Cytokine最新文献

{"title":"Role of interleukin-6, serum ferritin, and d-dimer in hospitalized COVID-19 patients","authors":"Praveen Gupta ,&nbsp;Anunay Gupta ,&nbsp;Sandeep Bansal ,&nbsp;Monica Sharma ,&nbsp;Sumita Saluja ,&nbsp;Ira Balakrishnan ,&nbsp;Kapil Gupta","doi":"10.1016/j.cyto.2024.156776","DOIUrl":"10.1016/j.cyto.2024.156776","url":null,"abstract":"<div><h3>Background</h3><div>Various studies have observed an association between interleukin-6 (IL-6), serum ferritin, <span>d</span>-dimer, and in-hospital mortality in COVID-19 patients. However, multivariate regression analysis was not done in the majority of the studies, Also, the role of interleukin-6 (IL-6), serum ferritin, and <span>d</span>-dimer in hospitalized COVID-19 patients was not adequately studied and reported from our region.</div></div><div><h3>Method</h3><div>It was a retrospective cohort study in which the serum IL-6, serum ferritin, and <span>d</span>-dimer of 305 hospitalized COVID-19 patients were analyzed, and their association with mortality was determined.</div></div><div><h3>Results</h3><div>In COVID-19 patients, the levels of IL-6 (<em>P = 0.007</em>), serum ferritin (<em>P = 0.011</em>), and <span>d</span>-dimer (<em>P = 0.004</em>) were significantly elevated in patients with severe SARS-CoV-2 illness (SpO2 &lt; 90 % at admission). IL-6 levels were significantly elevated (186 pg/ml vs. 215 pg/ml, <em>P = 0.003</em>) in non-survivors compared to survivors. However, <span>d</span>-dimer (mg/ml) (<em>P = 0.129)</em> and serum ferritin (mg/ml) (<em>P = 0.051</em>) levels were similar between the two groups. The ROC curve (receiver operating characteristic curve) analysis showed a significant but poor area under the curve (AUC) between elevated IL-6 (&gt;208 pg/ml) and in-hospital mortality (<em>P &lt;</em> 0.008, AUC = 0.61). Kaplan-Meir survival analysis showed poor survival in patients with elevated IL-6 (&gt;208 pg/ml) (<em>P<!--> </em>by log-rank: 0.010) and elevated <span>d</span>-dimer (&gt;1780 mg/ml) (<em>P</em> by log-rank: 0.036). The multivariate cox-regression analysis did not show any association between IL-6, serum ferritin, <span>d</span>-dimer, and in-hospital mortality (<em>P</em> &gt; 0.05). Also, no association was found between serum levels of IL-6, serum ferritin, <span>d</span>-dimer, and the use of a ventilator (<em>P &gt; 0.05)</em> and the severity of SARS-CoV-2 illness (<em>P &gt; 0.05</em>) on multivariate binary logistic regression analysis.</div></div><div><h3>Conclusion</h3><div>In this study, the serum levels of IL-6, serum ferritin, and <span>d</span>-dimer were not associated with in-hospital mortality in hospitalized COVID-19 patients on multivariate cox-regression analysis, and were the markers of severe SARS-CoV-2 illness.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156776"},"PeriodicalIF":3.7,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142386847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnostic value of IFN-gamma in tuberculous pleural effusion","authors":"Hongchun Huang ,&nbsp;Yonghuai Li ,&nbsp;Xiaohui Cao ,&nbsp;Minghui Yang ,&nbsp;Jilu Shen","doi":"10.1016/j.cyto.2024.156773","DOIUrl":"10.1016/j.cyto.2024.156773","url":null,"abstract":"<div><h3>Background</h3><div>Simple, rapid, and accurate diagnosis of tuberculous pleural effusion (TPE) remains challenging. This study aimed to determine the accuracy of IFN-γ in diagnosing TPE.</div></div><div><h3>Methods</h3><div>We quantified the expression of interferon-gamma (IFN-γ) in blood (B), adenosine deaminase (ADA), and IFN-γ in pleural effusions (PE) from 25 TPE patients and 31 non-TPE patients using a combination of immunological assays and flow cytometric analysis. The diagnostic performance of these three biomarkers was evaluated using receiver operating characteristic (ROC) curves.</div></div><div><h3>Results</h3><div>We found that IFN-γ levels in blood and pleural fluid were higher in the TPE group than in the non-TPE group. The mean concentration of IFN-γ in pleural fluid of the TPE group was 3140.90 (1817.94, 6611.05) pg/mL, while that of the non-TPE group was 4.91 (0.69, 8.6) pg/mL), and the difference was statistically significant (z = 6.39, P &lt; 0.001). The mean blood IFN-γ was 40.19 (16.45, 59.08) pg/mL in the TPE group and 2.76 (1.96, 6.02) pg/mL in the non-TPE group, which was statistically different (z = 5.12, P &lt; 0.001). The area under the ROC curve (AUC) for pleural fluid IFN-γ, blood IFN-γ, and ADA were 0.999 (95 % CI: 0.994–1.00), 0.901 (95 % CI: 0.798–1.00) and 0.996 (95 % CI: 0.987–1.00), respectively.