Journal of Interferon and Cytokine Research最新文献

Embryonic Lethal Abnormal Visual-Like Protein 1 Aggravates Caerulein-Induced AR42J Cell Injury and Macrophage M1 Polarization to Accelerate Acute Pancreatitis by Upregulating TRAF6. 胚胎致命性异常视觉样蛋白 1 通过上调 TRAF6 加剧了 Caerulein 诱导的 AR42J 细胞损伤和巨噬细胞 M1 极化，从而加速了急性胰腺炎的发生。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-11-13 DOI: 10.1089/jir.2024.0149

Wenyong Zhou, Xin Wang, Bin Yan, Yue Sun

{"title":"Embryonic Lethal Abnormal Visual-Like Protein 1 Aggravates Caerulein-Induced AR42J Cell Injury and Macrophage M1 Polarization to Accelerate Acute Pancreatitis by Upregulating TRAF6.","authors":"Wenyong Zhou, Xin Wang, Bin Yan, Yue Sun","doi":"10.1089/jir.2024.0149","DOIUrl":"https://doi.org/10.1089/jir.2024.0149","url":null,"abstract":"Tumor necrosis factor receptor-associated factor 6 (TRAF6) has been found to promote the progression of acute pancreatitis (AP). However, its underlying molecular mechanisms in AP need to be further revealed. Caerulein-induced AR42J cells were used to construct AP cell models. Cell viability and apoptosis were measured by Cell Counting Kit 8 assay and flow cytometry. Levels of inflammatory factors and oxidative stress-related markers were assessed. The medium of AR42J cells was collected for coculturing RAW264.7 cells. Macrophage marker CD86+ cell rates were checked with flow cytometry. The levels of TRAF6, embryonic lethal abnormal visual-like protein 1 (ELAVL1), and inducible nitric oxide synthase (iNOS) were examined by Western blot or quantitative real-time polymerase chain reaction. RNA immunoprecipitation assay was performed to evaluate the interaction between ELAVL1 and TRAF6. TRAF6 mRNA stability was tested using actinomycin D treatment. Caerulein treatment suppressed viability, induced AR42J cell apoptosis, inflammation, oxidative stress, and accelerated macrophage M1 polarization. TRAF6 downregulation could alleviate caerulein-induced AR42J cell injury and macrophage M1 polarization. ELAVL1 interacted with TRAF6 to stabilize its expression. Meanwhile, ELAVL1 knockdown relieved caerulein-induced AR42J cell injury and macrophage M1 polarization, while these effects were abolished by TRAF6 overexpression. TRAF6, stabilized by ELAVL1, promoted caerulein-induced AR42J cell injury and macrophage M1 polarization, suggesting that it might accelerate AP9 progression.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622229","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

Unraveling the Multifaceted Roles of Atypical Chemokine Receptors in Breast Cancer. 揭示非典型趋化因子受体在乳腺癌中的多重作用

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-11-11 DOI: 10.1089/jir.2024.0186

Qinan Yin, Yisha Yang, Zhifeng Qu, Mouna Ouchari, Li Zeng, Siya Tang, Jiayu Zheng, Shunshun Zhang, Haodi Ma, Youyou Chen, Jiayi Wang, Linlin Shi, Xuewei Zheng

{"title":"Unraveling the Multifaceted Roles of Atypical Chemokine Receptors in Breast Cancer.","authors":"Qinan Yin, Yisha Yang, Zhifeng Qu, Mouna Ouchari, Li Zeng, Siya Tang, Jiayu Zheng, Shunshun Zhang, Haodi Ma, Youyou Chen, Jiayi Wang, Linlin Shi, Xuewei Zheng","doi":"10.1089/jir.2024.0186","DOIUrl":"https://doi.org/10.1089/jir.2024.0186","url":null,"abstract":"Breast cancer (BC) remains one of the most prevalent and deadly malignancies among women globally. A deeper understanding of the molecular mechanisms driving BC progression and metastasis is essential for the development of effective therapeutic strategies. While traditional chemokine receptors are well known for their roles in immune cell migration and positioning, atypical chemokine receptors (ACKRs) have recently gained attention as key modulators in cancer-related processes. Unlike conventional receptors, ACKRs-comprising ACKR1, ACKR2, ACKR3, and ACKR4-primarily function by scavenging chemokines, regulating their availability, and modulating receptor signaling in a ligand-independent manner. This review aims to elucidate the roles of ACKRs in BC, focusing on their influence on the tumor microenvironment (TME), cancer cell proliferation, survival, metastasis, and angiogenesis. Additionally, we will explore the potential of ACKRs as diagnostic and prognostic markers and assess their viability as therapeutic targets. By synthesizing recent research findings and highlighting future research directions, this review seeks to provide a comprehensive understanding of the significance of ACKRs in BC and underscore the need for continued investigation into their therapeutic potential.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622232","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

