suggest that different body compositions have differential influences on glycaemic traits and type 2 diabetes through distinct inflammatory biomarkers. The findings may be helpful in tailoring management of body composition based on inflammatory biomarkers with different glycaemic statuses.

Background: Gout is a chronic inflammatory diseases caused by monosodium urate crystal deposition. However, the role of interleukin (IL)-36 in gout has not dbeen elucidated. Methods: We enrolled 75 subjects, including 20 healthy controls (HC), 30 patients with acute gout attack and 25 patients in remission. Baseline data were obtained through clinical interrogation and laboratory data were obtained through tests of blood samples. Serum levels of IL-36 alpha were detected using enzyme-linked immunosorbent assay. Spearman correlation analysis was used to investigate the correlation of IL-36 alpha with other parameters. The diagnostic value of IL-36 alpha was demonstrated using a receiver operating characteristic curve. Results: The serum IL-36 alpha level of gout patients in acute attack and remission stage was significantly higher than that of HC. Serum IL-36 alpha was positively correlated with alanine transaminase (ALT) and aspartate transaminase (AST). Serum amyloid A (SAA) levels positively correlated with C-reactive protein levels and erythrocyte sedimentation rates. Glutamyl transpeptidase levels positively correlated with AST and ALT levels. Conclusion: In conclusion, serum IL-36 alpha levels were elevated in patients with gout and correlated with the clinical markers of inflammation. Our findings suggest that IL-36 alpha may be a novel inflammatory indicator for gout.

Objective: Factors influencing chronic rhinosinusitis (CRS) are usually studied in terms of genetics and environment; however, clinical indicators have not been reported. This case-control study was conducted in Ningbo, China, to explore new independent risk factors for CRS. Methods: A total of 695 participants, including 440 healthy controls and 255 patients with CRS, were included in this study. Clinical data were retrieved from questionnaires and electronic medical record systems of hospitals. Independent risk factors were screened using logistic regression and 10-fold cross-validation combined with the least absolute shrinkage and selection operator. A CRS risk prediction model was established using logistic regression, and nomograms were visualized. The model was validated and evaluated using receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA). Results: Ten independent risk factors, including alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, creatinine, triglyceride, total cholesterol, red blood cell count, hemoglobin, lymphocyte percentage, and monocyte percentage were screened. ROC analysis showed that the area under the curve of the training set was 0.890, indicating that the predictive model had excellent discriminant ability. The calibration curves showed that the fitting curves of the training set were close to the reference curves, indicating that the model had a good fit. The DCA showed that the threshold probability range of the training set was 1% to 89%. Conclusions: Independent risk factors for CRS were screened, and a prediction model was constructed, which is of significance for the prevention, control, and treatment of the disease.

BackgroundInterleukin (IL)-38 is a newly discovered anti-inflammatory cytokine. However, its concentration and clinical significance in patients with gout remain unclear. This study aimed to investigate the levels of IL-38 in patients with gout and evaluate their clinical significance.MethodsThirty-two patients with active gout, 27 patients with inactive gout, and 20 negative controls (NCs) were included in the study. Clinical parameters, including white blood cell count, C-reactive protein, serum amyloid A, erythrocyte sedimentation rate, uric acid, urea, creatinine, alanine aminotransferase, aspartate aminotransferase, glutamyl transpeptidase, and glycoserated serum protein, were obtained from laboratory tests of blood samples. The serum concentration of IL-38 was determined using enzyme-linked immunosorbent assay. Spearman’s correlation analysis and receiver operating characteristic curve assessments were used to investigate the role and diagnostic value of IL-38 in gout.ResultsPatients with active and inactive gout exhibited significantly lower serum IL-38 levels than NCs. No significant differences were observed between the two gout groups. A negative correlation was observed between IL-38 and white blood cell counts, whereas a positive correlation was found between IL-38 and creatinine levels. Furthermore, IL-38, either alone or in combination with uric acid, demonstrated substantial diagnostic potential.ConclusionThe findings suggest that the decreased serum levels of IL-38 in patients with gout compared to that in NCs indicates that IL-38 may have immunomodulatory effects on gout inflammation and possesses clinical application value.

BACKGROUND:Interleukin (IL)-41 is upregulated in the synovial tissue of rheumatoid arthritis (RA) patients, but its serum level has not been reported. The present study aimed to determine IL-41 expression in serum from RA patients and to clarify the relationships between IL-41 and disease-related parameters in RA patients.METHODS:The study included 46 RA patients and 32 healthy controls (HC). Baseline data were obtained by routine physical examinations and immune-related parameters were measured by an automated chemiluminescent immunoassay analyzer. The correlations between IL-41 and disease activity score in 28 joints (DAS28) and serum clinical data were analyzed using the Pearson correlation test.RESULTS:Serum IL-41 concentrations were higher in RA patients than in HC. Serum IL-41 was positively correlated with DAS28 based on C-reactive protein (DAS28-CRP), CRP, erythrocyte sedimentation rate (ESR), mean platelet volume (MPV), and CRP-to-albumin ratio (CAR) and negatively correlated with platelet count, while rheumatoid factor was significantly correlated with ESR, CRP, and CAR. Receiver operating characteristic curve analysis showed that IL-41 had diagnostic value for RA, especially when combined with MPV.CONCLUSIONS:The present findings suggest that IL-41 is increased in the serum of RA patients and may be a potential new diagnostic biomarker for RA.

