Journal of Interferon and Cytokine Research最新文献_第8页

Association Between Serum Chemokine Ligand 20 Levels and Disease Activity and Th1/Th2/Th17-Related Cytokine Levels in Rheumatoid Arthritis. 类风湿性关节炎患者血清趋化因子配体20水平与疾病活性和Th1/Th2/Th17相关细胞因子水平的相关性。

IF 2.3 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2023-11-01 Epub Date: 2023-10-09 DOI: 10.1089/jir.2023.0057

Liuqing Wang, Xuelian Hong, Hongwei Du

{"title":"Association Between Serum Chemokine Ligand 20 Levels and Disease Activity and Th1/Th2/Th17-Related Cytokine Levels in Rheumatoid Arthritis.","authors":"Liuqing Wang, Xuelian Hong, Hongwei Du","doi":"10.1089/jir.2023.0057","DOIUrl":"10.1089/jir.2023.0057","url":null,"abstract":"Rheumatoid arthritis (RA) is a type of arthritis autoimmune disease characterized by systemic chronic inflammation. C-C Chemokine ligand 20 (CCL20) is the same as most chemokines with immunomodulatory and inflammatory processes. The correlation of CCL20 in RA remains unclear. This study aimed to explore the association among levels of CCL20, T helper cell (TH) subset (Th1/Th2/Th17)-related cytokine levels, and clinical indices of RA disease activity. Serum CCL20 levels were quantified by enzyme-linked immunosorbent assay, and a flow-fluorescence technique was used to assess Th1/Th2/Th17-related cytokine levels. The serum CCL20 levels in patients were significantly higher than those in healthy controls and positively associated with C-reactive protein levels, erythrocyte sedimentation rate, and disease activity score-28 (DAS28). Patients with RA were categorized into 4 major groups, including remission, low, moderate, and high disease activity, with related DAS28 scores for each group. CCL20 levels of the disease moderate/high activity group were moderately positively correlated with IL-6 levels, but not with the other Th1/Th2/Th17-related cytokines. Serum CCL20 levels correlate strongly with RA disease activity and clinical inflammation and were significantly elevated in patients compared to healthy individuals. CCL20 plays a key role in the immune response of patients with RA and is, therefore, a potential biomarker of disease activity.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"512-517"},"PeriodicalIF":2.3,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41182793","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

Proinflammatory Bone Marrow Mesenchymal Stem Cell-Derived Exosomal miR-150-3p Suppresses Proinflammatory Polarization of Alveolar Macrophages in Sepsis by Targeting Inhibin Subunit Beta A. 炎性骨髓间充质干细胞来源的外泌体miR-150-3p通过靶向抑制素亚单位βA抑制脓毒症中肺泡巨噬细胞的炎性极化。

IF 2.3 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2023-11-01 Epub Date: 2023-10-11 DOI: 10.1089/jir.2023.0068

Guojin Liang, Yueying Feng, Wan Tang, Lifeng Yao, Changshun Huang, Yijun Chen

{"title":"Proinflammatory Bone Marrow Mesenchymal Stem Cell-Derived Exosomal miR-150-3p Suppresses Proinflammatory Polarization of Alveolar Macrophages in Sepsis by Targeting Inhibin Subunit Beta A.","authors":"Guojin Liang, Yueying Feng, Wan Tang, Lifeng Yao, Changshun Huang, Yijun Chen","doi":"10.1089/jir.2023.0068","DOIUrl":"10.1089/jir.2023.0068","url":null,"abstract":"Bone marrow mesenchymal stem cell (BMSC)-derived exosomes can protect lung tissues against sepsis, but its related mechanism remains elusive. BMSCs were primed with or without lipopolysaccharide (LPS) before extracting exosomes. The isolated exosomes were identified by transmission electron microscopy, nanoparticle tracking analysis, and western blot. LPS-stimulated macrophages were cocultured with exosomes for 24 h, followed by enzyme-linked immunosorbent assay, flow cytometry, and molecular experiments. Bioinformatics and luciferase assay were employed to investigate the interaction between miR-150-3p and inhibin subunit beta A (INHBA). MiR-150-3p expression was increased in exosomes in a proinflammatory environment. Exosomes suppressed proinflammatory polarization by downregulating IL-6, IL-1β, iNOS, and CD86, as well as promoted anti-inflammatory polarization by upregulating IL-10, ARG-1, and CD206 in LPS-stimulated macrophages. Such effects were more pronounced by LPS-primed exosomes, which was reversed in the absence of miR-150-3p. MiR-150-3p targeted INHBA. INHBA silencing decreased CD86 expression and increased CD206 expression in macrophages, but these effects were reversed by exosomal miR-150-3p inhibition. Proinflammatory BMSC-derived exosomal miR-150-3p suppressed proinflammatory polarization and promoted anti-inflammatory polarization of alveolar macrophages to attenuate LPS-induced sepsis by targeting INHBA.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"518-530"},"PeriodicalIF":2.3,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41203392","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

