Journal of Interferon and Cytokine Research最新文献

筛选
英文 中文
IL-33 Has a Protective Effect Against Perinatal Listeriosis by Regulating Mitophagy of CD8+ T Lymphocytes. IL-33通过调节CD8+ T淋巴细胞自噬对围产期李斯特菌病的保护作用
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-06-13 DOI: 10.1089/jir.2025.0069
Tingjuan Shi, Yuxi Yang, Yingying Li, Ning Xu, Fei Chen, Tian Xia, Hongliang Wu, Yingyi Luan, Chenghong Yin
{"title":"IL-33 Has a Protective Effect Against Perinatal Listeriosis by Regulating Mitophagy of CD8<sup>+</sup> T Lymphocytes.","authors":"Tingjuan Shi, Yuxi Yang, Yingying Li, Ning Xu, Fei Chen, Tian Xia, Hongliang Wu, Yingyi Luan, Chenghong Yin","doi":"10.1089/jir.2025.0069","DOIUrl":"https://doi.org/10.1089/jir.2025.0069","url":null,"abstract":"<p><p>Listeriosis is a foodborne disease caused by <i>Listeria monocytogenes</i> (Lm) that usually leads to serious adverse outcomes in pregnant women. Interleukin (IL)-33/serum stimulation (ST)2 axis has an important impact on infectious diseases, but its role in listeriosis is rarely studied. Here, the immunomodulatory effects of IL-33/ST2 axis during perinatal Lm infection were investigated. In our study, the perinatal Lm infection model was constructed by injecting Lm into the tail vein of C57BL/6J mice. IL-33/ST2 axis was blocked by intraperitoneal injection of anti-IL-33Rα/ST2 antibody. <i>In vitro</i>, mouse cytotoxic T lymphocyte cell line (CTLL)-2 cells were activated by using CD3/CD28 antibodies. Perinatal Lm infection caused massive necrosis of liver tissue. Blocking IL-33/ST2 axis in pregnant mice inhibited the infiltration of CD8<sup>+</sup> T lymphocytes into the site of infection and further aggravated liver damage. We also found that IL-33 promotes mitochondrial autophagy in activated CTLL-2 cells <i>in vitro</i>. Mitochondrial autophagy was beneficial to the clearance of damaged mitochondria and reduced the production of reactive oxygen species. IL-33/ST2 axis affects the immune function of CD8<sup>+</sup> T lymphocytes by regulating mitophagy, which plays a very important role in the occurrence and development of perinatal Lm infection. Immunomodulation targeting IL-33/ST2 axis may be an effective way to adjuvant treatment of perinatal Lm infection.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inhibition of FKBP5 Alleviates Inflammation and Intestinal Barrier Dysfunction in Sepsis. 抑制FKBP5减轻脓毒症的炎症和肠屏障功能障碍。
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-06-04 DOI: 10.1089/jir.2025.0046
Jian Li, Anwaier Apizi, Tingting Song, Paiheriding Kamilijiang, Xiangyou Yu, Ruifeng Chai, Zhaoxia Yu
{"title":"Inhibition of FKBP5 Alleviates Inflammation and Intestinal Barrier Dysfunction in Sepsis.","authors":"Jian Li, Anwaier Apizi, Tingting Song, Paiheriding Kamilijiang, Xiangyou Yu, Ruifeng Chai, Zhaoxia Yu","doi":"10.1089/jir.2025.0046","DOIUrl":"https://doi.org/10.1089/jir.2025.0046","url":null,"abstract":"<p><p><b><i>Background:</i></b> The pro-apoptotic and pro-inflammatory effects of FK506 binding protein 5 (FKBP5) in sepsis-induced acute kidney injury have been previously reported. However, its biological functions and underlying mechanisms in regulating sepsis-induced intestinal injury remain elusive. Therefore, this study aimed to explore the effects of FKBP5 on sepsis-induced intestinal injury. <b><i>Methods:</i></b> A mouse model of sepsis was established by cecal ligation and puncture (CLP). A cell model was established by treating Caco-2 cells with lipopolysaccharide (LPS). The impacts of FKBP5 knockdown on apoptosis, barrier integrity, inflammation, and the nuclear factor kappa B (NF-κB) signaling were evaluated in ileal tissue and Caco-2 cells. <b><i>Results:</i></b> FKBP5 expression was elevated in the ileal tissue in response to CLP and LPS treatments. In mice with sepsis, FKBP5 knockdown reduced cell apoptosis and regulated Bax, Bcl-2, and cleaved PARP levels. FKBP5 knockdown also reduced the levels of D-lactic acid, tumor necrosis factor alpha, interleukin (IL)-6, and IL-1β, improved intestinal histopathological damage, and enhanced the expression of zonula occludens-1 and occludin. FKBP5 knockdown also displayed protective effects in LPS-stimulated cells. FKBP5 knockdown inhibited the NF-κB signaling in CLP and LPS groups. <b><i>Conclusion:</i></b> Inhibition of FKBP5 alleviates inflammation and intestinal barrier dysfunction in sepsis, partially by inhibiting the NF-κB signaling.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