Background: Imbalances in cytokine networks have been shown to be a possible cause of rheumatoid arthritis (RA). The interleukin (IL)-12 family is involved in the pathogenesis of autoimmune diseases including RA, while IL-39 is a newly discovered member of the IL-12 family, although its role in RA remains unclear. The purpose of the present study was to detect the expression of IL-39 in the sera of patients with RA and its relationship with RA activity.Methods: We recruited 46 patients with RA and 35 healthy controls at Ningbo Sixth Hospital. Blood samples were collected for biochemical analysis, and disease activity scores of 28 joints based on C-reactive protein were monitored. Serum concentrations of IL-39 were determined using an enzyme-linked immunosorbent assay. The Pearson correlation test was used to analyze the association between serum IL-39 levels and clinical indicators.Results: Serum levels of IL-39 were significantly higher in patients with RA compared with healthy controls (p < 0.0001). IL-39 levels positively correlated with rheumatoid factor (RF), erythrocyte sedimentation rate (ESR), and IgM; RF positively correlated with ESR. Receiver operating characteristic curve analysis showed that IL-39 has diagnostic value for RA (p < 0.0001).Conclusions: The significant increase of IL-39 levels in serum of patients with RA and its positive correlation with clinical indicators suggest that IL-39 may serve as biomarker for the diagnosis of RA.

Background: Interleukin (IL)-41 is a recently discovered secreted protein that is expressed in a variety of tissues, and it is associated with several immune and metabolic diseases. However, IL-41 has not been studied in hyperuricemia (HUA). Methods: Forty-four HUA patients and 44 healthy controls (HCs) were included in this study, and we collected theirgeneral and biochemical parameters, including white blood cell, neutrophil, lymphocyte, and platelet counts, mean platelet volume, platelet distribution width, serum creatinine, blood urea nitrogen, fasting blood glucose, total triglyceride, total cholesterol, high-density lipoprotein, low-density lipoprotein, total protein, albumin, alkaline phosphatase, gamma-glutamyltransferase, and hemoglobin concentration. The level of serum IL41 was determined using an enzyme-linked immunosorbent assay. Multivariate logistic regression analysis was exploited to identify the independent risk factors associated with HUA, and the clinical diagnostic value of IL-41 was analyzed by applying the receiver operating characteristic (ROC) curve. We assessed the association between IL-41 and clinical parameters with Spearman's rank correlation. Results: Circulating IL-41 levels were significantly higher in HUA patients than in the HCs group (460.3 pg/mL vs. 261.3 pg/mL, respectively; P < 0.001). The area under the ROC curve (AUC) for IL-41 in HUA patients was 0.7443 (with a cut-off value of 311.055 pg/mL, a sensitivity of 68.18 %, and a specificity of 72.73 %), while the AUC for IL-41 combined with the platelet count was 0.8109. Correlation analysis revealed that the circulating IL41 level was positively correlated with age in HCs and HUA patients. Conclusions: We herein demonstrated that serum IL-41 was elevated in HUA patients and that it may constitute a novel biomarker of anti-inflammatory response related to HUA.

白细胞介素(IL)-36家族包括IL-36α,IL-36β,IL-36γ及IL-36受体拮抗剂(IL-36Ra).这些细胞因子通过促进感染的消退或与其受体复合物结合而促进炎症反应,从而在固有免疫和适应性免疫中起重要作用.在体内平衡稳态下,这些细胞因子和受体的表达及活性受到良好的调节;相反,不受约束的表达或不受控制的激活可以引发或增强病理性炎症反应.有研究表明在皮肤与关节相关炎症发生期间,靶向IL-36有着潜在的治疗价值.本文重点综述IL-36细胞因子在皮肤和关节相关的3种代表性炎症疾病—银屑病、银屑病关节炎(PsA)和类风湿关节炎(RA)中的作用,并探讨它们作为银屑病、PsA和RA新型靶标的治疗潜力.

Ankylosing spondylitis (AS) is a chronic autoimmune disease. The purpose of this study was to investigate the levels of serum IL-36γ in AS patients and their association with AS. The study enrolled 131 subjects, including 45 with active AS, 46 with inactive AS, and 40 healthy controls (HCs). The basic clinical information of each participant was obtained through physical examination and relevant clinical medical records. Serum IL-36γ levels were detected through an enzyme-linked immunosorbent assay. Serum IL-36γ levels in the active AS group were significantly higher than those in the HC group (94.72 vs. 65.76 pg/mL, P = 0.0087). The serum IL-36γ concentration in the inactive AS group was increased as compared to that in the HC group (100.90 vs. 65.76 pg/mL, P = 0.0138). Correlation analysis indicated that serum IL-36γ was positively correlated with glutamyl transferase in the active AS group (P = 0.0172), while serum IL-36γ was positively correlated with uric acid in the inactive AS group (P = 0.0151). The area under the curve (AUC) for IL-36γ was 0.6824 (P = 0.0009), and the AUC for IL-36γ combined with the erythrocyte sedimentation rate and C-reactive protein levels was 0.8102 (P < 0.0001), according to receiver operating characteristic curve analysis. This study found that serum IL-36γ levels were elevated in AS patients and correlated with disease activity. Our results suggest that IL-36γ may be involved in the progression of AS disease and is a potential biomarker for AS.

