Cytokine最新文献

{"title":"FokI polymorphism of the vitamin D receptor gene: Linking COVID-19 risk to genetic susceptibility in children","authors":"Amal Ahmed Mohamed ,&nbsp;Abdullah Taher Alanazi ,&nbsp;Hoda H. Ahmed ,&nbsp;Samar Elfiky ,&nbsp;Muhammad T Abdel Ghafar ,&nbsp;Ingy Maher ,&nbsp;Sherin A. Taha ,&nbsp;Mohammed Zakaria Ali AbuRahma ,&nbsp;Waleed Elagawy ,&nbsp;Dina A. Mohareb ,&nbsp;Abeer M. Rawy ,&nbsp;Heba M. Abostate ,&nbsp;Amira AlSayed Youssef ,&nbsp;Dalia Saeed Elsayed ,&nbsp;Rasha M. Abdel-Hamid","doi":"10.1016/j.cyto.2025.156958","DOIUrl":"10.1016/j.cyto.2025.156958","url":null,"abstract":"<div><h3>Background</h3><div>Vitamin D receptor (VDR), influenced by gene polymorphisms like <em>FokI</em>, may affect susceptibility to infections, including coronavirus disease 2019 (COVID-19). Since studies in children are limited, we aimed to analyze the correlation between the VDR <em>FokI</em> variant and both the incidence and severity of COVID-19 in Egyptian children.</div></div><div><h3>Methods</h3><div>Seventy-seven COVID-19-positive and 107 COVID-19-negative pediatric patients were included. Participants' serum 25(OH)D levels, inflammatory biomarkers, and demographics were evaluated. Real-time polymerase chain reaction (PCR) was used for genotyping the VDR <em>FokI</em> (rs2228570) polymorphism.</div></div><div><h3>Results</h3><div>Absolute lymphocyte count (ALC) was significantly lower in COVID-19 patients than in controls, while interleukin-6 (IL-6), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), procalcitonin, and D-dimer were significantly higher (all <em>p</em> &lt; 0.001). Vitamin D insufficiency was significantly more common in COVID-19 cases (18.2 % versus 3.7 %, <em>p</em> = 0.002). Male sex, increased tumor necrosis factor-alpha (TNF-α), and CRP were significantly associated with severe COVID-19 (<em>p</em> = 0.032, 0.029, &lt; 0.001, respectively). The <em>FokI</em> TT genotype in codominant and recessive models and the T allele in the multiplicative model were significantly correlated with 2.4, 3.0, and 1.8 folds increased COVID-19 risk (<em>p</em> = 0.043, &lt; 0.001, and 0.004, respectively). However, VDR <em>FokI</em> variants did not significantly associate with severe COVID-19.</div></div><div><h3>Conclusion</h3><div>The T allele and TT genotype of the <em>FokI</em> variant in the <em>VDR</em> gene increase susceptibility to COVID-19 but not its severity in Egyptian children. Additional research is required to validate the potential role of vitamin D and its receptor polymorphism in COVID-19.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156958"},"PeriodicalIF":3.7,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143941118","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":"Eliminating myeloid-derived suppressor cells alleviates immunosuppression and reduces susceptibility to secondary infections in a two-hit sepsis model","authors":"Dongjie Liu ,&nbsp;Wei Fu ,&nbsp;Teng Zhang ,&nbsp;Jianyao Wang ,&nbsp;Yuxin He ,&nbsp;Xiao Wang ,&nbsp;Tongxiang Xu ,&nbsp;Cheng Wang ,&nbsp;Tao Ma","doi":"10.1016/j.cyto.2025.156955","DOIUrl":"10.1016/j.cyto.2025.156955","url":null,"abstract":"<div><div>Myeloid-derived suppressor cells (MDSCs) are known for their immunosuppressive effects on both innate and adaptive immunity, particularly targeting T cells, and they undergo continuous expansion during sepsis. However, the pathophysiological significance of MDSCs in sepsis-induced immunosuppression remains to be fully elucidated. In this study, we investigated the dynamic changes in MDSCs during sepsis and their contribution to sepsis-induced immunosuppression using a clinically relevant “two-hit” sepsis model. Our findings revealed that mice surviving cecal ligation and puncture (CLP) exhibited a significant accumulation and enhanced activity of MDSCs, which correlated with sepsis-related immune paralysis, impaired bacterial clearance, and heightened susceptibility to secondary infections. Importantly, administration of the liver X receptor (LXR) agonist GW3965 at the late stage of sepsis significantly restored immune function, decreased susceptibility to secondary infections, enhanced bacterial clearance, and improved prognosis by eliminating MDSCs. These results highlight the pivotal role of MDSCs in the development of sepsis-associated immunosuppression and indicate that targeting MDSCs could be a promising therapeutic approach to mitigate immunosuppression in sepsis.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156955"},"PeriodicalIF":3.