Nerve Growth Factor from Pancreatic Cancer Cells Promotes the Cancer Progression by Inducing Nerve Cell-Secreted Interleukin-6. 胰腺癌细胞的神经生长因子通过诱导神经细胞分泌白细胞介素-6促进癌症进展

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-11-08 DOI: 10.1089/jir.2024.0154

Jianbiao Xu, Yun Shang, Tongmin Wang, Jianlin Song, Wenchuan Zhu, Yunjun Zeng, Jianxun Wang, Xiaochun Yang

{"title":"Nerve Growth Factor from Pancreatic Cancer Cells Promotes the Cancer Progression by Inducing Nerve Cell-Secreted Interleukin-6.","authors":"Jianbiao Xu, Yun Shang, Tongmin Wang, Jianlin Song, Wenchuan Zhu, Yunjun Zeng, Jianxun Wang, Xiaochun Yang","doi":"10.1089/jir.2024.0154","DOIUrl":"https://doi.org/10.1089/jir.2024.0154","url":null,"abstract":"Pancreatic cancer (PC) is a cancer with a poor prognosis, and nerve growth factor (NGF) is involved in the pathogenesis of PC within the unknown exact role. Herein, SW1990 cells and PC12 cells were co-cultured using transwell co-culture system and subsequently revealed that NGF was overexpressed in SW1990 cells and promoted PC12 cell proliferation. Knockdown of NGF expression in SW1990 cells using lentiviral shRNA effectively inhibited NGF expression in SW1990 cells and reduced its stimulatory effect on PC12 cell proliferation. Additionally, NGF in SW1990 cells increased the expression of IL-6, dopamine, and c-FOS, as well as decreased the level of lactate dehydrogenase, in PC12 cells, whereas the inhibition of NGF expression significantly reduced the levels of IL-6, dopamine and c-FOS, indicating the critical role of IL-6/STAT3 signaling in PC progression. Finally, cell proliferation, migration, and invasion were assessed using cell counting kit-8, scratch, and Transwell assays, which showed that activated neurons promoted the proliferation, migration, invasion, and NGF secretion of SW1990 cells through the IL-6/STAT3 pathway. The results revealed that NGF secreted by PC cells played a pivotal role in PC progression via regulating activated neural cells-secreted IL-6, providing new theoretical insights for the treatment of PC.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605157","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

IL-4 Downregulates PD-L1 Level Via SOCS1 Upregulation-Induced JNK Deactivation to Enhance Antitumor Immunity in In Vitro Colorectal Cancer. IL-4 通过 SOCS1 上调诱导 JNK 失活下调 PD-L1 水平，增强体外结直肠癌抗肿瘤免疫力

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-11-01 Epub Date: 2024-10-04 DOI: 10.1089/jir.2024.0110

Ruiyan Huang, Baofan Zhang, Wanchun Ye, Zhongjie Tang, Qingsong Zheng

{"title":"IL-4 Downregulates PD-L1 Level Via SOCS1 Upregulation-Induced JNK Deactivation to Enhance Antitumor Immunity in In Vitro Colorectal Cancer.","authors":"Ruiyan Huang, Baofan Zhang, Wanchun Ye, Zhongjie Tang, Qingsong Zheng","doi":"10.1089/jir.2024.0110","DOIUrl":"10.1089/jir.2024.0110","url":null,"abstract":"Interleukin-4 (IL-4) controls cell growth and immune system regulation in tumorigenesis and can inhibit the growth of colon cancer cell lines, but the possible mechanism is unclear. In this study, we investigated the possible mechanism of IL-4 in colorectal cancer (CRC) through in vitro experiments. CRC cells received treatment with IL-4 (50 ng/mL), investigating the suppressor of cytokine signaling 1 (SOCS1)-related mechanism underlying the role of IL-4 in the progression and immunosuppression of CRC. The malignant processes of CRC cells and CD8+T cell-mediated immune response in CRC cells were determined by CCK-8, Transwell, wound healing, and flow cytometry assays. Programmed death ligand 1 (PD-L1), SOCS1 expressions, and c-Jun N-terminal kinase (JNK) activation in CRC cells were analyzed by quantitative reverse transcription polymerase chain reaction and/or Western blot. IL-4 repressed the malignant processes, yet promoted the apoptosis of CRC cells. Besides, IL-4 downregulated PD-L1 level, upregulated SOCS1 level, and restrained JNK activation in CRC cells, while enhancing CRC cell-killing effect of CD8+T cells. IL-4-induced effects on the aforementioned malignant processes of CRC cells and the killing effect of CD8+T cells toward CRC cells were all reversed when SOCS1 was knocked down in the CRC cells. IL-4 downregulates PD-L1 level via SOCS1 upregulation-induced JNK deactivation to enhance antitumor immunity in in vitro CRC. The study provides a theoretical basis for the clinical application of IL-4 in antitumor immunity in CRC.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"486-495"},"PeriodicalIF":1.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372066","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