CXCL13 as a Predictive Biomarker for Response to Methotrexate Monotherapy in Rheumatoid Arthritis. CXCL13作为类风湿性关节炎对甲氨蝶呤单药治疗反应的预测性生物标志物。
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-06-04 DOI: 10.1089/jir.2025.0041
Vishnu S Chandran, Mithun C B, Sajitha Krishnan, Sandeep Surendran, Clint Sunny, Manu Pradeep
{"title":"CXCL13 as a Predictive Biomarker for Response to Methotrexate Monotherapy in Rheumatoid Arthritis.","authors":"Vishnu S Chandran, Mithun C B, Sajitha Krishnan, Sandeep Surendran, Clint Sunny, Manu Pradeep","doi":"10.1089/jir.2025.0041","DOIUrl":"https://doi.org/10.1089/jir.2025.0041","url":null,"abstract":"<p><p>This prospective study investigated the utility of baseline CXCL13 levels in predicting methotrexate response and monitoring disease activity in 50 treatment-naive early rheumatoid arthritis (RA) patients (2010 American College of Rheumatology/European League Against Rheumatism criteria) treated with methotrexate. Participants were categorized into methotrexate responders (MTX-R, <i>n</i> = 29) and nonresponders (MTX-NR, <i>n</i> = 21) at 12 weeks. Baseline CXCL13 levels were significantly higher in MTX-R compared with MTX-NR (<i>P</i> = 0.035). Receiver operating characteristic curve analysis identified a baseline CXCL13 cutoff of >100 pg/mL for predicting methotrexate response, with 69% sensitivity, 52% specificity, and 62% accuracy. Posttreatment, CXCL13 levels decreased significantly in MTX-R (<i>P</i> < 0.001) but remained unchanged in MTX-NR. Disease activity parameters (eg, DAS-28) correlated with CXCL13 dynamics, though specific coefficients were not detailed. The study highlights CXCL13 as a potential biomarker for stratifying methotrexate therapy, with higher baseline levels favoring therapeutic response and posttreatment reductions reflecting clinical improvement. While moderate diagnostic accuracy limits standalone use, CXCL13 may complement existing tools to guide early personalized treatment. Further validation in larger cohorts is warranted to confirm its role in optimizing RA management.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
GPNMB Suppresses Inflammation and Extracellular Matrix Degradation in Nucleus Pulposus Cells by Inhibiting Pro-Inflammatory Cytokine Production and Activation of the NF-κB Signaling Pathway. GPNMB通过抑制促炎细胞因子的产生和NF-κB信号通路的激活,抑制髓核细胞的炎症和细胞外基质降解。
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-06-01 Epub Date: 2025-04-16 DOI: 10.1089/jir.2025.0022
Jun Zheng, Yaodong Song, Bing Yu
{"title":"GPNMB Suppresses Inflammation and Extracellular Matrix Degradation in Nucleus Pulposus Cells by Inhibiting Pro-Inflammatory Cytokine Production and Activation of the NF-κB Signaling Pathway.","authors":"Jun Zheng, Yaodong Song, Bing Yu","doi":"10.1089/jir.2025.0022","DOIUrl":"10.1089/jir.2025.0022","url":null,"abstract":"<p><p>Lumbar disc herniation is primarily caused by intervertebral disc degeneration (IVDD). Nucleus pulposus (NP) cell dysfunction leads to pro-inflammatory cytokines secretion increase, causing extracellular matrix (ECM) degradation. ECM is essential for maintaining normal disc function. Glycoprotein (Transmembrane) Nmb (GPNMB) is strongly associated with inflammation, and its expression and effects in IVDD are unclear. We categorized 40 clinically collected IVDD samples using the magnetic resonance imaging (MRI)-based Pfirrmann grading system. GPNMB mRNA expression was notably suppressed in patients with severe IVDD