TRPM2-L Participates in the Interleukin-6 Pathway to Enhance Tumor Growth in Prostate Cancer by Hypoxia-Inducible Factor-1α. TRPM2-L参与白细胞介素-6通路通过缺氧诱导因子-1α促进癌症前列腺肿瘤生长。

IF 2.3 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2023-11-01 Epub Date: 2023-10-31 DOI: 10.1089/jir.2023.0088

Kai Cheng, Qingmei Jia, Christopher Batbatan, Zhihua Guo, Fengtao Cheng

{"title":"TRPM2-L Participates in the Interleukin-6 Pathway to Enhance Tumor Growth in Prostate Cancer by Hypoxia-Inducible Factor-1α.","authors":"Kai Cheng, Qingmei Jia, Christopher Batbatan, Zhihua Guo, Fengtao Cheng","doi":"10.1089/jir.2023.0088","DOIUrl":"10.1089/jir.2023.0088","url":null,"abstract":"Interleukin-6 (IL-6) can promote cell proliferation in prostate cancer (PCa). Full-length transient receptor potential melastatin 2 (TRPM2-L) is highly expressed in PCa. However, the association between IL-6 and TRPM2-L in PCa is unclear. Here, human PCa cell lines, PC-3 and DU-145, were treated with 10 μg/mL tocilizumab, an IL-6 receptor (IL-6R) inhibitor, and the TRPM2-L protein expression in cells was significantly decreased. Cells were stably transfected with TRPM2 short-interfering RNA (siRNA) and cell survival clearly declined. Recombinant IL-6 treatment weakened the effects of TRPM2-siRNA on cell survival. TRPM2-L binds directly to IL-6R in PC-3 and DU-145 cells. The protein expression of hypoxia-inducible factor-1α was suppressed by reduction with TRPM2-L in PC-3 and DU-145 cells. Human umbilical vein endothelial cells (HUVECs) were indirectly cocultured with PCa cells, and the invasion and angiogenic activity of HUVECs were enhanced after coculture with PCa cells. However, TRPM2-L reduction in PCa cells significantly decreased the invasion and angiogenic activity of HUVECs compared to the control coculture. In vivo, xenograft tumors were induced using PC-3 cells. Tocilizumab treatment or TRPM2-L reduction clearly suppressed tumor growth. Meanwhile, the injection of mouse recombinant IL-6 weakened the antitumor effects of TRPM2-L reduction. These data demonstrate that the IL-6/TRPM2-L axis in PCa tumor growth is important, and interference of the IL-6/TRPM2-L axis may be a novel approach for PCa therapy.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"495-511"},"PeriodicalIF":2.3,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71412569","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

LINC00641/miR-378a and Their Cross-Talk with TNF-α/IFN-γ as Potential Biomarkers in Ulcerative Colitis and Crohn's Diseases. LINC00641/miR-378a及其与TNF-α/IFN-γ的交互作用作为溃疡性结肠炎和克罗恩病的潜在生物标志物

IF 2.3 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2023-11-01 DOI: 10.1089/jir.2023.0097