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143917576","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":"Mesenchymal stem cell transplantation ameliorates inflammation in spinal cord injury by inhibiting lactylation-related genes","authors":"Weiwei Zou ,&nbsp;Zelin Zhang ,&nbsp;Tingting Cao ,&nbsp;Mangmang Li","doi":"10.1016/j.cyto.2025.156960","DOIUrl":"10.1016/j.cyto.2025.156960","url":null,"abstract":"<div><h3>Background</h3><div>The immune microenvironment significantly influences neural regeneration in spinal cord injury (SCI). Lactate activates central nervous system (CNS) glial cells, prompting the secretion of proinflammatory cytokines and triggering an inflammatory response. Mesenchymal stem cells (MSCs) make a promising future for SCI therapy due to their immune regulation and anti-inflammatory properties. However, it is unclear whether MSCs inhibit inflammatory responses in the SCI microenvironment through lactylation regulation. This study aimed to identify lactylation-related genes (LRGs) in SCI and investigate their role in immune cell infiltration and MSC-mediated inflammation reduction.</div></div><div><h3>Methods</h3><div>Transcription datasets of SCI patients were acquired from Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) underwent functional enrichment analysis, and CIBERSORT assessed immune cell infiltration in SCI. Crucial lactylation-related differentially expressed genes (LRDEGs) associated with SCI were identified via machine learning. The association between LRDEGs and inflammatory response in SCI mediated by immune cell infiltration was confirmed using Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG). Rats with subacute thoracic SCI were transplanted with hUC-MSCs, and transcriptome analyses were conducted on their spinal cords and retrieved hUC-MSCs, respectively.</div></div><div><h3>Results</h3><div>The study identified 808 DEGs and 13 differentially infiltrated immune cell types in SCI patients compared to healthy controls. Multiple inflammatory response-related signaling pathways were activated in SCI. Seven LRDEGs, including LSP1, XRCC4, HSDL2, HNRNPH1, RPL14, IKZF1, and TP53, were recognized as key regulators. These genes are linked to immune cell infiltration and inflammatory responses in SCI. In SCI rats, the increased expression of LRDEGs and inflammatory cytokines were observed, which were significantly reduced after hUC-MSC transplantation. Differences in LRDEG expression patterns, enriched functions, and pathways between two SCI subtypes were statistically significant.</div></div><div><h3>Conclusions</h3><div>LRDEGs are involved in immune cell-mediated inflammatory response in SCI, and hUC-MSC transplantation reduces LRDEGs expression and inflammation response in the SCI microenvironment.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156960"},"PeriodicalIF":3.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143917577","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":"Association between frailty and inflammatory cytokines in patients with multiple sclerosis: a case-control study","authors":"Shucheng Xing,&nbsp;Xue Li,&nbsp;Chen Chen","doi":"10.1016/j.cyto.2025.156945","DOIUrl":"10.1016/j.cyto.2025.156945","url":null,"abstract":"<div><h3>Background</h3><div>Frailty is a common symptom in Multiple Sclerosis (MS), yet its precise mechanism remains elusive, and the clinical implications of frailty in MS are uncertain. Moreover, inflammation is closely linked to frailty. This study aims to assess serum cytokine levels in individuals with MS and explore their correlation with frailty.</div></div><div><h3>Methods</h3><div>A case-control study included 83 primary MS patients and 100 healthy individuals undergoing health check-ups. Serum cytokine levels were measured, and MS severity was determined using the Expanded Disability Status Scale (EDSS) score. Additionally, a comprehensive frailty index (FI) was calculated based on health deficits from various domains following standardized procedures.</div></div><div><h3>Results</h3><div>Serum IL-6 and TNF-α levels were significantly higher in the frail group than in the non-frail group, with a statistically significant difference (<em>P</em> &lt; 0.05). After adjusting for disease duration, sex, age, BMI, SBP, and DBP, serum IL-6 independently correlated with frailty in MS patients (OR = 1.46; 95 % CI = 1.02–1.93; <em>P</em> = 0.003). Moreover, increased serum IL-6 levels were associated positively with the frailty index (β = 0.123, <em>P</em> = 0.008).</div></div><div><h3>Conclusion</h3><div>Our initial findings suggest elevated levels of pro-inflammatory cytokines in MS patients with frailty, with IL-6 showing a positive correlation with frail indices. These results underscore the potential impact of inflammatory responses on frailty development in MS.