compared with patients with mild IVDD. Increased GPNMB mRNA expression correlated with decreased Interleukin-6 (IL-6) expression and increased collagen type II (COL2A1) expression levels. We utilized lentivirus to overexpress GPNMB in IL-1β-induced NP cells to explore its function in IVDD. GPNMB overexpression inhibited pro-inflammatory cytokines Tumor necrosis factor-alpha and IL-6 secretion in IL-1β-induced NP cells, while anti-inflammatory cytokine IL-10 content was increased. In addition, GPNMB overexpression inhibited NP ECM degradation by decreasing ECM-degrading enzymes matrix metalloproteinases-3/13 and a disintegrin and metalloproteinase with thrombospondin motifs-4/5 <i>in vitro</i>. Mechanism studies revealed that GPNMB was bound to CD44, a receptor expressed on the NP cell surface. GPNMB overexpression inhibited nuclear factor-κB (NF-κB) p65 phosphorylation and nuclear translocation <i>in vitro</i>, possibly through CD44. In conclusion, GPNMB suppressed the expression of pro-inflammatory cytokines and ECM degradation in NP cells by inhibiting activation of NF-κB.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"238-246"},"PeriodicalIF":1.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144015098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Lienal Polypeptide Decreases Immune Thrombocytopenia in a Mouse Model by Upregulating Cytokine Production and Increasing the Levels of CD4+, CD8+, and T Regulatory Cells. 连纳尔多肽通过上调细胞因子的产生并提高 CD4+、CD8+ 和 T 调节细胞的水平,减少小鼠模型中的免疫性血小板减少症。
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-06-01 Epub Date: 2025-03-21 DOI: 10.1089/jir.2024.0256
Zhaorong Yue, Fei Xie, Ruyue Wang, Xin Wang, Hongyu Li
{"title":"Lienal Polypeptide Decreases Immune Thrombocytopenia in a Mouse Model by Upregulating Cytokine Production and Increasing the Levels of CD4<sup>+</sup>, CD8<sup>+</sup>, and T Regulatory Cells.","authors":"Zhaorong Yue, Fei Xie, Ruyue Wang, Xin Wang, Hongyu Li","doi":"10.1089/jir.2024.0256","DOIUrl":"10.1089/jir.2024.0256","url":null,"abstract":"<p><p>Primary immune thrombocytopenia (ITP) is a condition marked by immune-mediated inadequate platelet production or excessive destruction. This study investigates the effects of Lienal polypeptide injection (LP) on T lymphocyte subgroups in the spleen and thymus, megakaryocyte counts in the bone marrow, and cytokine levels related to megakaryocyte development in mice with antibody-induced ITP, aiming to elucidate potential therapeutic mechanisms. We first assessed the effects of LP on Meg-01 megakaryocytic cells regarding proliferation, apoptosis, and differentiation using Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assays, Western blot analysis, and flow cytometry for apoptosis and CD41 expression as a differentiation marker. Following this, LP was administered intraperitoneally at 60 mg/(kg·d) for 11 days to ITP mice. We quantified peripheral blood platelets and bone marrow megakaryocytes, measured spleen and thymus indices, and assessed serum levels of stem cell factor (SCF), interleukin-3 (IL-3), interleukin-6 (IL-6), and platelet factor-4 (PF-4) via enzyme-linked immunosorbent assay (ELISA). Flow cytometry quantified T-helper cells (CD4<sup>+</sup>), cytotoxic T cells (CD8<sup>+</sup>), and regulatory T cells (Tregs). LP significantly induced apoptosis in Meg-01 cells while not markedly affecting differentiation. In ITP mice, LP effectively prevented platelet decline without affecting megakaryocyte counts or maturity. Increased SCF, IL-3, and IL-6 levels, alongside decreased PF-4 levels, correlated with enhanced platelet production. Moreover, CD4<sup>+</sup>/CD8<sup>+</sup> ratios and Treg populations increased, contributing to reduced platelet destruction. In conclusion, LP exerts a protective effect in ITP by modulating SCF, IL-3, IL-6, and PF-4 levels and restoring the balance of T cell subtypes, elucidating its therapeutic potential.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"214-226"},"PeriodicalIF":1.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
