Cytokine最新文献

{"title":"Shared inflammation in takotsubo syndrome and sepsis: Lipocalin-2 mediates neutrophil infiltration and cardiac damage","authors":"Yuxi Huang ,&nbsp;Piaorong Zeng ,&nbsp;Tianmin Liu ,&nbsp;Mei Xu ,&nbsp;Wenyi Tang ,&nbsp;Fangyuan Cheng ,&nbsp;Zhijuan Zhou ,&nbsp;Bairong Chen ,&nbsp;Kan Liu ,&nbsp;TouKun Chong ,&nbsp;Jian Chen","doi":"10.1016/j.cyto.2025.157102","DOIUrl":"10.1016/j.cyto.2025.157102","url":null,"abstract":"<div><h3>Background</h3><div>Takotsubo syndrome (TTS) and sepsis often co-occur with poor outcomes, yet their underlying molecular mechanisms remain to be elucidated. Transcriptomic analysis is employed to detect diagnostic biomarkers and reveal shared pathophysiological mechanisms in sepsis-associated TTS.</div></div><div><h3>Methods</h3><div>Myocardial gene expression data (TTS, sepsis, and controls) from GEO were analyzed to identify shared differentially expressed genes. WGCNA and PPI networks were used for candidate gene selection. Key genes were further refined using random forest and LASSO algorithms. Immune cell infiltration was assessed using CIBERSORT. Myocardial injury and gene expression in rat models were evaluated using HE staining, TUNEL assay, immunohistochemistry, qPCR, and Western blotting. Clinical validation was conducted using plasma samples from the China TTS Registry. <em>t</em>-tests and ANOVA were conducted via GraphPad Prism 8 software. A <em>P</em>-value &lt; 0.05 was considered statistically significant.</div></div><div><h3>Results</h3><div>Lipocalin-2 (LCN2) was recognized as an important biomarker through WGCNA, PPI network analysis, and machine learning algorithms, showing strong predictive performance. Its expression was significantly associated with neutrophil infiltration and myocardial injury in TTS. Consistent with the bioinformatics findings, the TTS-sepsis comorbidity model showed elevated mRNA and protein levels of LCN2 in myocardial tissue, accompanied by increased neutrophil infiltration and severe cardiac injury. Clinical validation confirmed elevated plasma LCN2 levels in patients with sepsis-associated TTS, correlating with neutrophil counts, NT-proBNP, and cTnI levels.</div></div><div><h3>Conclusion</h3><div>LCN2 is identified as a key inflammatory mediator linking neutrophil-driven inflammation to myocardial injury in sepsis-associated TTS, with dual potential as a diagnostic biomarker and therapeutic target.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"198 ","pages":"Article 157102"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877364","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":"Integrated experimental and computational approaches to analyze TNF superfamily ligand–receptor interactions","authors":"Anne-Laure Favier ,&nbsp;Cyril Salama ,&nbsp;Chloé Cervera ,&nbsp;Diane Riccobono ,&nbsp;Krisztina Nikovics","doi":"10.1016/j.cyto.2025.157100","DOIUrl":"10.1016/j.cyto.2025.157100","url":null,"abstract":"<div><div>The TNF superfamily, composed of cytokines and their receptors, plays a central role in regulating immune responses, apoptosis, inflammation, and tissue regeneration. TNF itself is a key orchestrator of the cytokine cascade in many diseases and is often described as a “master regulator.” It engages in complex ligand-receptor interactions, making the study of these dynamics essential for the development of new therapeutic strategies.</div><div>This review summarizes the current experimental and computational tools used to study ligand–receptor interactions within the TNF superfamily, highlighting both their strengths and limitations. Particular attention is given to methods for analyzing protein–protein interactions, which are fundamental to deciphering the regulatory functions of this family. While traditional <em>in vitro</em>, <em>in vivo</em>, and <em>in situ</em> approaches have confirmed numerous authentic ligand–receptor pairs, <em>in silico</em> analyses reveal a much broader landscape of predicted interactions. These computational predictions do not represent experimentally validated binding events; rather, they indicate possible ligand–receptor compatibilities based on structural homology, interface similarity, and docking-derived binding energies. Such predictions suggest that the TNF interaction network may be more extensive than previously recognized, underscoring the need for systematic experimental validation to uncover additional biologically relevant interactions.