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156945"},"PeriodicalIF":3.7,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906812","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":"Based on the IL-33/ST2-MyD88 signaling pathway to explore the mechanism of aerobic exercise in antagonizing the inflammatory response in depressive mice","authors":"Lei Gao ,&nbsp;Ruilian Liu ,&nbsp;He Qu ,&nbsp;Honglin Qu ,&nbsp;Qingyun Bai ,&nbsp;Yilin Chen","doi":"10.1016/j.cyto.2025.156956","DOIUrl":"10.1016/j.cyto.2025.156956","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Purpose&lt;/h3&gt;&lt;div&gt;This study examined how aerobic exercise affect the IL-33/ST2-MyD88 signaling pathway in mice with chronic unpredictable mild stress (CUMS) induced depression&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Method&lt;/h3&gt;&lt;div&gt;Thirty-six C57BL/6 mice were randomly assigned t three groups: a control group (CG), a model group (MG), and an exercise group (ME). We created a depression model using chronic unpredictable mild stress, after which the ME group underwent 8 weeks of aerobic training. After exercise intervention, neurobehavioral assessment was performed. ELISA was used to detect the levels of IL-33, IL-1β and IL-10 in the serum of mice. Toluidine blue Nissl staining was used to observe the structure of hippocampal neurons. Total RNA was extracted from blood samples using magnetic beads and from hippocampal tissue or neurons using Trizol. The levels of IL-33, ST2, MyD88, IL-1β, IL-10 and NF-κB mRNA in mice were detected by RT-PCR&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Result&lt;/h3&gt;&lt;div&gt;The number of lattice crossings and modification times were significantly reduced in MG group, the exercise time was significantly shortened, and the sugar and water preference index was significantly reduced, while the immobility time in forced swimming and tail suspension tests were significantly prolonged. The results indicated that CUMS successfully induced anhedonia and depression-like behaviors in the mice. In the ME group, there was a significant increase in the number of crossing lattices, modification times, exercise duration, and sugar and water preference index, while the immobility time in the forced swimming and tail suspension tests significantly decreased. Compared with the CG group, serum levels of inflammatory factors IL-33, IL-1β, and NF-κB significantly increased in the MG group, while these levels significantly decreased in the ME group. It decreased and IL-10 showed a very significant increase. Nissl staining results indicated that hippocampal nerve cells in MG group were sparsely arranged, with widened gaps, severe nucleus contraction, and shallow staining. The ME group had reduced neuronal vacuoles and improved nuclear shrinkage. Immunohistochemical results revealed that in MG group, the expression of pro-inflammatory factors IL-1β and MyD88 increased. In Contrast, the ME group exhibited a decrease in IL-1β and MyD88, alongside a significant increase in the anti-inflammatory factor IL-10. In the RT-PCR test results, the blood inflammation signal pathway IL-33/ST2 and its downstream factors MyD88, NF-κB, and IL-1β mRNA were significantly up-regulated, and the inhibitory factor IL-10 mRNA was up-regulated in MG group. Gene expression trends for IL-33 mRNA, ST2 mRNA, IL-1β mRNA, MyD88 mRNA and NF-κB mRNA in hippocampus tissue were similar to those in blood, all showing significant up-regulation. In contrast, IL-10 mRNA did not exhibit significant up-regulation. While IL-33/ST2 expression did not significantly decrease, other pro-inflammatory factors showed significant","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156956"},"PeriodicalIF":3.7,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143900055","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 role of interleukin (IL)-2 cytokine family in Parkinson's disease","authors":"Pouya Goleij ,&nbsp;Alireza Amini ,&nbsp;Mohammad Amin Khazeei Tabari ,&nbsp;Mahboube Hadipour ,&nbsp;Pantea Majma Sanaye ,&nbsp;Khalaf F. Alsharif ,&nbsp;Maria Daglia ,&nbsp;Danaé S. Larsen ,&nbsp;Haroon Khan","doi":"10.1016/j.cyto.2025.156954","DOIUrl":"10.1016/j.cyto.2025.156954","url":null,"abstract":"<div><div>Parkinson's disease (PD) is a neurodegenerative disorder, which primarily impacts the nervous system, marked by its immune and inflammatory characteristics. The interleukin-2 (IL-2) cytokine family has a crucial role in regulating both neuroinflammation and immune activity, positioning it as one of the critical immune pathways in PD. Balancing pro-inflammatory and anti-inflammatory signals in PD heavily depends on the IL-2 cytokine family, that includes IL-2, IL-4, IL-7, IL-9, IL-15 and IL-21. This balance is vital for neuron survival and resistance to