KLF13 Attenuates Lipopolysaccharide-Induced Alveolar Epithelial Cell Damage by Regulating Mitochondrial Quality Control via Binding PGC-1α. KLF13通过结合PGC-1α调节线粒体质量控制,减轻脂多糖诱导的肺泡上皮细胞损伤。
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-06-01 Epub Date: 2024-07-01 DOI: 10.1089/jir.2023.0234
Qiong Xi, Lin Liu, Qin Zhao, Shan Zhu
{"title":"KLF13 Attenuates Lipopolysaccharide-Induced Alveolar Epithelial Cell Damage by Regulating Mitochondrial Quality Control via Binding PGC-1α.","authors":"Qiong Xi, Lin Liu, Qin Zhao, Shan Zhu","doi":"10.1089/jir.2023.0234","DOIUrl":"10.1089/jir.2023.0234","url":null,"abstract":"<p><p>Sepsis is a clinically life-threatening syndrome, and acute lung injury is the earliest and most serious complication. We aimed to assess the role of kruppel-like factor 13 (KLF13) in lipopolysaccharide (LPS)-induced human alveolar type II epithelial cell damage and to reveal the possible mechanism related to peroxisome proliferator-activated receptor-γ co-activator 1-α (PGC-1α). In LPS-treated A549 cells with or without KLF13 overexpression or PGC-1α knockdown, cell viability was measured by a cell counting kit-8 assay. Enzyme-linked immunosorbent assay kits detected the levels of inflammatory factors, and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining measured cell apoptosis. Besides, mitochondrial reactive oxygen species (MitoSOX) and mitochondrial membrane potential were detected using MitoSOX red- and JC-1 staining. Expression of proteins related to mitochondrial quality control (MQC) was evaluated by western blot. Co-immunoprecipitation (Co-IP) assay was used to analyze the interaction between KLF13 and PGC-1α. Results indicated that KLF13 was highly expressed in LPS-treated A549 cells. KLF13 upregulation elevated the viability and reduced the levels of inflammatory factors in A549 cells exposed to LPS. Moreover, KLF13 gain-of-function inhibited LPS-induced apoptosis of A549 cells, accompanied by upregulated BCL2 expression and downregulated Bax and cleaved caspase3 expression. Furthermore, MQC was improved by KLF13 overexpression, as evidenced by decreased MitoSOX, JC-1 monomers and increased JC-1 aggregates, coupled with the changes of proteins related to MQC. In addition, Co-IP assay confirmed the interaction between KLF13 and PGC-1α. PGC-1α deficiency restored the impacts of KLF13 upregulation on the inflammation, apoptosis, and MQC in LPS-treated A549 cells. In conclusion, KLF13 attenuated LPS-induced alveolar epithelial cell inflammation and apoptosis by regulating MQC via binding PGC-1α.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"227-237"},"PeriodicalIF":1.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141476790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Differential Expression of Th17-Related Cytokines in Patients of Chronic Kidney Disease with and Without Systemic Lupus Erythematosus. 慢性肾病伴与不伴系统性红斑狼疮患者th17相关细胞因子的差异表达
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-06-01 Epub Date: 2025-05-23 DOI: 10.1089/jir.2024.0265
Farhad Seif, Karrar Hadi Kadhim, Milad Ahmadaghdami, Paria Bayati, Somayeh Sadani, Homa Davoodi, Ali Memarian, Somayeh Ghorbani, Yasser Bagheri
{"title":"Differential Expression of Th17-Related Cytokines in Patients of Chronic Kidney Disease with and Without Systemic Lupus Erythematosus.","authors":"Farhad Seif, Karrar Hadi Kadhim, Milad Ahmadaghdami, Paria Bayati, Somayeh Sadani, Homa Davoodi, Ali Memarian, Somayeh Ghorbani, Yasser Bagheri","doi":"10.1089/jir.2024.0265","DOIUrl":"10.1089/jir.2024.0265","url":null,"abstract":"<p><p>Dysregulation of immune cells and cytokines, particularly T helper 17 (Th17) cells and their associated cytokines, is implicated in the pathogenesis of both systemic lupus erythematosus (SLE) and chronic kidney disease (CKD). This study aimed to investigate the serum levels of Th17-related cytokines (interleukin [IL]-17A, IL-21, IL-22, and IL-23) in CKD patients with and without SLE and explore their potential role in disease progression. A total of 118 participants were included, comprising 78 patients with CKD (stages 3-5) and 40 healthy controls. Cytokine levels were measured using enzyme-linked immunosorbent assay kits. Patients with CKD exhibited significantly lower IL-21 levels and higher IL-22 and IL-17A levels compared with controls, while patients with end-stage renal disease showed elevated IL-21 and IL-23 levels. Among SLE-negative nephrotic patients, IL-23 and IL-17A were significantly upregulated, whereas SLE-positive nephrotic patients had increased IL-22 and IL-17A levels. In addition, IL-21 and IL-17A were significantly correlated in patients with CKD, suggesting a potential immunoregulatory interplay. These findings indicate that Th17-related cytokines are differentially expressed depending on CKD stage and SLE status, potentially influencing immune responses, inflammation, and kidney fibrosis. Understanding alterations of these cytokines may aid in identifying targeted therapeutic, particularly for patients with CKD at risk of SLE-related complications.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"205-213"},"PeriodicalIF":1.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Role of Interleukin-8 in Hemolytic Uremic Syndrome Severity in Children with Shiga Toxin-Producing Escherichia Coli Infection. 白细胞介素-8在产志贺毒素大肠杆菌感染儿童溶血性尿毒症严重程度中的作用
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-05-29 DOI: 10.1089/jir.2025.0031
Analía Toledano, Ana Caratozzolo, Romina Lanfranchi, Mayra Martinez, Marian Chacoff, Carolina Carballo, Laura B Talarico, María M Contrini, Eduardo Luis López
{"title":"Role of Interleukin-8 in Hemolytic Uremic Syndrome Severity in Children with Shiga Toxin-Producing <i>Escherichia Coli</i> Infection.","authors":"Analía Toledano, Ana Caratozzolo, Romina Lanfranchi, Mayra Martinez, Marian Chacoff, Carolina Carballo, Laura B Talarico, María M Contrini, Eduardo Luis López","doi":"10.1089/jir.2025.0031","DOIUrl":"https://doi.org/10.1089/jir.2025.0031","url":null,"abstract":"<p><p>We aimed to measure serum concentrations of interleukin (IL) 8, tumor necrosis factor-α (TNF-α), IL-6, IL-1β, and human neutrophil gelatinase-associated lipocalin (N-gal) in children with Shiga toxin-producing <i>Escherichia coli</i> (STEC) infection to determine the inflammatory cytokine profile and the role of these molecules in hemolytic uremic syndrome (HUS) development and severity. Three groups of patients with evidence of STEC infection were incorporated: bloody diarrhea (BD), patients with HUS requiring dialysis (HUSD), and patients with HUS and no dialysis requirement (HUSND). Serum samples were assayed for cytokines and N-gal using immunoassays. Thirty-six children were enrolled: 13 with BD, 10 with HUSND, and 13 with HUSD. We found significantly higher levels of IL-8, TNF-α, IL-6, and N-gal in patients with HUSD compared to patients with BD. Only TNF-α levels were significantly higher in patients with HUSND than in patients with BD. Higher IL-8 and N-gal levels were evidenced in HUSD than in patients with HUSND at the initial stages of disease. Principal component analysis revealed that children with HUSD exhibited an immune profile different from the other study groups. These results suggest a possible involvement of IL-8 in disease severity in patients with STEC-HUS. Furthermore, our results indicate a potential role of N-gal in HUS development.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Significant Associations Between Blood Cell Counts and a Large Number of Salivary Cytokines, Chemokines, and Growth Factors. 血细胞计数与大量唾液细胞因子、趋化因子和生长因子之间的显著关联。
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-05-20 DOI: 10.1089/jir.2025.0048
Lars B Eriksson, Mats Eriksson, Torsten Gordh, Anders Larsson