Nour A Abdel Hameed, Olfat G Shaker, Nabil A Hasona

{"title":"LINC00641/miR-378a and Their Cross-Talk with TNF-α/IFN-γ as Potential Biomarkers in Ulcerative Colitis and Crohn's Diseases.","authors":"Nour A Abdel Hameed, Olfat G Shaker, Nabil A Hasona","doi":"10.1089/jir.2023.0097","DOIUrl":"10.1089/jir.2023.0097","url":null,"abstract":"The most well-known forms of inflammatory bowel disease (IBD) that affect the entire gastrointestinal tract are ulcerative colitis (UC) and Crohn's disease (CD). The serum profile of inflammatory biomarkers and noncoding RNA and their role in the propagation of the inflammatory process remains controversial. Thus, this study was designed to examine the relationship between hematological profile, C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interferon-gamma (INF-γ), and the expression of LINC00641 and miR-378a in individuals with IBDs. In addition, we elucidated the correlation between the expression of LINC00641 and miR-378a and the biochemical variables analyzed. This retrospective study analyzed 94 unrelated participants. Group I included healthy controls, Group II consisted of participants diagnosed with UC, and Group III consisted of participants diagnosed with CD. Patients with IBDs experienced significant elevations in CRP, total leukocyte count, platelets, erythrocyte sedimentation rate, TNF-α, and INF-γ. However, participants with IBD had lower hemoglobin and albumin levels than healthy control participants. Moreover, the expression levels of LINC00641 and miR-378a were elevated in participants with IBD, with a significant difference between participants with IBD and healthy controls. The most striking observation was a clear association between serum LINC00641 and miR-378a levels and the biochemical variables assessed. This study demonstrated a positive correlation between the expression of LINC00641/miR-378a and TNF-α in patients with UC and CD patients. This study suggests that LINC00641 and miR-378a are prospective biomarkers and noninvasive screening tools for IBDs, which may help predict the progression of complications.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":"43 11","pages":"531-537"},"PeriodicalIF":2.3,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92154760","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

The Many Faces of Oligoadenylate Synthetases. 低聚腺苷酸合成酶的多面性。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2023-11-01 Epub Date: 2023-09-25 DOI: 10.1089/jir.2023.0098

Saumendra N Sarkar, Munesh K Harioudh, Lulu Shao, Joseph Perez, Arundhati Ghosh

引用次数: 0

Annihilation of Non-small Cell Lung Cancer by NKG2D CAR-T Cells Produced from T Cells from Peripheral Blood of Healthy Donors. 健康供体外周血T细胞产生的NKG2D CAR-T细胞对非小细胞肺癌癌症的杀伤作用。

IF 2.3 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2023-10-01 DOI: 10.1089/jir.2023.0043

Jinhong Jiang, Yonghua Liu, Yuxiao Zeng, Bingmu Fang, Yongping Chen

{"title":"Annihilation of Non-small Cell Lung Cancer by NKG2D CAR-T Cells Produced from T Cells from Peripheral Blood of Healthy Donors.","authors":"Jinhong Jiang, Yonghua Liu, Yuxiao Zeng, Bingmu Fang, Yongping Chen","doi":"10.1089/jir.2023.0043","DOIUrl":"10.1089/jir.2023.0043","url":null,"abstract":"Some progress has been made in immunotherapy with chimeric antigen receptor (CAR)-T cells targeting NKG2D-NKG2DL with the purpose of eradicating solid tumors. Non-small cell lung cancer (NSCLC) has been shown to express NKG2DL. This study hence evaluated the therapeutic effect of NKG2D CAR-T cells on NSCLC. Accordingly, NKG2D CAR-T cells were obtained from diverse human autologous T cell sources. T cells from peripheral blood T lymphocytes of healthy volunteers (without NKG2D CAR insertion) were used as NT-T cells. Coculture of effector cells (CAR-T cells or NT-T cells) with target cells (NSCLC cells such as PC-9 or NCL-H460 cells) was performed at different ratios. The cytotoxicity of CAR-T cells was examined using lactate dehydrogenase assay kits. Murine xenograft assay was conducted to investigate the in vivo antitumor effect of CAR-T cells. Cytokines secreted from CAR-T cells were assessed by enzyme-linked immunosorbent assay. CAR-T cell infiltration into xenografts was observed through immunochemical assay. Based on the results, NKG2DL was highly expressed in NSCLC cells. Compared with NT-T cells, NKG2D CAR-T cells from different sources of T cells delivered stronger toxicity, and secreted more effector and memory function-related cytokines to NSCLC cells, and those from the peripheral blood of healthy donors (H-T cells) exhibited the strongest effect. Furthermore, compared with NT-T cells, H-T cells and NKG2D CAR-T cells from NSCLC patients' peripheral blood diminished tumor, improved survival, increased body weight and tumor-infiltrating capacity, and upregulated serum IFN-γ level in NOG mice. Collectively speaking, NKG2D CAR-T cells exhibit a robust effect on eradicating NSCLC in a NKG2DL-dependent manner, thus making themselves a promising therapeutic candidate for NSCLC patients.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":"43 10","pages":"445-454"},"PeriodicalIF":2.3,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41203395","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

A Conversation with Judy Lieberman. 与朱迪·利伯曼的对话。

IF 2.3 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2023-10-01 DOI: 10.1089/jir.2023.29055.int