degeneration. Disruptions in IL-2 signaling can upset the equilibrium among regulatory T cells (Tregs) and pro-inflammatory T cells, such as Th1 and Th17, further aggravating the chronic neuroinflammation typical of PD. In PD, a decline in IL-2 or receptor dysfunction can hinder Treg activity, leading to increased inflammation and neurodegeneration. Similarly, IL-15 and IL-21 supports cytotoxic immune cell function, including natural killer (NK) cells and CD8+ T cells, which may exacerbate neuronal damage by sustaining pro-inflammatory processes. Moreover, IL-4 and IL-7 have anti-inflammatory roles in maintaining T cell homeostasis, and their dysregulation can contribute to interruption of the blood-brain barrier and increased infiltration of immune cells into the central nervous system. Targeting the IL-2 cytokine family in Parkinson's disease has shown therapeutic potential by expanding Tregs, which reduce neuroinflammation and promote dopaminergic neuron survival. Recombinant IL-2 and IL-2/anti-IL-2 complexes have demonstrated efficacy in animal models, enhancing Treg function and leading to improved neuroprotection. Additionally, IL-4-based therapies have been explored for their ability to shift microglia toward a neuroprotective phenotype, further enhancing neuronal survival by modulating inflammatory responses and cellular metabolism. Current research is exploring how to optimize cytokine delivery while minimizing immune side effects, with the goal of developing more targeted therapies for PD.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156954"},"PeriodicalIF":3.7,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143900054","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":"Unraveling the immune activation mechanisms of DAMPs in coronary artery disease through transcriptomic and single-cell analyses","authors":"Yinghao Li,&nbsp;Henghe Shi,&nbsp;Yifei Zou,&nbsp;Yinuo Guan,&nbsp;Ning Liu,&nbsp;Bin Liu","doi":"10.1016/j.cyto.2025.156952","DOIUrl":"10.1016/j.cyto.2025.156952","url":null,"abstract":"<div><div>This study employs transcriptomics and single-cell analysis to delve into the mechanisms by which damage-associated molecular patterns (DAMPs) trigger immune activation in coronary artery disease (CAD). We obtained RNA-seq data from the GSE202625 and GSE242046 datasets, as well as single-cell RNA-seq data from the GSE159677 dataset, all sourced from the GEO database. Through differential expression analysis, we identified 821 differentially expressed genes (DEGs), comprising 389 upregulated and 432 downregulated genes, which are likely closely associated with the pathological processes of CAD. Notably, the genes P2RY14 and IFIH1 exhibited significant expression differences in CAD, suggesting their potential involvement in immune responses and inflammatory processes. Our findings indicate a significant infiltration and activation of immune cells in CAD patients, particularly T cells and macrophages. The activation of these cells is likely linked to the release of DAMPs and the activation of pattern recognition receptors (PRRs), thereby triggering local and systemic inflammatory responses. Single-cell analysis further revealed distinct clustering patterns of immune cells, especially T cells and B cells, in CAD patients compared to healthy controls. Dendritic cells and macrophages play particularly critical roles in the development of CAD. Dendritic cells bridge innate and adaptive immune responses by presenting antigens to T lymphocytes, potentially either promoting or inhibiting the progression of atherosclerosis. Macrophages exhibit polarization during the atherosclerosis process, with M1-type macrophages tending to promote inflammatory responses, while M2-type macrophages may exert anti-inflammatory effects.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156952"},"PeriodicalIF":3.7,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882371","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":"Augmented hippocampal up-regulation of immune modulators following a peripheral immune challenge in a hemizygous mouse model of the 15q13.3 microdeletion","authors":"Katherine A. Rees ,&nbsp;Kristin M. McCamy ,&nbsp;Conner I. Danao,&nbsp;Ursula H. Winzer-Serhan","doi":"10.1016/j.cyto.2025.156951","DOIUrl":"10.1016/j.cyto.2025.156951","url":null,"abstract":"<div><div>The strongest known genetic risk factor for generalized epilepsy is the human hemizygous 15q13.3 microdeletion (MD). This 1.5 Mb MD encompasses six genes, including CHRNA7 encoding the alpha7 subunit that forms the homo-pentameric nicotinic acetylcholine receptor, a known regulator of the immune system. In the CNS, hyper activation of neuroimmune responses contributes to increased