Cytokine最新文献

{"title":"Long-term cytokine profile in multisystem inflammatory disease among children","authors":"Valeria Calcaterra ,&nbsp;Cristian Loretelli ,&nbsp;Davide Biganzoli ,&nbsp;Ahmed Abdelsalam ,&nbsp;Giuseppe Marano ,&nbsp;Stephana Carelli ,&nbsp;Laura Fiori ,&nbsp;Savina Mannarino ,&nbsp;Enza D’Auria ,&nbsp;Elvira Verduci ,&nbsp;Raffaella De Santis ,&nbsp;Dario Dilillo ,&nbsp;Valentina Fabiano ,&nbsp;Patrizia Carlucci ,&nbsp;Erika Maghraby ,&nbsp;Letizia Messa ,&nbsp;Cristina Cereda ,&nbsp;Paolo Fiorina ,&nbsp;Elia Biganzoli ,&nbsp;Gianvincenzo Zuccotti","doi":"10.1016/j.cyto.2024.156744","DOIUrl":"10.1016/j.cyto.2024.156744","url":null,"abstract":"<div><h3>Background</h3><p>Multisystem inflammatory disease in children (MIS-C) is a post-infectious condition following coronavirus disease-19 infection. Long-term follow-up data suggests that initial clinical severity does not necessarily correlate with long-term outcomes. The long-term immunological response in children with MIS-C remains poorly understood. We analyzed cytokine profiles at diagnosis and during follow-up, in pediatric patients with MIS-C, exploring correlations among cytokine expressions and standard biochemical and hormonal test results.</p></div><div><h3>Methods</h3><p>Twenty-five MIS-C patients (mean 9.4 ± 3.9) with complete test results at diagnosis and at 6- and 12-months follow-up were included in the study. Selected cytokines, such as IL-9, eotaxin, IP-10, MIP-1β, RANTES, MCP-1(MCAF), TNF-α, PDGF-B, IL-4, and MIP-1α, were included in the analysis.</p></div><div><h3>Results</h3><p>IP-10, MCP-1 (MCAF), and MIP-1α levels normalized or nearly normalized at 6–12 months, the remaining cytokines, including IL-9, eotaxin, MIP-1β, RANTES, TNF-α, PDGF-B, IL-4, remained higher in MIS-C than in controls at our last follow-up time. At 6 months post-diagnosis, a mild negative correlation between triglycerides and HOMA-IR with MCP-1 (MCAF), IL-4, and Eotaxin was noted. At the 12-month follow-up we found a mild positive correlation of cortisol and ACTH levels with PDGF-B, MIP-1α, and TNF-α. Conversely, a negative correlation between these cytokines with fasting glucose and HOMA-IR was observed.</p></div><div><h3>Conclusions</h3><p>Our study findings highlight a notable cytokine-mediated inflammatory response in pediatric patients with MIS-C, characterized by sustained elevated levels over a 12-month monitoring period compared to the control group. We have identified various interrelationships among different cytokines, as well as correlations between heightened cytokine levels and metabolic and hormonal patterns. The pronounced inflammatory response underscores its involvement in acute organ damage, while its persistence suggests potential implications for long-term metabolic disorders.</p></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"183 ","pages":"Article 156744"},"PeriodicalIF":3.7,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142083671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The lipoteichoic acid of Lactobacillus plantarum effect on lymphocyte, VEGF-A and TGF-β expression in male rat dental pulp","authors":"Nirawati Pribadi ,&nbsp;Sri Kunarti ,&nbsp;Sylvia ,&nbsp;Wulan Tri Maulinda ,&nbsp;Cindy Ramadhan Putri ,&nbsp;Necdet Adanir ,&nbsp;Meircurius Dwi Condro Surboyo ,&nbsp;Maya Safitri","doi":"10.1016/j.cyto.2024.156741","DOIUrl":"10.1016/j.cyto.2024.156741","url":null,"abstract":"<div><h3>Objective</h3><p>Lipoteichoic acid from <em>Lactobacillus plantarum (L. plantarum)</em> is a significant virulence factor that exacerbates pulp inflammation. Lipoteichoic acid plays a role in modulating the inflammatory to proliferative phase transition is crucial in determining the outcome of pulp healing or necrosis. This study explores the role of <em>L. plantarum</em> on lymphocytes and the expression of transforming growth factor β1 (TGF-β1) and vascular endothelial growth factor A (VEGF-A) in a male rat model of acute dental pulp injury.