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"198 ","pages":"Article 157100"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145880905","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":"SMAD signaling in cancer: integrative roles in tumor progression, immune evasion, and therapeutic resistance","authors":"Hai Zhao ,&nbsp;Fan Yang ,&nbsp;Jiaxin Yang ,&nbsp;Sheng Yang","doi":"10.1016/j.cyto.2025.157090","DOIUrl":"10.1016/j.cyto.2025.157090","url":null,"abstract":"<div><div>Transforming growth factor-beta (TGF-β)/SMAD signaling exerts pleiotropic effects in cancer, orchestrating epithelial–mesenchymal transition (EMT), immune evasion, stemness, and therapeutic resistance. While canonically regarded as tumor-suppressive, emerging data reposition SMAD proteins, particularly SMAD2, SMAD3, and SMAD4, as central effectors of pro-tumorigenic reprogramming in advanced malignancies. Here, we delineate the multifaceted contributions of SMAD signaling across tumor-intrinsic and microenvironmental contexts, highlighting post-translational regulation, immune remodeling, and crosstalk with non-coding RNAs. We show how SMADs mediate dynamic EMT programs, modulate innate and adaptive immune landscapes, and drive chemoresistance through transcriptional and metabolic rewiring. In the tumor microenvironment (TME), SMAD-driven axes involving macrophages, neutrophils, and CAFs reinforce immune suppression and metastasis. Moreover, engineering SMAD pathways in CAR-T and NK cells enhances immunotherapeutic efficacy. We also identify SMAD-based transcriptional and epigenetic signatures with prognostic and predictive utility across multiple tumor types. This integrative review provides a unified framework for understanding the SMAD signaling network as both a mechanistic driver and therapeutic vulnerability in cancer.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"198 ","pages":"Article 157090"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145749531","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":"Unlocking potentials of a prenylated flavonoid: Xanthohumol's role in combating inflammatory conditions and Rhematic diseases","authors":"Farag M.A. Altalbawy ,&nbsp;Ahmed Hussein Zwamel ,&nbsp;Ashok Kumar Bishoyi ,&nbsp;Suhas Ballal ,&nbsp;Rishiv Kalia ,&nbsp;Kamal Kant Joshi ,&nbsp;Subhashree Ray ,&nbsp;Atreyi Pramanik ,&nbsp;Jasur Rizaev ,&nbsp;Khursheed Muzammil","doi":"10.1016/j.cyto.2025.157092","DOIUrl":"10.1016/j.cyto.2025.157092","url":null,"abstract":"<div><div>Xanthohumol, a prenylated flavonoid derived from hops (<em>Humulus lupulus</em>), has garnered significant attention for its multifaceted therapeutic potential. This review highlights xanthohumol's ability to modulate key signaling pathways, including NF-κB, STAT3, and Nrf2, which are central to inflammation, oxidative stress, and cancer progression. As a flavonoid, xanthohumol exhibits potent antioxidant and anti-inflammatory properties, making it effective in alleviating inflammatory conditions such as osteoarthritis, rheumatoid arthritis, and inflammatory bowel disease. In cancer, xanthohumol demonstrates remarkable efficacy by inhibiting tumor growth, angiogenesis, and metastasis through the suppression of critical pathways like CXCR4 and STAT3. Preclinical studies have shown that xanthohumol selectively targets cancer cells while sparing normal cells, underscoring its potential as a safe and effective anticancer agent. Beyond its anti-inflammatory and anticancer effects, xanthohumol also plays a significant role in metabolic regulation. It improves glucose homeostasis, lipid metabolism, and gut microbiota composition, offering therapeutic benefits for metabolic syndrome and diabetes. Clinical trials and preclinical research further validate xanthohumol's safety and efficacy, with emerging evidence supporting its use in managing chronic diseases. This review provides a comprehensive overview of xanthohumol's mechanisms of action, therapeutic applications, and future directions in clinical research, positioning it as a promising natural compound for the prevention and treatment of a wide range of diseases.