</div></div><div><h3>Conclusion</h3><div>This study confirms that IFN-γ has high diagnostic validity in patients with TPE and can potentially be an excellent biomarker.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156773"},"PeriodicalIF":3.7,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictive value of IL-8 for mortality risk in elderly sepsis patients of emergency department","authors":"Xiangqun Zhang,&nbsp;Junyu Wang ,&nbsp;Shubin Guo","doi":"10.1016/j.cyto.2024.156774","DOIUrl":"10.1016/j.cyto.2024.156774","url":null,"abstract":"<div><h3>Background</h3><div>Sepsis significantly impacts morbidity and mortality, particularly among older adults. Despite extensive research, early recognition and prognosis prediction of sepsis remain challenging. IL-8, a chemokine produced by inflammatory cells like monocytes and endothelial cells, has shown potential in predicting mortality in sepsis patients, though its role in elderly sepsis remains unexplored.</div></div><div><h3>Objectives</h3><div>The present study aimed to explore the predictive ability of interleukin-8 (IL-8) for mortality risk in elderly septic patients.</div></div><div><h3>Methods</h3><div>220 elderly sepsis patients were included in the present study. Serum samples were obtained within 1 h of admission to assess serum IL-8, white blood cell (WBC), procalcitonin (PCT), C-reactive protein (CRP), and lactic acid (LAC) levels. The Sequential Organ Failure Score (SOFA) and Acute Physiological and Chronic Health Assessment II (APACHE II) were recorded. Logistic regression analysis was employed to identify independent predictors of mortality within 28 days for elderly patients diagnosed with sepsis. Further, the capacity of these factors to predict 28-day mortality within this patient cohort was evaluated.</div></div><div><h3>Results</h3><div>SOFA score, APACHE II score, LAC, and IL-8 were all significant independent predictors for 28-day mortality in elderly sepsis patients (P &lt; 0.05). The AUC of the ROC curve for IL-8 was calculated to be 0.701, indicating a moderately predictive performance. In comparison, the AUC for LAC was marginally higher at 0.708. Nevertheless, the results of the statistical analysis revealed no significant difference in the predictive value between IL-8 and LAC. Moreover, the present findings indicate that the combined assessment of IL-8 and SOFA score demonstrated superior predictive value for mortality compared to using IL-8 alone.</div></div><div><h3>Conclusions</h3><div>IL-8 LAC, APACHE II, and SOFA can be considered independent predictors factors for mortality of elderly sepsis patients. Utilizing the combination of IL-8 and SOFA demonstrates a heightened predictive capability compared to using any single index alone.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156774"},"PeriodicalIF":3.7,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The surfactant protein B polymorphisms (rs7316 and rs1130866) and their correlation with disease progression of COVID-19","authors":"Amir Behrouzi ,&nbsp;Fatemeh Sakhaee ,&nbsp;Morteza Ghazanfari Jajin ,&nbsp;Iraj Ahmadi ,&nbsp;Enayat Anvari ,&nbsp;Fattah Sotoodehnejadnematalahi ,&nbsp;Abolfazl Fateh","doi":"10.1016/j.cyto.2024.156775","DOIUrl":"10.1016/j.cyto.2024.156775","url":null,"abstract":"<div><h3>Background</h3><div>It is critical to examine the pathogenic pathways in coronavirus disease 2019 (COVID-19) that resulted in the development of severe lung injury. Surfactant protein B (<em>SFTPB</em>) is a vital component for sustaining life and serves pivotal functions in the host’s defensive mechanisms and alveolar surface tension reduction. Our study aimed to determine the effect of <em>SFTPB</em> rs7316 and rs1130866 variants on the course of disease in COVID-19 patients.</div></div><div><h3>Methods</h3><div>The study cohort comprised 3,184 individuals diagnosed with COVID-19. We employed the RFLP approach to determine the variations of the <em>SFTPB</em> genes.</div></div><div><h3>Results</h3><div>SFTPB rs7316 did not exhibit a statistically significant correlation with COVID-19 mortality across different inheritance models. But, after making more changes for SARS-CoV-2 variants, it was found that there was a strong link between the TT and TC genotypes of <em>SFTPB</em> rs7316 and death rates, especially for the Delta variant. Furthermore, our study’s findings indicate a significant association between the <em>SFTPB</em> rs1130866 G allele and an elevated risk of mortality in COVID-19 across all variants of SARS-CoV-2.