</p></div><div><h3>Design</h3><p>The acute dental pulp model was created in the upper molar of <em>Rattus novergicus</em> using a round bur. Then, the dental pulp was exposed to 10 µg/ml of the lipoteichoic acid of <em>L. plantarum</em> and filled with a temporary filling. In the next 24, 48, and 72 h, each animal was decapitated, and the expression of TGF-β1 and VEGF-A in dental pulp was analyzed using indirect immunohistochemistry, while the lymphocytes analyzed using hematoxyline-eosin staining.</p></div><div><h3>Result</h3><p>Lipoteichoic acid of <em>L. plantarum</em> induced acute dental pulp by increasing the lymphocyte number after 48 and 72 h of exposure (p &lt; 0.05). While, inhibiting TGF-β1 expression after 48 and 72 h of exposure (p &lt; 0.05), and VEGF-A was inhibiting after 72 h of exposure (p &lt; 0.05).</p></div><div><h3>Conclusion</h3><p>Exposure to lipoteichoic acid from <em>L. plantarum</em> significantly accelerates the inflammatory response in the dental pulp. However, this accelerated inflammation disrupts the proliferative phase, potentially leading to more extensive damage to the dental pulp.</p></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"183 ","pages":"Article 156741"},"PeriodicalIF":3.7,"publicationDate":"2024-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142054361","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":"Genetic insights into the association between serum cytokines and frozen shoulder risk: A bidirectional mendelian randomization study","authors":"Xuefei Li ,&nbsp;Han Long ,&nbsp;Dusu Wen ,&nbsp;Biao Chen ,&nbsp;Liaobin Chen ,&nbsp;Bin Li","doi":"10.1016/j.cyto.2024.156736","DOIUrl":"10.1016/j.cyto.2024.156736","url":null,"abstract":"<div><h3>Background</h3><p>Although existing studies have indicated a connection between chronic low-grade inflammation and the onset of frozen shoulder (FS), the precise causal relationship between distinct circulating inflammatory factors and FS has yet to be thoroughly evaluated. In this study, we employed a bidirectional two-sample Mendelian randomization (MR) analysis to investigate the potential causal relationship between systemic cytokines and FS.</p></div><div><h3>Methods</h3><p>A genome-wide association dataset comprising 41 serum cytokines from 8,293 individuals of Finnish descent was utilized, along with FS data from the UK Biobank included 10,104 FS cases and 451,099 controls. The primary MR method was the inverse variance weighted approach, and four additional MR techniques (MR-Egger, weighted median, simple mode, and weighted mode) were also employed to support and validate the findings. Heterogeneity and horizontal pleiotropy assessments were assessed using Cochrane’s Q and MR-Egger intercept tests. Moreover, a series of sensitivity analyses were conducted to strengthen the accuracy and credibility of these findings.</p></div><div><h3>Results</h3><p>Based on the IVW method, genetically predicted increasing levels of growth regulated oncogene alpha (GROa) (OR=1.08, 95 % CI 1.02–1.13, <em>P</em>=0.005), interferon gamma-induced protein 10 (IP-10) (OR=1.09, 95 % CI 1.02–1.17, <em>P</em>=0.010), regulated on activation, C–C Motif Chemokine Ligand 5 (CCL5) (OR=1.11, 95 % CI 1.03–1.20, <em>P</em>=0.007) were suggestively associated with an increased risk of FS. Reverse MR analysis revealed no significant causal effect of FS on the 41 systemic inflammatory factors. No heterogeneity or horizontal pleiotropy was observed in our analysis.</p></div><div><h3>Conclusion</h3><p>This study established a causal association between 41 systemic inflammatory factors and FS, indicating that elevated levels of GROa, IP-10 and CCL5 were associated with a higher risk of FS. Further research is warranted to explore the potential of these biomarkers as early predictors and therapeutic targets for FS.