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"198 ","pages":"Article 157092"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145808859","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":"The role of HMGB1 in central nervous system (CNS) diseases: mechanisms and therapeutic perspectives","authors":"Ou Du,&nbsp;Yi-Jin Wu,&nbsp;Meng-Yang Li,&nbsp;Jun-Rong Du","doi":"10.1016/j.cyto.2025.157099","DOIUrl":"10.1016/j.cyto.2025.157099","url":null,"abstract":"<div><div>Central nervous system (CNS) diseases represent a major global health burden and are among the leading causes of disability and mortality worldwide. The pathological mechanisms underlying CNS disorders are complex and multifactorial, involving processes such as neuroinflammation, oxidative stress, neuronal damage, and synaptic dysfunction. High-mobility group box 1 (HMGB1), a member of the high-mobility group box (HMGB) protein family, is predominantly localized in the nucleus under physiological conditions, where it contributes to DNA repair, transcriptional regulation, and other cellular functions. However, in various CNS pathologies—including stroke, traumatic brain injury (TBI), Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), glioblastoma (GBM), epilepsy, depression, multiple sclerosis (MS), and schizophrenia—HMGB1 is released or secreted into the extracellular space. There, it plays a key role in regulating neuroinflammation, cell death, cell migration, and tissue damage and repair, thereby contributing to disease pathogenesis and progression. HMGB1 not only functions as a critical regulator in the progression of CNS diseases but also serves as a biomarker for predicting poor clinical outcomes. Moreover, a growing body of evidence indicates that therapeutic strategies targeting HMGB1 can significantly alleviate pathological damage in various CNS disorders, highlighting its potential as a promising therapeutic target. This review comprehensively summarizes the structure, post-translational modifications, release mechanisms, and receptor systems of HMGB1, along with its roles and mechanisms in CNS diseases. It also discusses the potential of HMGB1 as a biomarker and examines emerging HMGB1-targeted therapeutic strategies, aiming to provide a theoretical foundation for the treatment and drug development of CNS disorders.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"198 ","pages":"Article 157099"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145837306","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":"Group 2 innate lymphoid cells (ILC2s) in childhood allergic diseases: A review of the mechanisms and therapeutic advances","authors":"Yun Zhang ,&nbsp;Yaling Wu ,&nbsp;Yingying Wang ,&nbsp;Haoquan Zhou","doi":"10.1016/j.cyto.2025.157101","DOIUrl":"10.1016/j.cyto.2025.157101","url":null,"abstract":"<div><div>Recent advances in pediatric immunology have clarified the pivotal role of group 2 innate lymphoid cells (ILC2s) in the pathophysiology of childhood allergic diseases. As key components of the innate immune system, ILC2s mediate the initiation and progression of these disorders. Their activation is triggered primarily by epithelial-derived cytokines, whose expression is highly elevated in children with allergies. Upon activation, ILC2s rapidly secrete type 2 cytokines, driving disease-specific pathogenesis. In allergic asthma, airway ILC2 expansion exacerbates eosinophilic inflammation, airway hyperresponsiveness, and remodeling; in allergic rhinitis, nasal mucosal ILC2 activation induces typical symptoms; and in food allergies, intestinal mucosal ILC2s cause epithelial damage and increased permeability, promoting allergic progression. These mechanistic insights have underpinned the development of innovative therapies. Clinical trials have confirmed the efficacy of treatments targeting ILC2-derived cytokines or their receptors: anti-IL-5 monoclonal antibodies (targeting the IL-5 ligand), anti-IL-13 monoclonal antibodies (targeting the IL-13 ligand), and anti-IL-4Rα monoclonal antibodies (targeting IL-4 receptor α and blocking IL-4/IL-13 signaling) are promising treatments for specific childhood allergic diseases. Emerging strategies targeting ILC2 activation pathways and modulating the microbiome to regulate ILC2 activity are under active investigation. Collectively, the past five years of research have improved the understanding of the mechanisms underlying childhood allergic diseases and established new treatment paradigms, with great potential to optimize clinical management and improve the outcomes of pediatric patients with allergies.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"198 ","pages":"Article 157101"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145837275","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":"Promoter variants of tumor necrosis factor-alpha (G-308 a: rs1800629 and C-857 T:rs1799724) are linked to type 1 diabetes: A meta-analysis and trial sequential analysis","authors":"Shengnan Zhang,&nbsp;Zhenyu Li,&nbsp;Xiaodong Yang","doi":"10.1016/j.cyto.2025.157082","DOIUrl":"10.1016/j.cyto.2025.157082","url":null,"abstract":"<div><h3>Introduction</h3><div>Tumor necrosis factor-alpha (TNF-α) is associated with type 1 diabetes through complex immunological and metabolic pathways, highlighting its multifaceted role. Genetic differences, particularly in the TNF-α gene promoter region, influence individual susceptibility to type 1 diabetes by altering gene expression. Numerous studies have examined the link between TNF-α polymorphisms and type 1 diabetes in various populations, yielding inconsistent results. This research explores the relationship between TNF-α and type 1 diabetes through a detailed meta-analysis of existing studies.