</div></div><div><h3>Conclusions</h3><div>The use of the SFTPB rs1130866 marker has the potential to facilitate the prediction of COVID-19 severity. On the other hand, for SFTPB rs7316, this kind of prediction seems to depend on the particular SARS-CoV-2 variants.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156775"},"PeriodicalIF":3.7,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378850","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":"Chemerin, TNF − α and the degree of albuminuria in patients with diabetic kidney disease","authors":"Fatima El-Tahir ,&nbsp;Asmaa Esh ,&nbsp;Adel Ghorab ,&nbsp;Ali M Shendi","doi":"10.1016/j.cyto.2024.156772","DOIUrl":"10.1016/j.cyto.2024.156772","url":null,"abstract":"<div><h3>Background</h3><div>Chronic inflammation has been increasingly recognized as an essential pathogenic mechanism for the development and progression of diabetic kidney disease (DKD). Chemerin is an adipokine which has been suggested to be related to inflammation and has been correlated with the development of diabetic complications. We aimed to explore the potential links between chemerin, TNF – α, as a marker of systemic inflammation, and the level of albuminuria in patients with type 2 diabetes mellitus (T2DM).</div></div><div><h3>Method</h3><div>The study included 84 patients with T2DM and 10 normoalbuminuric non-diabetic controls. Demographic, clinical and laboratory data including chemerin and TNF-α levels were collected.</div></div><div><h3>Results</h3><div>A total of 84 diabetic patients were enrolled, 32 males (38.1 %), with mean age 57.9 ± 10.7 years. They were divided into 3 groups: A1: 14 with normalbuminuria, A2: 27 with microalbuminuria, and A3: 43 with macroalbuminuria (uACR &lt; 30, 30–300 and &gt; 300 mg/gm respectively). Chemerin and TNF-α levels increased with the progress of albuminuria (control: 21.3 (14.7 –77), A1: 794 (683–925), A2: 1150 (962.9 – 1221.5) and A3: 1466 (1197.5 – 2002.5) ng/ml; p &lt; 0.001) and (control: 77.9 (59 – 96.8), A1: 85.2 (71–116.3), A2: 87.3 (81 – 97.5) and A3: 99 (85.1 – 142.5) pg/ml; p = 0.009) respectively. Among the diabetics, a significant association was evident between serum chemerin and serum TNF-α (r = 0.53; p &lt; 0.001). On linear stepwise regression analysis, chemerin was significantly associated with TNF-α and HbA1c (unstandardized β 10.881 and 272.68 respectively, p &lt; 0.001); and TNF-α was significantly correlated with chemerin, uACR (unstandardized β 0.059 and 0.004 respectively, p &lt; 0.001) and HbA1c (unstandardized β −13.699, p = 0.014).</div></div><div><h3>Conclusion</h3><div>Our findings suggest a potential role of chemerin and TNF-α in the development and progression of DKD, and thus support the role of the inflammatory pathway. Larger follow up studies are warranted to further explore the potential links between chemerin, inflammation and DKD.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156772"},"PeriodicalIF":3.7,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142374725","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":"Synthetic trimeric interleukin-6 receptor complexes with a STAT3 phosphorylation dominated activation profile","authors":"Christiane Seibel ,&nbsp;Silke Pudewell ,&nbsp;Puyan Rafii ,&nbsp;Julia Ettich ,&nbsp;Hendrik T. Weitz ,&nbsp;Alexander Lang ,&nbsp;Patrick Petzsch ,&nbsp;Karl Köhrer ,&nbsp;Doreen M. Floss ,&nbsp;Jürgen Scheller","doi":"10.1016/j.cyto.2024.156766","DOIUrl":"10.1016/j.cyto.2024.156766","url":null,"abstract":"<div><div>In Interleukin (IL)-6 signalling, IL-6 site I binds to the IL-6 receptor (IL-6R) first, following by IL-6 site II interaction to domain 2/3 of gp130 to form premature trimeric IL-6:IL–6R:gp130 receptor complexes. Formation of the mature hexameric receptor complex is then facilitated by the inter-trimeric interaction of IL-6 site III with domain 1 of the opposing gp130. The two gp130-associated Janus kinases (JAKs) <em>trans</em>-phosphorylate when their spatiotemporal pairing is correct, which causes the activation of STAT, ERK, and AKT pathways in a balanced manner. Since the intracellular domain (ICD) of IL-6R is not needed for STAT/ERK/AKT phosphorylation, we investigated the conditions under which a chimeric IL-6R_ECD-gp130_TMD/ICD receptor protein