</p></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"183 ","pages":"Article 156736"},"PeriodicalIF":3.7,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142020393","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":"Correlation between inflammatory cytokines and the likelihood of developing multiple types of digestive system cancers: A Mendelian randomization study","authors":"Su-Lan Chen ,&nbsp;Bin Zhang ,&nbsp;Song Wang ,&nbsp;Ming Yang ,&nbsp;Qiao-Hui Shen ,&nbsp;Rui Zhang ,&nbsp;Zhuang Xiong ,&nbsp;Yan Leng","doi":"10.1016/j.cyto.2024.156735","DOIUrl":"10.1016/j.cyto.2024.156735","url":null,"abstract":"<div><h3>Objective</h3><p>Inflammatory cytokines have been linked to digestive system cancers, yet their exact causal connection remains uncertain. Consequently, we conducted a Mendelian randomization (MR) analysis to gauge how inflammatory cytokines are linked to the risk of five prevalent digestive system cancers (DSCs).</p></div><div><h3>Methods</h3><p>We collected genetic variation data for 41 inflammatory cytokines from genome-wide association studies (GWAS), and the results data for five common diseases from the Finnish database. Our primary analytical approach involved employing the inverse-variance weighted, residual sum (IVW) method, complemented by the MR-Egger method, the weighted median method, simple mode analysis, and weighted mode analysis as supplementary analytical techniques. Furthermore, we conducted multiple sensitivity analyses.</p></div><div><h3>Results</h3><p>Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), macrophage colony-stimulating factor (M-CSF), and interleukin (IL)-18 showed a negative association with the risk of hepatocellular carcinoma. Conversely, TRAIL was inversely linked to the risk of gastric cancer, while IL-16 exhibited a positive correlation with gastric cancer risk. Stem cell factor (SCF) acted as a protective factor against pancreatic cancer. For colorectal cancer, IL-7, IL-9, IL-13, and vascular endothelial growth factor (VEGF) were identified as risk factors. Notably, our results did not indicate a significant correlation between inflammatory cytokines and the risk of esophageal cancer.</p></div><div><h3>Conclusion</h3><p>Our research unveils potential connections between 41 inflammatory cytokines and the risk of five common DSCs through a MR analysis. These associations offer valuable insights that could aid in the development of diagnostic biomarkers and the identification of novel therapeutic targets for DSCs.</p></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"183 ","pages":"Article 156735"},"PeriodicalIF":3.7,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1043466624002382/pdfft?md5=9c98d93e97fdc16e1a72ab1f3c39470e&pid=1-s2.0-S1043466624002382-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142020394","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-2 in graft-versus-host disease pathogenesis, prevention and therapy","authors":"Hila Najaf Khosravi ,&nbsp;Sepideh Razi ,&nbsp;Nima Rezaei","doi":"10.1016/j.cyto.2024.156723","DOIUrl":"10.1016/j.cyto.2024.156723","url":null,"abstract":"<div><p>Graft-versus-host disease (GVHD) is a significant complication following allogeneic hematopoietic cell transplantation (allo-HCT), posing substantial risks to patient survival. In the late follow-up phase of transplanted patients, GVHD is also a major cause of morbidity and disability, mostly due to low response to first-line steroids and the lack of effective standard therapies in the second line.</p><p>This review provides a description of GVHD pathogenesis, with a focus on the central role of Interleukin-2 (IL-2). IL-2 is one of the critical mediators in the complex pathogenesis of GVHD, contributing to the intricate balance between regulatory T cells (Tregs) and effector T cells (Teffs). Due to this pivotal role, several studies investigate the potential of IL-2 as a therapeutic option for GVHD management. We discuss the outcomes of low-dose IL-2 therapies and their impact on Treg proliferation and steroid dependency reduction. Additionally, the effects of combining IL-2 with other treatments, such as extracorporeal photopheresis (ECP) and Treg-enriched lymphocyte infusions, are highlighted. Novel approaches, including modified IL-2 complexes and IL-2 receptor blockade, are explored for their potential in selectively enhancing Treg function and limiting Teff activation. The evolving understanding of IL-2′s pivotal role in immune regulation presents promising prospects for applying treatment and prevention strategies for GVHD.