{"title":"Significant Associations Between Blood Cell Counts and a Large Number of Salivary Cytokines, Chemokines, and Growth Factors.","authors":"Lars B Eriksson, Mats Eriksson, Torsten Gordh, Anders Larsson","doi":"10.1089/jir.2025.0048","DOIUrl":"https://doi.org/10.1089/jir.2025.0048","url":null,"abstract":"<p><p>The association between local oral inflammation and cardiovascular risk has been extensively studied, with results indicating a bidirectional relationship. The aim of the present study was to investigate the associations between blood cells and a large number of salivary cytokines, chemokines, and growth factors. The study consisted of 165 individuals who were referred to the Oral and Maxillofacial Surgery clinic at Falun County hospital, Sweden, for surgical removal of impacted lower third molar. The study subjects did not have any known inflammatory disorders. Complete blood cell counts were analyzed using the routine laboratory at Falun Hospital, Falun, Sweden. Proteomic analysis of 92 inflammation-related protein biomarkers in saliva was performed using a multiplex proximity extension assay. After adjustment for multiplicity testing using the false discovery rate approach, there remained significant association between several saliva cytokines, chemokines, and growth factors and white blood cell counts (<i>n</i> = 19), neutrophil counts (<i>n</i> = 18), erythrocyte counts (<i>n</i> = 13), hemoglobin concentrations (<i>n</i> = 20), erythrocyte volume fractions (<i>n</i> = 22), and platelet counts (<i>n</i> = 12). There are several significant associations between local inflammatory cytokines in the oral cavity and blood cell parameters indicating a relationship between local and systemic inflammatory activity.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Epigenome-Wide DNA Methylation Profiling of Peripheral Blood Shows Lymphocyte Dysfunction in Children with Kawasaki Disease. 外周血全基因组DNA甲基化分析显示川崎病患儿淋巴细胞功能障碍
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-05-09 DOI: 10.1089/jir.2025.0029
Jayakanthan Kabeerdoss, Rakesh Kumar Pilania, Taru Goyal, Abarna Thangaraj, Manpreet Dhaliwal, Surjit Singh
{"title":"Epigenome-Wide DNA Methylation Profiling of Peripheral Blood Shows Lymphocyte Dysfunction in Children with Kawasaki Disease.","authors":"Jayakanthan Kabeerdoss, Rakesh Kumar Pilania, Taru Goyal, Abarna Thangaraj, Manpreet Dhaliwal, Surjit Singh","doi":"10.1089/jir.2025.0029","DOIUrl":"https://doi.org/10.1089/jir.2025.0029","url":null,"abstract":"<p><p>Kawasaki disease (KD) is an acute childhood vasculitis, commonly seen in children under the age of five. Despite extensive research over the past five decades, the pathogenesis of KD remains elusive. The objective of this epigenetic reanalysis study is to delineate common pathways involved in KD using a bioinformatics approach. Array datasets from the Gene Expression Omnibus repository were extracted and subjected to analysis using the Chip Analysis Methylation Pipeline in the R statistical tool for the identification of differential methylation probes and differential methylation regions. Adaptive immune genes <i>CD8B, RAG1, IL-7R, STAT1</i>, and <i>CCR7</i> were significantly hypermethylated in acute KD as compared to healthy controls. Gene enrichment analysis showed that genes involved in T-cell receptor activation and differentiation, antigen processing and presentation of MHC class I were hypermethylated, whereas neutrophil degranulation was hypomethylated in the acute phase of KD as compared to healthy controls. The proportion of neutrophils significantly increased, while the proportions of CD4 T-cells and CD8 T-cells decreased in the peripheral blood of children with acute KD as compared to healthy controls. Reduced proportions of CD4 T cells and CD8 T cells, as well as hypermethylation of their genes, have been observed in the peripheral blood of patients with acute KD. [Figure: see text].</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144015430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信