seizure susceptibility. In a mouse model with a hemizygous deletion of the orthologous region (Df(h15q13)/+) (Het), we previously demonstrated increased hippocampal expression of inflammatory cytokines compared to wildtype (WT) mice following a mild peripheral immune challenge. To further characterize neuroimmune responses, hippocampal mRNA expression of the chemokines CXCL2 and CXCL10, and the Gap junction protein connexin 43 (GJA1), all of which are implicated in neuronal hyperexcitability, were determined along with additional immune related targets. Three hours after a lipopolysaccharide (LPS, 0.1 mg/kg) or polyinosinic:polycytidylic acid (Poly(I:C), 5 mg/kg) injection (i.p.), hippocampi were collected, mRNA extracted, and cDNA prepared for qPCR. The results demonstrate extensive upregulation of CXCL2 and CXCL10 expression by LPS and Poly(I:C) (up to 200-fold CXCL2, up to 600-fold CXCL10) (<em>p</em> &lt; 0.0001) with genotype x treatment interactions for CXCL2 by LPS (<em>p</em> &lt; 0.007). Responses to treatment were far smaller in magnitude for all other targets. LPS and Poly(I:C) induced statistically similar increases for Toll-like receptor (TLR)2, TLR4, HMGB1, and C3, but Poly(I:C) had stronger effects on GJA1, TLR3, C1qA and MARCO expression. Remarkably, TLR3 was the only target with significant downregulation of expression after Poly(I:C) (<em>p</em> &lt; 0.0001). In addition, genotype x treatment interactions were detected for TLR3, TLR4, HMGB1, and C1qA (<em>p</em> &lt; 0.02). Thus, a peripheral immune challenge caused extensive increases for CXCL2 and CXCL10, and the genotype-treatment interactions that was seen for several targets, underscored the augmented neuroinflammatory response in mice carrying the MD. Of note is the dramatic upregulation of CXCL10 by low dose Poly(I:C). CXCL10 causes hyperexcitability via neuronal CXCR3 activation. Thus, even an asymptomatic viral infection may increase seizure susceptibility. In summary, a peripheral immune challenge causes strong upregulation of hippocampal inflammatory mediators implicated in neuronal excitability which is particularly detrimental for individuals with high seizure susceptibility, such as carriers of the 15q13.3 MD.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156951"},"PeriodicalIF":3.7,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882471","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":"IL-4 exerts beneficial anti-tumor effect dependent on a short-range manner","authors":"J.D. Zhang ,&nbsp;X.Y. Xue ,&nbsp;Y.F. Zhang ,&nbsp;S.Q. Lin ,&nbsp;Z.J. Sun ,&nbsp;L.X. Yan ,&nbsp;Y.G. Zhang ,&nbsp;W. Wang","doi":"10.1016/j.cyto.2025.156950","DOIUrl":"10.1016/j.cyto.2025.156950","url":null,"abstract":"","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156950"},"PeriodicalIF":3.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874245","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":"Anti-inflammatory effects of apigenin on LPS-induced mastitis in lactating SD rats through inhibiting TLR4/NF-κB signaling pathway","authors":"Yihan Hu ,&nbsp;Yingying Xie ,&nbsp;Yiming Sun ,&nbsp;Linghuan Luo ,&nbsp;Haibin Wang ,&nbsp;Ruili Zhang ,&nbsp;Ming Ge","doi":"10.1016/j.cyto.2025.156944","DOIUrl":"10.1016/j.cyto.2025.156944","url":null,"abstract":"<div><div>Mastitis is an important disease of the mammary gland in all kinds of lactating mammals, endangering the development of animal husbandry and human health. Apigenin is one chemical constituent of Taraxacum and Philippine Violet Herb which are effective Chinese herbs for the treatment of mastitis. It is reported that apigenin possesses anti-inflammatory activity and other pharmacological effects. However, the attenuation of apigenin on mastitis has not yet been reported. The present study investigated the protection of apigenin against lipopolysaccharide (LPS)-induced mastitis in SD rats both in vivo and in vitro. The results suggested that apigenin relieved the lesions of mammary tissues induced by LPS, decreased mRNA and protein levels of pro-inflammatory cytokines:tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). Simultaneously, apigenin reduced the increasing content of myeloperoxidase (MPO) and Toll-like receptor 4 (TLR4), and phosphorylation of nuclear factor kappa B (NF-κB) induced by LPS. The results showed that apigenin was able to attenuate the LPS-induced mastitis in rats by inhibiting the TLR4/NF-κB signaling pathway in vivo and in vitro, which provides scientific references for further research.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"191 ","pages":"Article 156944"},"PeriodicalIF":3.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874244","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}