</p></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"183 ","pages":"Article 156723"},"PeriodicalIF":3.7,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142011674","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":"Poly I:C vaccination drives transient CXCL9 expression near B cell follicles in the lymph node through type-I and type-II interferon signaling","authors":"Alexander G. Ball ,&nbsp;Katerina Morgaenko ,&nbsp;Parastoo Anbaei ,&nbsp;Sarah E. Ewald ,&nbsp;Rebecca R. Pompano","doi":"10.1016/j.cyto.2024.156731","DOIUrl":"10.1016/j.cyto.2024.156731","url":null,"abstract":"<div><p>Subunit vaccines drive immune cell–cell interactions in the lymph node (LN), yet it remains unclear how distinct adjuvants influence the chemokines responsible for this interaction in the tissue. Here, we tested the hypothesis that classic Th1-polarizing vaccines elicit a unique chemokine signature in the LN compared to other adjuvants. Polyinosinic:polycytidylic acid (Poly I:C) vaccination resulted in dynamic upregulation of CXCL9 that was localized in the interfollicular region, a response not observed after vaccination with alum or a combination of alum and poly I:C. Experiments using in vivo mouse models and live ex vivo LN slices revealed that poly I:C vaccination resulted in a type-I IFN response in the LN that led to the secretion of IFNγ, and type-I IFN and IFNγ were required for CXCL9 expression in this context. CXCL9 expression in the LN was correlated with an IgG2c antibody polarization after vaccination; however, genetic depletion of the receptor for CXCL9 did not prevent the development of this polarization. Additionally, we measured secretion of CXCL9 from ex vivo LN slices after stimulation with a variety of adjuvants and confirmed that adjuvants that induced IFNγ responses also promoted CXCL9 expression. Taken together, these results identify a CXCL9 signature in a suite of Th1-polarizing adjuvants and determined the pathway involved in driving CXCL9 in the LN, opening avenues to target this chemokine pathway in future vaccines.</p></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"183 ","pages":"Article 156731"},"PeriodicalIF":3.7,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142011675","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":"IL10 and CXCL10 mRNA expression in food protein–induced enterocolitis syndrome","authors":"Ilaria Galliano ,&nbsp;Paola Montanari ,&nbsp;Giovanna Monti ,&nbsp;Maddalena Dini ,&nbsp;Cristina Calvi ,&nbsp;Anna Clemente ,&nbsp;Anna Pau ,&nbsp;Stefano Gambarino ,&nbsp;Massimiliano Bergallo","doi":"10.1016/j.cyto.2024.156720","DOIUrl":"10.1016/j.cyto.2024.156720","url":null,"abstract":"<div><h3>Background</h3><p>Food protein-induced enterocolitis syndrome (FPIES) is a rare non-IgE-mediated food allergy that mainly impacts babies and 7toddlers. The exact mechanism of FPIES is not completely understood. By studying the expression of IL-10 and CXCL10 in pediatric FPIES patients, researchers can gain insights into the immune mechanisms underlying this disorder.</p></div><div><h3>Methods</h3><p>Peripheral venous blood was collected and subsequently stabilized with RNA pro. Total RNA was extracted and mRNA levels of CXCL10 and IL-10 was determined with real time PCR.</p></div><div><h3>Results</h3><p>Children with FPIES had significantly higher values than the healthy control group (HC) for CXCL10 while FPIES had a significant lower values than the control group for IL-10.</p></div><div><h3>Conclusions</h3><p>Our results show a high production of CXCL10 and a concomitant reduced production of IL-10 in FPIES subjects who have not yet reached tolerance. These data may represent a molecular diagnostic marker for FPIES.