BACKGROUND:Interleukin (IL)-38 and IL-41 are novel cytokines, but their role in male infertility (MI) is unknown. The purpose of this study was to measure the levels of serum IL-38 and IL-41 in patients with MI and correlate these levels with semen indexes. METHODS:Eighty-two patients with MI and 45 healthy controls (HC) were recruited for this study. Semen parameters were detected using computer-aided sperm analysis, Papanicolaou staining, ELISA, flow cytometry, peroxidase staining and enzyme methods. Serum IL-38 and IL-41 levels were determined by ELISA. RESULTS:Serum IL-38 levels were decreased (P < 0.01) in patients with MI compared with HC. Serum IL-41 levels were significantly higher in patients with MI than in HC (P < 0.0001). In patients with MI, serum IL-38 levels were positively correlated with semen white blood cell counts (r = 0.29, P = 0.009), and there was a positive correlation between semen white blood cell counts and sperm concentration (r = 0.28, P = 0.0100) and seminal plasma elastase (r = 0.67, P < 0.0001). Receiver operating characteristic curve analysis showed that the area under the curve of IL-38 for diagnosing MI was 0.5637 (P > 0.05), and the area under the curve of IL-41 for diagnosing MI was 0.7646 (P < 0.0001). CONCLUSIONS:Serum IL-38 levels were significantly lower, and serum IL-41 levels were higher in patients with MI. These results suggest that IL-38 and IL-41 may be novel biomarkers for the diagnosis of MI.

Introduction: Kawasaki disease (KD) is a systemic vasculitis that causes abnormalities in the coronary arteries. Interleukin (IL)-41 is a novel immunoregulatory cytokine involved in the pathogenesis of some inflammatory and immune-related diseases. However, the role of IL-41 in KD is unclear. The purpose of this study was to detect the expression of IL-41 in the plasma of children with KD and its relationship with the disease.Methods: A total of 44 children with KD and 37 healthy controls (HC) were recruited for this study. Plasma concentrations of IL-41 were determined by ELISA. Correlations between plasma IL-41 levels and KD-related clinical parameters were analyzed by Pearson correlation and multivariate linear regression analysis. Receiver operating characteristic curve analysis was used to assess the clinical value of IL-41 in the diagnosis of KD.Results: Our results showed that plasma IL-41 levels were significantly elevated in children with KD compared with HC. Correlation analysis demonstrated that IL-41 levels were positively correlated with D-dimer and N -terminal pro-B-type natriuretic peptide, and negatively correlated with IgM, mean corpuscular hemoglobin concentration, total protein, albumin and pre-albumin. Multivariable linear regression analysis revealed that IgM and mean corpuscular hemoglobin concentrations were associated with IL-41. Receiver operating characteristic curve analysis showed that the area under the curve of IL-41 was 0.7101, with IL-41 providing 88.64 % sensi-tivity and 54.05 % specificity.Conclusion: Our study indicated that plasma IL-41 levels in children with KD were significantly higher than those in HC, and may provide a potential diagnostic biomarker for KD.

BACKGROUND:Gout is a common metabolic rheumatic disease, and there have been no reports on the serum levels of interleukin (IL)-41 in gout patients. The purpose of this study was to therefore determine the expression of IL-41 in the serum of gout patients.METHODS:Eighty-one participants were enrolled in this study, including 34 patients with acute gout, 27 gout patients in remission, and 20 healthy controls (HCs). Baseline data were obtained through interviews and laboratory parameters were acquired via blood sample testing. We measured serum IL-41 concentrations with an enzyme-linked immunosorbent assay, and executed Spearman's correlation analysis to investigate the correlation between IL-41 and other parameters, and the diagnostic value for IL-41 was demonstrated using a receiver operating characteristic curve. Multivariate analysis was conducted by adopting logistic regression.RESULTS:Serum IL-41 concentrations in acute-gout patients were higher than those in HCs and there was no significant difference in serum IL-41 levels between remission gout patients and HCs. In addition, IL-41 was positively correlated with white blood cell count, erythrocyte sedimentation rate, and C-reactive protein and serum amyloid A concentrations, while it was negatively correlated with triglyceride levels. IL-41 showed good diagnostic value for gout, and the combination of IL-41 and uric acid produced a superior diagnostic value. We also noted that IL-41 was an independent risk factor for acute gout.CONCLUSIONS:This study revealed that serum IL-41 was elevated in patients with acute gout, and suggests that IL-41 may constitute a novel diagnostic marker for acute gout.