Cytokine最新文献

{"title":"A novel genetic association of IL32 with tuberculosis","authors":"Anuradha Gautam ,&nbsp;Chandrika Bhattacharyya ,&nbsp;Ahana Dasgupta ,&nbsp;Samsiddhi Bhattacharjee ,&nbsp;Bhaswati Pandit","doi":"10.1016/j.cyto.2024.156783","DOIUrl":"10.1016/j.cyto.2024.156783","url":null,"abstract":"<div><h3>Aim</h3><div>IL32 is a pleiotropic intracellular cytokine with an emergent role in tuberculosis. The different isoforms of IL32: α, β, γ and δ have varying pro and anti-inflammatory potentials. We studied the role of genetic variants of <em>IL32</em> and its isoforms in susceptibility to tuberculosis using a case-household contact association study.</div></div><div><h3>Methodology</h3><div>Using a targeted sequencing approach, <em>IL32</em> (+1kb) gene was sequenced in 64 pairs of culture positive TB cases and their culture negative household contacts. Subsequently the identified variants were validated in an independent cohort of cases and household contacts using TaqMan genotyping assay. Regulatory role of the associated variants was assessed using GTExPortal, RegulomeDB score, HaploReg and ENCODE histone ChIP-seq data. Expression of IL32 and its isoforms was evaluated by RT-PCR in PBMC from unexposed healthy controls (N = 25) with different genotype background and stimulated with TB antigens ESAT6 and CFP10. ∼ 200 bp around the associated variant was cloned into pGL3 promoter vector to assess enhancer activity by dual luciferase assay in cell lines.</div></div><div><h3>Results</h3><div>Intronic variant rs9927163(G/T) was found associated with pulmonary TB, T being the risk allele (OR = 2.3(1.40–3.83, p = 0.03)), while G is the protective allele. This finding was validated in independent set of TB cases and household contacts (p = 0.0435). rs9927163 is an eQTL for the genes <em>IL32</em> (p = 4.1e-10) and <em>BICDL2</em> (p = 2.1e-7) in whole blood and interrupts an AP-1 binding site. ENCODE histone ChIP-seq data shows rs9927163 residing within T cell specific H3K4me3 peak. The G allele is associated with greater enhancer activity in a T cell line (2.12 fold, p = 0.0059). The TT genotype showed greater normalized expression of IL32δ, a less proinflammatory isoform compared to the GT and GG genotypes together following ESAT6 (p = 0.02288) and CFP10 (p = 0.04595) treatment. This indicates that greater expression of a potentially less protective IL32 isoform within individuals with the TT genotype might be a risk factor for developing TB.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156783"},"PeriodicalIF":3.7,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal relationship between circulating inflammatory proteins and risk of different types of encephalitis: A two-sample Mendelian randomization study","authors":"Shiqiang Yang ,&nbsp;Yanwei Liu ,&nbsp;Shiqiang Wang ,&nbsp;Hua Peng ,&nbsp;Xuhui Hui ,&nbsp;Anqiang Yang","doi":"10.1016/j.cyto.2024.156789","DOIUrl":"10.1016/j.cyto.2024.156789","url":null,"abstract":"<div><h3>Background</h3><div>Cytokines are potent molecules of the immune response. They act at the site of inflammation and circulate in the bloodstream. However, there are few studies on encephalitis and circulating inflammatory proteins.</div></div><div><h3>Methods</h3><div>In this study, Mendelian randomization (MR) was used to explore the potential causal effect of 91 circulating inflammatory proteins on 3 different types of encephalitis. Causal effects were examined using Steiger, MR-Egger, weighted median, and inverse variance weighting (IVW) methods. IVW methods were primarily used for results interpretation. In addition, sensitivity analyses were performed, including assessment of heterogeneity, horizontal pleiotropy, and Leave-one-out techniques.