</p></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"182 ","pages":"Article 156720"},"PeriodicalIF":3.7,"publicationDate":"2024-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1043466624002230/pdfft?md5=8076843e6a7f46118214f440112ca6bb&pid=1-s2.0-S1043466624002230-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141964346","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":"Revealing of TLR-9 gene polymorphisms by qPCR HRM technique and their influence on TLR-9 serum level in acute myeloid leukemia patients: Case-control study","authors":"Maryam Qasim Mohammed ,&nbsp;Ali Hussein Alwan ,&nbsp;Asmaa Amer Almukhtar ,&nbsp;Mohanad Kareem Aneed Al-Saedi","doi":"10.1016/j.cyto.2024.156730","DOIUrl":"10.1016/j.cyto.2024.156730","url":null,"abstract":"<div><p>Acute myeloid leukemia (AML) is one of the most common and fatal malignancies that affect adults, which can quickly become aggressive if left untreated, and leukemia cells invade the bone marrow. TLR-9 is an innate immune cell receptor sensitive to various PAMPs and encoded by the <em>TLR-9</em> gene. As is often known, genetic polymorphisms in any gene can help the development of the disease, and these three polymorphisms, rs187084, rs5743836, and rs352140 of <em>TLR-9</em>, have been studied in many different cancer disorders. Therefore, this study aimed to discover the multiple forms of a <em>TLR-9</em> gene in a sample of Iraqi AML patients. A total of 120 participants in a case-control study were enrolled in the current study. Using CBC, some hematological parameters were evaluated, and the serum level of TLR-9 was assessed using the ELISA technique. DNA was extracted directly from blood, and a high-resolution melting (HRM) analysis was then carried out. The results revealed a significant difference in some blood parameters among patients and healthy control, while WBC and lymphocytes were without an evident difference between the two groups of the current investigation. The serum concentration of TLR-9 showed an elevated level in patients (P value &lt; 0.01). Nonetheless, this increase was not affected by the genotype patterns of polymorphisms. According to the P-value, there was a significant difference in wild genotypes of the three polymorphisms (rs187084, rs5743836, and rs352140). At the same time, the odds ratio revealed the association with the disease as a protective factor. In contrast, there was a significant difference in the heterozygous and mutant genotypes of <em>TLR-9</em> polymorphisms, though the odds ratio confirmed the association with the AML as a risk factor. The results of rs352140 were compatible with H.W.E since there were no significant differences between the observed and expected values for either patients or healthy controls. In contrast, the result of rs5743836 was not consistent with the HWE. Furthermore, although it corresponds with the healthy one, the finding of rs187084 conflicted with H.W.E. in the patient group. In conclusion, High serum levels of TLR-9 in patients could act as biomarkers for AML. The <em>TLR-9</em> gene polymorphisms (rs187084, rs5743836, and rs352140) have been linked to an increased risk of AML and may impact the disease progression in the Iraqi population.</p></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"182 ","pages":"Article 156730"},"PeriodicalIF":3.7,"publicationDate":"2024-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141964345","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":"COX-2 optimizes cardiac mitochondrial biogenesis and exerts a cardioprotective effect during sepsis","authors":"Leijing Yin ,&nbsp;Ludong Yuan ,&nbsp;Zhengyang Luo ,&nbsp;Yuting Tang ,&nbsp;Xiaofang Lin ,&nbsp;Shuxin Wang ,&nbsp;Pengfei Liang ,&nbsp;Lingjin Huang ,&nbsp;Bimei Jiang","doi":"10.1016/j.cyto.2024.156733","DOIUrl":"10.1016/j.cyto.2024.156733","url":null,"abstract":"<div><h3>Background</h3><p>Septic cardiomyopathy is a component of multiple organ dysfunction in sepsis. Mitochondrial dysfunction plays an important role in septic cardiomyopathy. Studies have shown that cyclooxygenase-2 (COX-2) had a protective effect on the heart, and prostaglandin E₂ (PGE₂), the downstream product of COX-2, was increasingly recognized to have a protective effect on mitochondrial function.</p></div><div><h3>Objective</h3><p>This study aims to demonstrate that COX-2/PGE₂ can protect against septic cardiomyopathy by regulating mitochondrial function.