Dual Time-Dependent Effects of Interleukin-33 Administration on the Kidney Postmyocardial Infarction. 心肌梗死后服用白细胞介素-33对肾脏的双重时间依赖效应

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-11-01 Epub Date: 2024-09-23 DOI: 10.1089/jir.2024.0127

Ghadir Amin, Rana Ghali, Nada J Habeichi, Ziad Mallat, George W Booz, Fouad A Zouein

{"title":"Dual Time-Dependent Effects of Interleukin-33 Administration on the Kidney Postmyocardial Infarction.","authors":"Ghadir Amin, Rana Ghali, Nada J Habeichi, Ziad Mallat, George W Booz, Fouad A Zouein","doi":"10.1089/jir.2024.0127","DOIUrl":"10.1089/jir.2024.0127","url":null,"abstract":"Kidney damage is a serious prevalent complication that occurs after a myocardial infarction (MI) and is associated with worse outcomes. Interleukin-33 (IL-33), a member of the IL-1 superfamily, functions as an alarmin that is released upon necrosis or tissue damage to alert immune cells expressing the ST2L receptor. IL-33 is increased in kidney disease, and recent studies have shown that the IL-33/ST2 axis is instrumental in both disease progression and repair. In this study, we investigated the effect of IL-33 administration on kidneys in C57BL6/J male mice 4 and 7 days after the induction of MI. The mice received either IL-33 or vehicle (PBS) treatment. Cardiac systolic function and systemic inflammation were assessed, and kidneys were subjected to histological and molecular analysis. The administration of IL-33 for 4 days post-MI improved renal structure consistent with reduced expression of profibrotic markers, reduced apoptosis, and increased expression of the anti-inflammatory cytokine IL-4. In addition, IL-33 administration enhanced the levels of Sirtuin3, nicotinamide phosphoribosyltransferase, and the renal nicotinamide adenine dinucleotide pool which are critical for mitochondrial function and energy production, indicating metabolic benefits. However, this protection seems to be lost with the continued administration of IL-33 for 7 days post-MI coinciding with aggravated cardiac dysfunction and increased systemic inflammation. These findings demonstrate that while IL-33 treatment can help improve kidney damage post-MI in the short term, extended treatment may not be beneficial. This may be due to the direct effects of IL-33 on the kidneys or indirectly mediated by adverse cardiac remodeling influencing the cardiorenal crosstalk.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"496-509"},"PeriodicalIF":1.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289343","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

Multifarious Aspect of Cytokines as an Immuno-Therapeutic for Various Diseases. 细胞因子作为各种疾病免疫疗法的多面性。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-11-01 Epub Date: 2024-10-11 DOI: 10.1089/jir.2024.0090

Yash Sharma, Kumud Bala

引用次数: 0

Integrated Analysis of Noncoding RNAs (PVT-1 and miR-200c) and Their Correlation with STAT4/IL-6 Axis as Reliable Biomarkers for COVID-19 Severity. 综合分析非编码 RNA（PVT-1 和 miR-200c）及其与 STAT4/IL-6 轴的相关性，作为 COVID-19 严重程度的可靠生物标志物。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-11-01 Epub Date: 2024-09-20 DOI: 10.1089/jir.2024.0132

Ghada Ayeldeen, Bahaa Mohammed Badr, Mohamed R Herzalla, Eman Amer, Mahmoud Elsabahy, Olfat G Shaker, Nabil A Hasona