</div></div><div><h3>Results</h3><div>We subjected 91 circulating inflammatory proteins to MR analysis of causality with each of the three types of encephalitis. The results suggested that the inflammatory factors with a potential causal relationship with viral encephalitis were caspase 8, C-X-C motif chemokine 6, interleukin-10, interleukin-15 receptor subunit alpha, interleukin-7, and TNF-beta. Inflammatory factors potentially causally associated with acute disseminated encephalomyelitis are beta-nerve growth factor, cystatin D, interleukin-7,</div><div>Latency-associated peptide transforming growth factor beta 1,and neurotrophin-3.Inflammatory factors potentially causally associated with autoimmune encephalitis are C–C motif chemokine 25, hepatocyte growth factor, latency-associated peptide transforming growth factor beta 1, programmed cell death 1 ligand 1, sulfotransferase 1A1, and tumor necrosis factor.</div></div><div><h3>Conclusion</h3><div>This finding identifies potential causal effects of certain circulating inflammatory factors on susceptibility to three types of encephalitis. It also suggests the therapeutic potential of modulating the levels of these cytokines. A basis for further research is provided.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156789"},"PeriodicalIF":3.7,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic insights into the causal linkage between systemic inflammatory regulators and frailty","authors":"Xingzhi Guo ,&nbsp;Rong Zhou ,&nbsp;Ge Tian ,&nbsp;Wenzhi Shi ,&nbsp;JuanJuan Lu ,&nbsp;Rui Li","doi":"10.1016/j.cyto.2024.156791","DOIUrl":"10.1016/j.cyto.2024.156791","url":null,"abstract":"<div><h3>Objectives</h3><div>Previous studies have suggested the associations between systemic inflammation and the risk of frailty, but causal relationships between them remain not well established. We conducted a bi-directional Mendelian randomization (MR) analysis to investigate the causal links between systemic inflammatory regulators and frailty.</div></div><div><h3>Methods</h3><div>Genetic variants associated with systemic inflammatory regulators were obtained from a comprehensive genetic study on 41 circulating cytokines, such as interleukin-4 (IL-4), eotaxin, and macrophage inflammatory protein-1β (MIP1β). We integrated summary-level data on frailty from two independent genetic studies on frailty index (FI) and Fried frailty score (FFS). The inverse-variance weighted method was used to assess the causal estimate. Sensitivity and heterogeneity analysis was performed to evaluate the stability of the estimates. The false discovery rate (FDR) method was used for P value adjustment of multiple comparisons.</div></div><div><h3>Results</h3><div>Genetically elevated levels of MIP1β and decreased levels of eotaxin were suggestively associated with increased FI (MIP1β: β = 0.016, P_raw = 0.006, P_FDR = 0.083; eotaxin: β = -0.030, P_raw = 0.007, P_FDR = 0.083) and FFS (MIP1β: β = 0.008, P_raw = 0.027, P_FDR = 0.247; eotaxin: β = -0.015, P_raw = 0.014, P_FDR = 0.247). In contrast, genetically predicted FI was suggestively associated with decreased levels of IL-4 (β = -0.395, P_raw = 0.040, P_FDR = 0.638) and platelet-derived growth factor BB (PDGF-BB, β = -0.385, P_raw = 0.047, P_FDR = 0.638) and increased levels of stem cell factor (SCF, β = 0.527, P_raw = 0.005, P_FDR = 0.204). Similar results were obtained from different sensitivity analysis.</div></div><div><h3>Conclusions</h3><div>The present study demonstrates that increased MIP-1β levels and decreased eotaxin levels might lead to a higher risk of frailty, whereas frailty might reduce the levels of IL-4 and PDGF-BB and increase the levels of SCF.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156791"},"PeriodicalIF":3.7,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neutrophil-derived IL-10 increases CVB3-induced acute pancreatitis pathology via suppressing CD8+T cell activation while increasing macrophage STAT3-IL-6 cascade","authors":"Yue Yang,&nbsp;Zhirong Sun,&nbsp;Jingrou Li,&nbsp;Yahui Song,&nbsp;Wei Xu","doi":"10.1016/j.cyto.2024.156784","DOIUrl":"10.1016/j.cyto.2024.156784","url":null,"abstract":"<div><div>Acute pancreatitis (AP) is a lethal inflammatory disease of the pancreas. Its pathogenesis remains obscure and specific treatments are lacking. An increase in Interleukin-10 (IL-10) in