</p></div><div><h3>Methods</h3><p>Cecal ligation and puncture (CLP) was used to establish a mouse model of sepsis and RAW264.7 macrophages and H9C2 cells were used to simulate sepsis <em>in vitro</em>. The NS-398 and celecoxib were used to inhibit the activity of COX-2. ZLN005 and SR18292 were used to activate or inhibit the PGC-1α activity. The mitochondrial biogenesis was examined through the Mitotracker Red probe, mtDNA copy number, and ATP content detection.</p></div><div><h3>Results</h3><p>The experimental data suggested that COX-2 inhibition attenuated PGC-1α expression thus decreasing mitochondrial biogenesis, whereas increased PGE₂ could promote mitochondrial biogenesis by activating PGC-1α. The results also showed that the effect of COX-2/PGE₂ on PGC-1α was mediated by the activation of cyclic adenosine monophosphate (cAMP) response element binding protein (CREB). Finally, the effect of COX-2/PGE₂ on the heart was also verified in the septic mice.</p></div><div><h3>Conclusion</h3><p>Collectively, these results suggested that COX-2/PGE₂ pathway played a cardioprotective role in septic cardiomyopathy through improving mitochondrial biogenesis, which has changed the previous understanding that COX-2/PGE₂ only acted as an inflammatory factor.</p></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"182 ","pages":"Article 156733"},"PeriodicalIF":3.7,"publicationDate":"2024-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141915651","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":"Elevated serum IGFBP-1 levels correlate with cognitive deficits in treatment-resistant and chronic medicated schizophrenia patients","authors":"Haidong Yang ,&nbsp;Man Yang ,&nbsp;Yuting Zhang ,&nbsp;Zhihui Shi ,&nbsp;Xiaobin Zhang ,&nbsp;Caiyi Zhang","doi":"10.1016/j.cyto.2024.156728","DOIUrl":"10.1016/j.cyto.2024.156728","url":null,"abstract":"<div><h3>Background</h3><p>Schizophrenia is a debilitating psychiatric disorder with diverse cognitive impairments. Insulin-like growth factor binding protein 1 (IGFBP-1), a ubiquitous negative regulator of IGF signaling, crosses the blood–brain barrier after peripheral synthesis. Given the crucial role of IGF signaling in cognitive function, we reasoned that altered serum IGFBP-1 concentrations might be associated with cognitive impairments in schizophrenia. To test this hypothesis, we examined the relationship between serum IGFBP-1 levels and cognitive performance in both medicated and treatment-resistant schizophrenia (TRS) patients.</p></div><div><h3>Methods</h3><p>Serum IGFBP-1 was measured in 31 TRS patients, 49 chronic medicated schizophrenia (CMS) patients, and 53 healthy controls. Clinical symptom severity was evaluated using the Positive and Negative Syndrome Scale (PANSS) and cognitive functions using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS).</p></div><div><h3>Results</h3><p>Both TRS and CMS patients exhibited cognitive deficits compared to healthy controls (p &lt; 0.05). Serum IGFBP-1 concentration differed significantly among groups (F=36.805, p &lt; 0.001) and post hoc tests demonstrated significantly higher concentrations in both schizophrenia groups compared to controls (p &lt; 0.001). Further, serum IGFBP-1 concentration was higher in the TRS group than the CMS group (p = 0.048). Correlation analysis identified a significant relationship between serum IGFBP-1 and attention in the TRS group (r = 0.411, p = 0.021), immediate memory in the CMS group (r = -0.417, p = 0.003), and RBANS total score in the CMS group (r = -0.368, p = 0.009). Multiple regression analysis adjusting for confounding factors revealed that serum IGFBP-1 was independently associated with attention in TRS patients (p = 0.016, 95 %CI.</p><p>0.002–0.015) and immediate memory in CMS patients (p = 0.022, 95 %CI-0.012 to −0.001).</p></div><div><h3>Conclusions</h3><p>Elevated serum IGFBP-1 concentration may serve as a predictive biomarker for distinct cognitive deficits in TRS and CMS patients. Further investigations are warranted.</p></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"182 ","pages":"Article 156728"},"PeriodicalIF":3.7,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141911013","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}