</div></div><div><h3>Materials and methods</h3><div>This meta-analysis examined four SNPs in the TNF-α gene promoter region: G-238 A, G-308 A, C-587 T, and T-1031C. Literature searches were conducted using PubMed, ScienceDirect, Google Scholar, Embase, Web of Science, and Scopus. Relevant articles were systematically reviewed, and qualifying studies were selected based on specific inclusion and exclusion criteria. The analysis was performed using Comprehensive Meta-Analysis software, version 4.</div></div><div><h3>Results</h3><div>Twenty-four case-control studies were suitable for examining the link between TNF-α polymorphisms and T1D susceptibility. Genetic comparison models showed an association between the TNF-α G-308 A and C-857 T variants and T1D risk, and sensitivity analysis confirmed these findings. Trial sequential analysis further validated the genetic relationship between TNF-α promoter variants (G-308 A and C-857 T) and indicated that sufficient studies were available for a conclusive meta-analysis. Conversely, no significant association was found between the promoter polymorphisms G-238 A and T-1031C and T1D onset, and TSA suggested the need for further research across diverse populations.</div></div><div><h3>Conclusions</h3><div>Variations in the TNF-α promoter at positions G-308 A and C-857 T are linked to an increased risk of T1D.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"198 ","pages":"Article 157082"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145665481","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":"Clinical observation of anti-PD-1/PD-L1 immunotherapy plus concurrent chemoradiotherapy for locally advanced esophageal squamous cell carcinoma","authors":"Xudong Sun ,&nbsp;Dongmei Wu ,&nbsp;Guangcheng Ding ,&nbsp;Xueying Zhang ,&nbsp;Changli Shi ,&nbsp;Yulong Tian","doi":"10.1016/j.cyto.2025.157096","DOIUrl":"10.1016/j.cyto.2025.157096","url":null,"abstract":"<div><h3>Objective</h3><div>This study analyzed the efficacy of the PD-1 inhibitor Sintilimab combined with concurrent chemoradiotherapy (CCRT) in patients with unresectable locally advanced esophageal squamous cell carcinoma (ESCC).</div></div><div><h3>Methods</h3><div>A retrospective study involved 177 individuals with unresectable advanced ESCC, treated with anti-PD-1/PD-L1 immunotherapy combined with CCRT. Patients were categorized into three groups: combined positive score (CPS) ≥ 50, 1 &lt; CPS &lt; 50, and CPS &lt; 1. Clinical data and laboratory markers (carcinoembryonic antigen [CEA] and squamous cell carcinoma antigen [SCC-Ag]) were collected at baseline, 6, 12, and 24 months. PET/CT and CT scans assessed tumor response, ORR, and DCR. Kaplan-Meier curves analyzed the impact of CPS scores on progression-free survival (PFS) and overall survival (OS). Baseline data were matched at a 1:1 ratio by propensity score matching, followed by Cox regression analyses.</div></div><div><h3>Results</h3><div>No noticeable differences were present among the groups regarding gender, tumor location, prior chemotherapy, prior radiotherapy, or laboratory markers. After treatment, CEA and SCC-Ag levels significantly decreased, with the lowest levels observed at 24 months post-treatment. Higher CPS scores were associated with reduced CEA and SCC-Ag levels. PD-L1-positive groups (CPS &gt; 1) had higher ORR and DCR than the PD-L1-negative group. As CPS scores increased, PFS and OS were significantly prolonged. Serum fibrinogen, CEA and SCC-Ag were identified as independent risk factors for OS; Serum CEA and SCC-Ag were independent risk factors affecting PFS.</div></div><div><h3>Conclusion</h3><div>Higher CPS scores are associated with improved PFS and OS in patients with locally advanced ESCC receiving anti-PD-1/PD-L1 immunotherapy combined with CCRT.