the early stage of AP patients is closely related to AP severity. In Coxsackievirus B3 (CVB3) induced murine AP model, we found early IL-10 increased viral replication and pancreatic inflammation, yet the cellular source of IL-10 and the immunomodulatory role of neutrophils during viral infection remains unknown. Here we show that CVB3 infection enhanced neutrophil infiltration and IL-10 expression in the pancreas at day3 post infection (p.i.). Neutrophils served as an important early source of pancreatic IL-10 at the initiation of infection. Day3 pancreas extracts (D3P) also induced bone-marrow derived neutrophils (BMneu) to secrete IL-10. Adoptive transfer of D3P-pretreated BMneu into IL-10 KO mice increased viral replication and pancreas histopathology, which effect was blunted by the absence of IL-10 in BMneu. Mechanically, IL-10⁺ neutrophil increased IL-10R1 expression on MΦs and activated STAT3-IL-6/IL-10 signaling cascade while decreased IL-12 and MHC II expression in MΦs, thus impairing IFN-γ⁺Granzyme B⁺CD8⁺T cell activation and viral clearance. Adoptive transferring infected mice with activated CD8⁺T cells 4 days p.i. attenuated viral load and AP pathology indicating an AP-protective effect. Our findings document a novel immunoregulatory function of neutrophils in acute CVB3 infection, in which neutrophil-derived IL-10 impairs anti-viral CD8⁺T activation, and amplifies intrapancreatic inflammation via activating MΦ STAT3-IL-6 signaling cascade. An IL-10-targeting option is suggested for the future treatment of viral AP.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156784"},"PeriodicalIF":3.7,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated serum and cerebrospinal fluid levels of Interleukin-4 related to poor outcome of Aneurysmal subarachnoid hemorrhage","authors":"Xuemei Hu ,&nbsp;Mingyang Zhao ,&nbsp;Meixue Wang ,&nbsp;Dongsen Wang ,&nbsp;Liangzhen Zhu ,&nbsp;Chunhai Su ,&nbsp;Qingjian Wu","doi":"10.1016/j.cyto.2024.156780","DOIUrl":"10.1016/j.cyto.2024.156780","url":null,"abstract":"<div><div>Aneurysmal subarachnoid hemorrhage (aSAH) is a hemorrhagic cerebrovascular disease that seriously jeopardizes human life and health. Some studies have shown that although Interleukin-4 (IL-4) acts as an anti-inflammatory factor, IL-4 levels are elevated when the disease occurs. This study focuses on exploring the relationship between IL and 4 concentrations in the serum and cerebrospinal fluid (CSF) and poor outcome in patients with aSAH. This study was a prospective observational study and 210 aSAH patients who met the inclusion criteria were divided into two groups according to the mRS score at 3 months after discharge, and 210 healthy people were selected as controls. The IL-4 concentrations were quantitatively determined with enzyme-linked adsorption assay (ELISA). We can draw a conclusion that Serum and CSF IL-4 concentrations are generally elevated in patients with poor outcome(<em>P</em> &lt; 0.05), and the CSF IL-4 concentration decreased gradually over the progress of time (<em>P</em> &lt; 0.05). The IL-4 concentration in the CSF was positively correlated with age, platelet-lymphocyte ratio (PLR), C-reactive protein (CRP), Hunt-Hess grade, mRS score, and World Federation of Neurological Surgeons score (WFNS) (<em>P</em> &lt; 0.0001). Additionally, IL-4 concentrations in the CSF were correlated with complications such as intracranial infection (<em>P</em> = 0.01), cerebral edema (<em>P</em> &lt; 0.01), hydrocephalus (<em>P</em> = 0.02), and complications by DCI (<em>P</em> = 0.02). Elevated serum and CSF concentrations of IL-4 may associated with the outcome of aSAH and may be a candidate early biomarkers for outcome of aSAH.