{"title":"Integrated Analysis of Noncoding RNAs (PVT-1 and miR-200c) and Their Correlation with STAT4/IL-6 Axis as Reliable Biomarkers for COVID-19 Severity.","authors":"Ghada Ayeldeen, Bahaa Mohammed Badr, Mohamed R Herzalla, Eman Amer, Mahmoud Elsabahy, Olfat G Shaker, Nabil A Hasona","doi":"10.1089/jir.2024.0132","DOIUrl":"10.1089/jir.2024.0132","url":null,"abstract":"Inefficient control of elevated inflammatory mediators in coronavirus disease 2019 (COVID-19) has led to health complications, prompting the exploration of efficient biomarkers for monitoring this condition. We herein sought to investigate the implications of plasmacytoma variant translocation 1 (PVT-1), microRNA-200c (miR-200c), signal transducer and activator of transcription 4 (STAT-4), and interleukin-6 (IL-6), as well as how they correlated with creatinine, C-reactive protein (CRP), and lactate dehydrogenase (LDH) activity to identify biomarkers able to the early prognosis and diagnosis of COVID-19. Our study included a total of 105 infected COVID-19 patients and 35 healthy subjects as controls. Individuals with COVID-19 showed a significant increase in CRP, creatinine, and LDH activity. In addition, COVID-19 patients exhibited significantly higher levels of IL-6. These patients also demonstrated notably elevated expressions of miR-200c and PVT-1. The expression level of STAT4 decreased in the COVID-19 patients, and this decrease was negatively correlated with creatinine and LDH activity. The levels of miR-200c and PVT-1 expressions, and their connections with IL-6 and STAT4 levels, increased significantly with the severity of COVID-19 cases. In addition, receiver operating characteristic analysis showed that PVT-1 and miR-200c could be reliable biomarkers for determining the severity of COVID-19.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"510-517"},"PeriodicalIF":1.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289344","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 Impact of Chemokine-Like Receptor 1 Gene Knockout on Lipopolysaccharide-Induced Epididymo-Orchitis in Mice. 类趋化因子受体 1 基因敲除对脂多糖诱导的小鼠附睾炎的影响

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-10-29 DOI: 10.1089/jir.2024.0152

Zhonglin Xiao, Jie Chen, Xiujun Fan, Wei Zhao, Chiawei Chu, Jian V Zhang

{"title":"The Impact of Chemokine-Like Receptor 1 Gene Knockout on Lipopolysaccharide-Induced Epididymo-Orchitis in Mice.","authors":"Zhonglin Xiao, Jie Chen, Xiujun Fan, Wei Zhao, Chiawei Chu, Jian V Zhang","doi":"10.1089/jir.2024.0152","DOIUrl":"10.1089/jir.2024.0152","url":null,"abstract":"This comprehensive study delved into the pivotal function of chemokine-like receptor 1 (CMKLR1) in lipopolysaccharide (LPS)-triggered epididymo-orchitis in mice. Upon LPS exposure, wild-type (WT) mice exhibited marked elevations in serum pro-inflammatory markers, including G-CSF, IL-6, and RANTES, along with heightened levels of TNF-α and IL-6 in testicular and epididymal tissues, which accompanied by pronounced structural damage within the testicular tissue and a concurrent decline in serum testosterone, estradiol (E2) levels, and testicular steroid synthetase expression. Remarkably, Cmklr1 gene ablation intensified the pro-inflammatory response in the serum (especially IFN-γ), testes, and epididymis of epididymo-orchitis models. Furthermore, Cmklr1 deficiency uniquely induced structural alterations within the epididymis, which is absent in the WT model. This genetic manipulation also exacerbated the decline in serum testosterone and E2 levels and testicular steroid synthase activity. While chemerin levels were significantly diminished in WT epididymo-orchitis models, Cmklr1 knockout had no discernible effect on chemerin expression in the model. In addition, a noteworthy observation was the elevation of the serum low density lipoprotein/high density lipoprotein (LDL/HDL) ratio in Cmklr1-deficient mice. Collectively, these findings underscore that the lack of chemerin/CMKLR1 signaling axis could potentially worsen the symptoms during LPS-induced epididymo-orchitis, highlighting its potential as a therapeutic target in related pathologies.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522124","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

Overview of Immunological Response in Urological Membranous Nephropathy: Focus on Cytokine and Treatment Options. 泌尿系统膜性肾病的免疫反应概述：关注细胞因子和治疗方案。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-10-25 DOI: 10.1089/jir.2024.0165

Chao Luo, Chengcheng Wei, Zhaoxian He, Renlei Feng

引用次数: 0

A Message from Editor-in-Chief David L. Woodland. 主编 David L. Woodland 的致辞。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-10-17 DOI: 10.1089/jir.2024.0193

David L Woodland

引用次数: 0