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"198 ","pages":"Article 157096"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145831883","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":"Advances in lipid nanoparticle delivery systems for targeted cytokine immunotherapy in autoimmune disorders","authors":"Dilpreet Singh","doi":"10.1016/j.cyto.2025.157098","DOIUrl":"10.1016/j.cyto.2025.157098","url":null,"abstract":"<div><div>Autoimmune diseases result from dysregulated immune responses, primarily driven by CD4+ T cell imbalances, leading to chronic inflammation and tissue destruction. Conventional cytokine-based therapies, including IL-2 for regulatory T cell (Treg) expansion and IL-6 or IL-17 inhibition for inflammation suppression, have shown promise in modulating immune responses. However, challenges such as systemic toxicity, short half-life, and off-target effects limit their therapeutic efficacy. Lipid nanoparticles (LNPs) have emerged as a next-generation drug delivery platform, offering enhanced cytokine stability, targeted cellular uptake, and controlled release, thereby overcoming limitations associated with free cytokine administration. Preclinical studies have demonstrated that LNP-IL-2 selectively expands Tregs in type 1 diabetes models, while IL-10-loaded LNPs suppress synovial inflammation in rheumatoid arthritis more effectively than conventional cytokine therapies. Optimization of ligand density and affinity on LNP surfaces is emerging as a key determinant of CD4⁺ T cell targeting efficiency. Additionally, LNP-encapsulated siRNA targeting IL-6 and IL-23 has shown superior suppression of inflammatory pathways in lupus and psoriasis. These findings underscore the potential of LNP-mediated cytokine delivery to precisely modulate CD4+ T cell function, restoring immune homeostasis in autoimmune diseases. Despite promising preclinical and early clinical data, challenges remain, including optimizing biodistribution, ensuring selective T cell targeting, and mitigating immune activation risks. This review provides an in-depth analysis of CD4+ T cell subsets in autoimmunity, the advantages of LNP-based cytokine therapies, and their translational potential. The integration of LNP technology into cytokine immunotherapy offers a novel, minimally toxic, and durable approach to reprogramming immune responses, paving the way for precision medicine in autoimmune disease management.</div></div><div><h3>Significance</h3><div>Autoimmune disorders are characterized by chronic inflammation driven by dysregulated cytokine activity. Traditional cytokine therapies often suffer from systemic toxicity and limited targeting precision. This manuscript highlights recent advancements in lipid nanoparticle (LNP) technology for the targeted delivery of cytokines, offering enhanced therapeutic efficacy and safety. By enabling precise modulation of immune responses at disease sites, LNP-based delivery systems represent a transformative approach in immunotherapy. This review underscores the potential of LNPs to overcome current limitations in autoimmune treatment, paving the way for next-generation precision medicine strategies.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"198 ","pages":"Article 157098"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145825443","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":"IL-8-, IL-12-, and VEGF-producing peripheral blood mononuclear cells enable differentiation between vertebral osteomyelitis and degenerative spinal diseases","authors":"Julia Schenk ,&nbsp;Martin Thelen ,&nbsp;Hans Anton Schlößer ,&nbsp;Esther Mahabir","doi":"10.1016/j.cyto.2025.157104","DOIUrl":"10.1016/j.cyto.2025.157104","url":null,"abstract":"<div><div>Vertebral osteomyelitis (VO) is a rare but serious spinal infection that presents significant challenges in early diagnosis and treatment. Diagnostic delays can result in severe complications, including neurological deficits, sepsis, organ failure, and death. In this study, we investigated the immune cell source of candidate cytokines – IL-6, IL-8, IL-12, and VEGF – with the aim of distinguishing VO from degenerative spinal diseases. Peripheral blood samples were collected pre-operatively and 40 to 56 days post-operatively. Cytokine production by major immune cell subsets within peripheral blood mononuclear cells (PBMCs) was analyzed using intracellular flow cytometry. Our findings indicate that pre-operative differentiation between VO and degenerative spinal diseases is feasible, particularly based on IL-8-positive CD8⁺ T-cells, IL-12-positive CD45⁺ lymphocytes, and VEGF-positive cells (including CD45⁺ cells, B-cells, T-cells, and CD8⁺ T-cells).</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"198 ","pages":"Article 157104"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877336","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}