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156780"},"PeriodicalIF":3.7,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142454517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammation and thrombotic risk in late-stage cervical cancer: An exploratory study of coagulation and cytokine profiles in a South African cohort","authors":"Louise Fourie ,&nbsp;Claudia Christowitz ,&nbsp;Carla Eksteen ,&nbsp;Haynes van der Merwe ,&nbsp;Hennie Botha ,&nbsp;Chantelle Venter ,&nbsp;Anna-Mart Engelbrecht","doi":"10.1016/j.cyto.2024.156782","DOIUrl":"10.1016/j.cyto.2024.156782","url":null,"abstract":"<div><h3>Purpose</h3><div>This exploratory study investigates the possible relationship between inflammation and thrombosis in cervical cancer patients in South Africa, highlighting the need for improved thrombotic risk profiling.</div></div><div><h3>Methods</h3><div>Thromboelastography (TEG) was used to assess coagulation parameters in platelet-poor plasma (PPP) from a small cohort of late-stage (III and IV) cervical cancer patients (n = 19) and healthy controls (n = 15). Parameters assessed included clotting time, clot formation speed, and clot strength. A Luminex Multiplex assay was used to measure interferon-γ (IFN-γ), interleukin-1β (IL-1β), IL-6, vascular endothelial growth factor-A (VEGF-A), and tumour necrosis factor-α (TNF-α) in PPP. Haematological profiles were also evaluated.</div></div><div><h3>Results</h3><div>Cervical cancer patients displayed a significantly shortened clotting time (<em>p</em> = 0.0044) and increased clot strength (<em>p</em> = 0.0003), suggesting enhanced coagulation. IL-1β was notably elevated (<em>p</em> = 0.0200), consistent with an inflammatory environment. Higher lymphocyte, neutrophil, and platelet counts (<em>p</em> = 0.0162, 0.0420, and 0.0374, respectively) were observed, indicating a possible prothrombotic state.</div></div><div><h3>Conclusion</h3><div>These findings suggest a potential link between inflammation and thrombosis in cervical cancer patients. However, due to this study’s small sample size and exploratory nature, direct relationships between these factors have yet to be definitively established and remain speculative. Thrombotic risk profiling may still offer value in managing patients, but further investigation is required to confirm these preliminary observations.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156782"},"PeriodicalIF":3.7,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142454518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The association of serum level and polymorphisms of IFN-γ (rs2069705) with the susceptibility to cutaneous leishmaniasis","authors":"Ula Farooq Ramzi ,&nbsp;Entsar Jabbar Saheb ,&nbsp;Watheq Muhammed Hussein","doi":"10.1016/j.cyto.2024.156785","DOIUrl":"10.1016/j.cyto.2024.156785","url":null,"abstract":"<div><div>Leishmaniasis, a broad range of parasitic diseases, caused by <em>Leishmania</em> which is a flagellated intracellular protozoan parasite of the family Trypanosomatidae. The severity of leishmaniasis diseases ranges from minor cutaneous lesions to severe visceral illnesses that can be disfiguring and life-threatening. Cytokines are glycoprotein molecules produced by various cells in response to various immunological triggers. They regulate the body’s innate and adaptive immunological responses. The aim of this study was to clarify the association of serum level and polymorphisms of IFN-γ with susceptibility to cutaneous leishmaniasis (CL). The whole blood 200 samples were collected from patients and controls from Diyala Governorate/ Iraq from October 2022 to February 2023 which were used to measure IFN-γ polymorphisms using High Resolution Melting technique. Enzyme-linked immunosorbent assay was used to detect the serum level of IFN-γ. The findings of this investigation showed that the IFN-γ serum concentration elevated significantly in patients compared to controls (P &lt; 0.01). Also, the study found that the highest mean level IFN-γ concentrations were found in adults aged 46–55 years old for patients compared with controls with significant differences (P &lt; 0.01). While, no significant differences were observed in the rest age groups except children aged 5–15 years old. Additionally, significant differences between patients and controls were revealed by polymorphisms data in all genetic models for genotypes GA, AA, (GA + AA) and allele A with (P &lt; 0.01) and OR &gt; 1. However, the distribution of IFN-γ serum levels by SNP (rs2069705) demonstrated no differences between genotypes except GG genotype which has significant differences for patients comparing to the same genotype in controls. Taking together, the SNP for IFN-γ (rs2069705) could be a risk factor for susceptibility infection with CL. Also, considered the mutant allele A as a risk allele and genotype AA in codominant genetic model as more risk factor than the genotype GA.