confers biological activity. For IL–6R_ECD–gp130_TMD/ICD, the extracellular domain (ECD) of IL-6R was fused to the transmembrane domain (TMD) and ICD of gp130. Co-expression of IL–6R_ECD–gp130_TMD/ICD with signalling-deficient gp130 variants did not induce IL-6 signalling, suggesting that the assembly of hexameric complexes failed to dimerize the IL-6R-associated JAKs correctly. By mimicking the premature trimeric receptor complex, IL-6-mediated dimerization of IL-6R_ECD-gp130_TMD/ICD with the single-cytokine-binding variant gp130_ΔD1 induced signalling. Of note, IL-6 signalling via these synthetic gp130_ΔD1:IL-6R_ECD-gp130_TMD/ICD complexes resulted predominantly in STAT3 phosphorylation. A STAT3-dominated profile was also observed after IL-6-induced signalling mediated by a JAK-deficient IL–6R_ECD–gp130_TMD/ICDΔJAK variant in complex with the JAK-proficient but STAT/ERK/AKT-deficient gp130_JAKΔICD variant. Our data showed that effective ERK/AKT signalling could not be executed after intracellular domain swapping from gp130 to the IL-6R. Taken together, the chimeric IL-6R/gp130 receptor may be helpful in the creation of customized synthetic IL-6 signalling.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156766"},"PeriodicalIF":3.7,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142338144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of Interleukin-38 in modulating T cells in chronic Colitis: A mouse model study","authors":"Ying Xu ,&nbsp;Xuan Zhang ,&nbsp;Shanshan Liu ,&nbsp;Nanfang Qu ,&nbsp;Yi Gao ,&nbsp;Changlong Lu ,&nbsp;Jingbo Zhai ,&nbsp;Junfeng Zhu","doi":"10.1016/j.cyto.2024.156769","DOIUrl":"10.1016/j.cyto.2024.156769","url":null,"abstract":"<div><h3>Background</h3><div>Interleukin (IL)-38 belongs to the IL-36 subfamily within the IL-1 family. Patients with inflammatory bowel diseases (IBD) exhibit higher levels of IL-38 in their intestinal tissue compared to healthy controls, suggesting that IL-38 may play a role in the pathogenesis of IBD. However, IL-38′s impact on T cell-mediated immune responses in gastrointestinal inflammation has not been investigated. Therefore, the objective of this work was to elucidate the role of IL-38 in modulating T cells in a mouse model of dextran sulfate sodium (DSS)-induced chronic colitis.</div></div><div><h3>Methods</h3><div>Recombinant IL-38 (rIL-38) was administered intraperitoneally (i.p.) to mice with chronic colitis induced by DSS. Clinical symptoms, length of colon, and histologic alterations were assessed. Cytokine production was quantified using ELISA, and helper T (Th) cell subsets were evaluated via flow cytometry.</div></div><div><h3>Results</h3><div>Administration of recombinant IL-38 (rIL-38) alleviated DSS-induced chronic colitis. In addition, animals with chronic colitis treated with rIL-38 exhibited a significant decrease in the spontaneous production of inflammatory cytokines by neutrophils in the lamina propria. Furthermore, rIL-38 treatment increased the absolute numbers and percentages of regulatory T cells (Tregs) but decreased the absolute numbers and percentages of Th1 and Th17 cells. Moreover, rIL-38 treatment also decreased IL-17A-producing γδT cells substantially.</div></div><div><h3>Conclusion</h3><div>This study’s results show that IL-38 reduces the effects of chronic colitis caused by DSS by boosting Treg reactions and reducing Th1/Th17 reactions and IL-17A-producing γδT cells in LPL. Therefore, we propose that IL-38 has the potential to be utilized as a biological therapy agent for IBD.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156769"},"PeriodicalIF":3.7,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142338145","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":"Contribution of macrophage polarization in bone metabolism: A literature review","authors":"Qiqi Yan,&nbsp;Haixia Liu,&nbsp;Ruyuan Zhu ,&nbsp;Zhiguo Zhang","doi":"10.1016/j.cyto.2024.156768","DOIUrl":"10.1016/j.cyto.2024.156768","url":null,"abstract":"<div><div>Macrophage polarization divides macrophages into two main cell subpopulations, classically and alternatively activated macrophages (M1 and M2, respectively). M1 polarization promotes osteoclastogenesis, while M2 polarization promotes osteogenesis. The physiological homeostasis of bone metabolism involves a high dynamic balance between osteoclastic-mediated bone resorption and formation. Reportedly, M1/M2 imbalance causes the onset and persistence of inflammation-related