引用次数: 0

The Role and Potential Regulatory Mechanism of STING Modulated Macrophage Apoptosis and Differentiation in Severe Acute Pancreatitis-Associated Lung Injury. STING调节巨噬细胞凋亡和分化在严重急性胰腺炎相关肺损伤中的作用及其潜在调控机制。

IF 2.3 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2023-10-01 DOI: 10.1089/jir.2023.0077

Yiqiu Peng, Yingying Li, Yuxi Yang, Tingjuan Shi, Ruixia Liu, Yingyi Luan, Chenghong Yin

{"title":"The Role and Potential Regulatory Mechanism of STING Modulated Macrophage Apoptosis and Differentiation in Severe Acute Pancreatitis-Associated Lung Injury.","authors":"Yiqiu Peng, Yingying Li, Yuxi Yang, Tingjuan Shi, Ruixia Liu, Yingyi Luan, Chenghong Yin","doi":"10.1089/jir.2023.0077","DOIUrl":"10.1089/jir.2023.0077","url":null,"abstract":"This study aims to investigate the role of STING in promoting macrophage apoptosis and regulating macrophage polarization in severe acute pancreatitis (SAP)-associated lung injury in vitro and in vivo. A murine model was established by intraperitoneal injection of caerulein and lipopolysaccharide (LPS). Meanwhile, ANA-1 cells were stimulated with LPS to induce apoptosis in vitro. More primary alveolar macrophages underwent apoptosis and M1 macrophage polarization in the SAP group compared with the control group, which was reversed by inhibiting STING. When ANA-1 cells were induced into M2-type macrophages, the reduction of M1 macrophage markers was accompanied by a decrease of LPS-induced apoptosis. Finally, the inhibitory effect of C-176 on STING ameliorates lung injury and inflammation by adjusting macrophage polarization and rescuing apoptosis. Therefore, inhibiting STING could be a new therapeutic strategy for treating acute pancreatitis-associated lung injury.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":"43 10","pages":"455-468"},"PeriodicalIF":2.3,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41203396","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

DNA-Dependent Interferon Induction and Lung Inflammation in Bordetella pertussis Infection. 百日咳杆菌感染中DNA依赖性干扰素的诱导和肺部炎症。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2023-10-01 Epub Date: 2023-08-31 DOI: 10.1089/jir.2023.0066

Jeremy Ardanuy, Karen M Scanlon, Ciaran Skerry, Nicholas H Carbonetti

{"title":"DNA-Dependent Interferon Induction and Lung Inflammation in Bordetella pertussis Infection.","authors":"Jeremy Ardanuy, Karen M Scanlon, Ciaran Skerry, Nicholas H Carbonetti","doi":"10.1089/jir.2023.0066","DOIUrl":"10.1089/jir.2023.0066","url":null,"abstract":"Pertussis, caused by Bordetella pertussis, is a resurgent respiratory disease but the molecular mechanisms underlying pathogenesis are poorly understood. We recently showed the importance of type I and type III interferon (IFN) induction and signaling for the development of lung inflammation in B. pertussis-infected mouse models. Classically, these IFNs are induced by signaling through a variety of pattern recognition receptors (PRRs) on host cells. Here, we found that the PRR signaling adaptor molecules MyD88 and TRIF contribute to IFN induction and lung inflammatory pathology during B. pertussis infection. However, the PRRs Toll-like receptors (TLR) 3 and TLR4, which signal through TRIF and MyD88, respectively, played no role in IFN induction. Instead, the DNA-sensing PRRs, TLR9 and STING, were important for induction of type I/III IFN and promotion of inflammatory pathology, indicating that DNA is a major inducer of lung IFN responses in B. pertussis infection. These results increase our understanding of this host-pathogen interaction and identify potential targets for host-directed therapies to reduce B. pertussis-mediated pathology.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"478-486"},"PeriodicalIF":1.9,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10599430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10483283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Call for Special Issue Papers: The "Yin-Yang" Activities of Tumor-Induced Inflammatory Cytokines for Cancer Immunotherapy, Detection and Prognosis. 特刊论文征集：癌症免疫治疗、检测和预后肿瘤诱导炎症细胞因子的“阴阳”活性。

IF 2.3 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2023-10-01 DOI: 10.1089/jir.2023.29056.cfp

Yan Ma, Sanjay Mukherjee, Jing Ma

引用次数: 0