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156785"},"PeriodicalIF":3.7,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142444836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence for a sex-dependent effect modification in the association between IFN-λ DNA polymorphisms and expression of IFN-λ and interferon-stimulated genes in human PBMCs","authors":"Debarati Guha Roy ,&nbsp;Manjarika De ,&nbsp;Seema Bharatiya ,&nbsp;Dhanashree A. Khedekar ,&nbsp;Kallol Datta ,&nbsp;Samsiddhi Bhattacharjee ,&nbsp;Sreedhar Chinnaswamy","doi":"10.1016/j.cyto.2024.156779","DOIUrl":"10.1016/j.cyto.2024.156779","url":null,"abstract":"<div><div>Human interferon (IFN) lambda (IFNL, IFN-L or IFN-λ) locus has several functional genetic variants but their role in regulating <em>in vivo</em> gene expression, and whether they associate with antiviral states in healthy individuals, is not clear. In this study, we recruited ∼550 healthy individuals belonging to both sexes, genotyped them for several <em>IFNL</em> genetic variants and measured, by qPCR, the expression of <em>IFNL2/3, IFNL4</em> and four IFN-stimulated genes (ISGs) (<em>MX1, OAS1, ISG15</em> and <em>RSAD2</em>) from their peripheral blood mononuclear cells (PBMC) both before and after stimulation with a viral mimic, poly I: C. We also measured secreted levels of several cytokines including IFN-λ1 and IFN-λ3 in poly I:C stimulated PBMCs. We found that males secrete higher levels of IFN-λs than females. The <em>IFNL3/4</em> genetic variants significantly associated with secreted levels of both IFN-λ1 and IFN-λ3 in opposite directions, only in males. While the <em>IFNL3/4</em> variants significantly associated with ISG expression either in basal or poly I:C induced or in both states, the direction of effect was opposite for the two sexes, suggesting that sex was a strong effect modifier. We did not see this trend in the association of ISG expression with the <em>IFNL1</em> polymorphism, rs7247086, whose association with ISG expression and secreted IFN-λ3 levels was seen in females but not in males. Further, expression of several genes was associated with the IFN-λ4 activity-modifying variant rs117648444. However, we neither saw any strong correlation between levels of IFN-λ1/3 and ISG expression, nor did we see any strong evidence of <em>IFNL4</em> expression that could be responsible for the association between ISG expression and <em>IFNL</em> genetic variants. These results suggest that there are complex interactions involving gender, IFN-λs, IFN-λ genetic variants and antiviral states in humans.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156779"},"PeriodicalIF":3.7,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142444835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory cytokines and carpal tunnel syndrome: A causal relationship revealed","authors":"Chen-fei Yang ,&nbsp;Ying Pu ,&nbsp;Li Li ,&nbsp;Ming-gang Guo ,&nbsp;Zhi-wei Feng","doi":"10.1016/j.cyto.2024.156777","DOIUrl":"10.1016/j.cyto.2024.156777","url":null,"abstract":"<div><h3>Objectives</h3><div>Carpal tunnel syndrome (CTS) and certain inflammatory cytokines have been linked in observational studies; however, the exact causative linkages remain unknown. The purpose of this study is to investigate any possible link between the onset of CTS and 91 inflammatory cytokines.</div></div><div><h3>Methods</h3><div>A two-sample bidirectional Mendelian randomization (MR) approach was used in this investigation. 