bone diseases. Therefore, understanding the research advances in functions and roles of macrophages in such diseases will provide substantial guidance for improved treatment of bone diseases. In this review, we underscore and summarize the research advances in macrophage polarization, and bone-related diseases, such as rheumatoid arthritis, osteoarthritis, and osteoporosis, over the last 5 years. Our findings showed that targeting macrophages and balancing macrophage polarization can effectively reduce inflammation and decrease bone destruction while promoting bone formation and vascular repair. These results indicate that regulating macrophage and macrophage polarization to restore homeostasis is a prospective approach for curing bone-related diseases.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156768"},"PeriodicalIF":3.7,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142327728","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":"Ang-1 promotes tumorigenesis and mediates the anti-cancer effects of Artesunate on Choroidal melanoma via the regulation of Akt/mTOR signaling pathway","authors":"Ningning Yao ,&nbsp;Qingyue Ma ,&nbsp;Wendan Yi ,&nbsp;Yichong Liu ,&nbsp;Qian Zhang ,&nbsp;Xiaodi Gao ,&nbsp;Xintong Zhao ,&nbsp;Haowen Wang ,&nbsp;Ke Lei ,&nbsp;Aihua Sui ,&nbsp;Wenjuan Luo","doi":"10.1016/j.cyto.2024.156771","DOIUrl":"10.1016/j.cyto.2024.156771","url":null,"abstract":"<div><div>The impact of Ang-1 on tumors remains a subject of contention, with its mechanism of action exhibiting complexity in the progression of diverse tumor types. Ang-1 has been shown to promote the progression of glioma, glioma, esophageal and human cervical cancer, whereas it exerts inhibitory effects on the growth of breast and colon cancer. However, the specific function of Ang-1 in CM has not been clarified. This research aims to explore the function of Ang-1 on CM and the underlying mechanism. WB and qPCR were utilized to measure the expression levels of different factors in CM cells. Clonogenic, CCK-8 and Transwell migration assay were used to probe CM cells’ proliferation and migration ability. Xenograft tumor model was used to testify the effect of Ang-1 and Artesunate (ART) on the growth of CM in vivo. We found Ang-1 promoted CM proliferation and migration, while it was inhibited by ART in vitro. Moreover, both ART treatment and Ang-1 knockdown had the effect of suppressing tumor growth in CM xenograft model. Mechanically, Ang-1 activated Akt/mTOR pathway and induced epithelial-mesenchymal transition (EMT) in CM cells. Furthermore, ART regulated Akt/mTOR pathway by decreasing the expression of Ang-1 in CM cells. Ang-1 promotes tumorigenesis of CM by regulating Akt/mTOR pathway, which can be inhibited by ART.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156771"},"PeriodicalIF":3.7,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142327533","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":"Chemokines and chemokine receptors: Potential therapeutic targets in systemic lupus erythematosus","authors":"Lishuang Duan ,&nbsp;Yongxing Yao ,&nbsp;Haiying Kong ,&nbsp;Yanfeng Zhou ,&nbsp;Dawei Cui","doi":"10.1016/j.cyto.2024.156770","DOIUrl":"10.1016/j.cyto.2024.156770","url":null,"abstract":"<div><div>Systemic lupus erythematosus (SLE) is an autoimmune disease that affects connective tissue and can lead to multisystem organ damage. Chemokines are a class of small proteins that interact with receptors and participate in a variety of physiological functions, including cell growth, differentiation, apoptosis and distribution. They also play important roles in pathological processes, such as the inflammatory response, wound repair, tumor formation and metastasis. Previous studies have shown that the levels of chemokines and their receptors are elevated in the blood and inflamed tissues of SLE patients. In addition, chemokine ligand-receptor interactions control the recruitment of leukocytes into tissues, suggesting that chemokines and their receptors may be biomarkers and therapeutic targets for SLE. This review summarizes the causative role of chemokines and their receptors in SLE, as well as their clinical values and challenges as potential biomarkers and therapeutic targets.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"184 ","pages":"Article 156770"},"PeriodicalIF":3.7,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142319127","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}