91 circulating inflammatory cytokines’ genetic variants were retrieved from the European ancestry genome-wide association study (GWAS) database. From germline GWAS, summary data for 24,766 CTS patients and 360,538 controls were gathered. The instrumental variables were single nucleotide polymorphisms (SNPs) that were highly correlated with the 91 inflammatory cytokines. The random-effects inverse-variance weighted (IVW) approach was employed in the primary analysis, and multiple comparisons were subjected to the Bonferroni correction. Sensitivity analysis was performed to evaluate the validity of the causal relationship.</div></div><div><h3>Results</h3><div>Our findings showed a negative correlation between CCL19, FGF-19, IL-5, TGF-alpha, TRAIL, and the risk of CTS. Specifically, CCL19 (odds ratio [OR]: 0.944, 95 % confidence interval [CI]: 0.894–0.996, <em>p</em> = 0.0349), FGF-19 (OR: 0.940, 95 % CI: 0.894–0.987, <em>p</em> = 0.0133), IL-5 (OR: 0.936, 95 % CI: 0.885–0.990, <em>p</em> = 0.0212), TGF-alpha (OR: 0.902, 95 % CI: 0.838–0.970, <em>p</em> = 0.0057), and TRAIL (OR: 0.926, 95 % CI: 0.881–0.974, <em>p</em> = 0.0026) were inversely related to CTS risk. Conversely, CCL20, IL-2RB, and IL-6 were positively associated with an increased risk of CTS. Specifically, CCL20 (OR: 1.072, 95 % CI: 1.005–1.142, <em>p</em> = 0.0334), IL-2RB (OR: 1.067, 95 % CI: 1.001–1.137, <em>p</em> = 0.0463), and IL-6 (OR: 1.088, 95 % CI: 1.005–1.177, <em>p</em> = 0.0365) were positively correlated with CTS risk. Reverse Mendelian randomization analyses indicated no evidence of a reverse causal relationship between CTS and inflammatory cytokines.</div></div><div><h3>Conclusion</h3><div>According to this study, there is a causal link between CTS and certain inflammatory cytokines, which suggests that these cytokines may be important in the pathophysiology of CTS. To confirm these results and investigate the specific function of these cytokines in the beginning and development of CTS, more investigation is necessary.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156777"},"PeriodicalIF":3.7,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142428611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnostic accuracy of pleural fluid complement C1q for tuberculous pleural effusion in elderly patients","authors":"Wen Zhao ,&nbsp;Yan Niu ,&nbsp;Jian-Xun Wen ,&nbsp;Xi-Shan Cao ,&nbsp;Yu-Ling Han ,&nbsp;Xu-Hui Wen ,&nbsp;Mei-Ying Wang ,&nbsp;Ling Hai ,&nbsp;Wen-Hui Gao ,&nbsp;Li Yan ,&nbsp;Wen-Qi Zheng ,&nbsp;Zhi-De Hu","doi":"10.1016/j.cyto.2024.156778","DOIUrl":"10.1016/j.cyto.2024.156778","url":null,"abstract":"<div><h3>Background</h3><div>Previous studies indicated that pleural fluid complement C1q was helpful for diagnosing tuberculous pleural effusion (TPE), but the participants in these studies were young. The diagnostic accuracy of C1q for TPE in elderly patients remains unknown. This study aimed to investigate the diagnostic accuracy of C1q for TPE in elderly patients.</div></div><div><h3>Methods</h3><div>We prospectively recruited patients with undiagnosed pleural effusion who visited the Affiliated Hospital of Inner Mongolia Medical University between September 2018 and July 2021. Their C1q in pleural fluid was detected, and the diagnostic accuracy of C1q was assessed by the receiver operating characteristic (ROC) curve analysis.</div></div><div><h3>Results</h3><div>The median ages of patients with TPE and non-TPE were 75 and 71 years, respectively. TPE patients had significantly higher C1q than non-TPE. The area under the ROC curve (AUC) of C1q was 0.67 (95 %CI: 0.51–0.82). At the threshold of 100 mg/L, C1q had a sensitivity of 0.44 (95 %CI: 0.19–0.69) and specificity of 0.79 (95 %CI: 0.71–0.86).</div></div><div><h3>Conclusion</h3><div>C1q in pleural fluid has low diagnostic accuracy for TPE in elderly patients.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156778"},"PeriodicalIF":3.7,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142428626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}