Journal of Inflammation-London最新文献

{"title":"Progress of CCL20-CCR6 in the airways: a promising new therapeutic target.","authors":"Ya -Jing Li, Wan-Li Geng, Chen-Chen Li, Jia-Hao Wu, Fei Gao, Yong Wang","doi":"10.1186/s12950-024-00427-5","DOIUrl":"10.1186/s12950-024-00427-5","url":null,"abstract":"<p><p>The chemokine CCL20, a small cytokine that belongs to the C-C chemokine family, interacts with its homologous receptor CCR6, which is expressed on wide range of cell types. According to current research, the CCL20-CCR6 has been established as acritical player in a diverse range of inflammatory, oncogenic, and autoimmune diseases. Within the respiratory system, CCL20-CCR6 demonstrates heightened expression in conditions such as allergic asthma, chronic airway inflammation, non-small cell lung cancer (NSCLC), chronic obstructive pulmonary disease (COPD), and other respiratory diseases, which is conducive to the inflammatory mediators recruitment and tumor microenvironment remodeling. Numerous studies have demonstrated that therapeutic interventions targeting CCL20 and CCR6, including antibodies and antagonists, have the potential to mitigate disease progression. Despite the promising research prospects surrounding the CCL20-CCR6 chemokine axis, the precise mechanisms underlying its action in respiratory diseases remain largely elusive. In this review, we delve into the potential roles of the CCL20-CCR6 axis within the respiratory system by synthesizing and analyzing current research findings. Our objective is to provide a comprehensive understanding of the CCL20-CCR6 axis and its implications for respiratory health and disease. And we aspire to propel research endeavors in this domain and furnish valuable insights for the development of future therapeutic strategies.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"21 1","pages":"54"},"PeriodicalIF":4.4,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681768/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142900922","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":"Basement membranes' role in immune cell recruitment to the central nervous system.","authors":"Shaun A Wright, Rachel Lennon, Andrew D Greenhalgh","doi":"10.1186/s12950-024-00426-6","DOIUrl":"10.1186/s12950-024-00426-6","url":null,"abstract":"<p><p>Basement membranes form part of the extracellular matrix (ECM), which is the structural basis for all tissue. Basement membranes are cell-adherent sheets found between cells and vascular endothelia, including those of the central nervous system (CNS). There is exceptional regional specialisation of these structures, both in tissue organisation and regulation of tissue-specific cellular processes. Due to their location, basement membranes perform a key role in immune cell trafficking and therefore are important in inflammatory processes causing or resulting from CNS disease and injury. This review will describe basement membranes in detail, with special focus on the brain. We will cover how genetic changes drive brain pathology, describe basement membranes' role in immune cell recruitment and how they respond to various brain diseases. Understanding how basement membranes form the junction between the immune and central nervous systems will be a major advance in understanding brain disease.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"21 1","pages":"53"},"PeriodicalIF":4.4,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11660997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142873609","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":"Effect of statins on arterial wall inflammation as assessed by 18F-FDG PET CT: an updated systematic review and meta-analysis.","authors":"Tannaz Jamialahmadi, Željko Reiner, Luis E Simental-Mendia, Wael Almahmeed, Sercan Karav, Ali H Eid, Francesco Giammarile, Amirhossein Sahebkar","doi":"10.1186/s12950-024-00421-x","DOIUrl":"10.1186/s12950-024-00421-x","url":null,"abstract":"<p><strong>Background: </strong>Pathogenesis of atherosclerosis is largely mediated by inflammatory process. Statins are lipid-lowering drugs which also have anti-inflammatory effects. 18 fluorine radiolabeled fluorodeoxyglucose (18 F-FDG) positron emission tomography-computed tomography (PET-CT) is considered to be a good indicator of arterial wall inflammation. Therefore, in this meta-analysis the role of statins on inflammatory process in the artery wall was evaluated using this method since its actual validity for this purpose is not yet well established.</p><p><strong>Methods: </strong>PubMed, Scopus, Web of Science, ClinicalTrials.gov, and Google Scholar databases were searched using MESH terms and keywords. Funnel plot, Begg's rank correlation, and Egger's weighted regression tests evaluated publication bias in the meta-analysis. In cases where funnel plot asymmetry was observed, the \"trim and fill\" method was used to check the input of potentially missing studies.</p><p><strong>Results: </strong>Findings of 10 clinical trials involving 373 subjects showed a remarkable reduction of arterial wall 18 F-FDG uptake according to target-to-background ratio (TBR) index after treatment with statins. Subgroup analysis showed a significant decrease in TBR with high-intensity and non-significant reduction of TBR with low-to-moderate-intensity statin therapy.</p><p><strong>Conclusion: </strong>Treatment with statins suppressed arterial wall inflammation as shown by using 18 F-FDG PET-CT.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"21 1","pages":"52"},"PeriodicalIF":4.4,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11658251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142857009","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":"Regulatory effects of statins on CCL2/CCR2 axis in cardiovascular diseases: new insight into pleiotropic effects of statins.","authors":"Hanieh Gholamalizadeh, Behzad Ensan, Sercan Karav, Tannaz Jamialahmadi, Amirhossein Sahebkar","doi":"10.1186/s12950-024-00420-y","DOIUrl":"10.1186/s12950-024-00420-y","url":null,"abstract":"<p><strong>Background: </strong>HMG-CoA reductase inhibitors are well-known medications in the treatment of cardiovascular disorders due to their pleiotropic and lipid-lowering properties. Herein, we reviewed the effects of statins on the CCL2/CCR2 axis.</p><p><strong>Method: </strong>Scopus and Pubmed databases were systematically searched using the following keywords:\" Hydroxymethylglutaryl CoA Reductase Inhibitors\",\" HMG-CoA Reductase Inhibitors\",\" Statins\", \"CCL2, Chemokine\", \"Monocyte Chemoattractant Protein-1\" and \"Chemokine (C-C Motif) Ligand 2\". Evidence investigating the role of statin on MCP-1 in CVD was identified and bibliographies were completely evaluated to gather further related studies.</p><p><strong>Results: </strong>The anti-inflammatory effects of statins on the CCL2/CCR2 pathway have been widely investigated. Despite inconclusive results, a great body of research supports the regulatory roles of statins on this pathway due to their pleiotropic effects. By disrupting the CCL2/CCR2 axis, statins attenuate the infiltration of monocytes and macrophages into the zone of inflammation and hence down-regulate the inflammatory cascades in various CVDs including atherosclerosis, cardiac remodeling, and stroke, among others.</p><p><strong>Conclusion: </strong>CCL2 plays a major role in the pathogenesis of cardiovascular disorders. Down-regulation of CCL2 is proposed as one of the pleiotropic properties of statins. However, more investigations are required to elucidate which statin in what dose exerts a more potent effect on CCL2/CCR2 pathway.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"21 1","pages":"51"},"PeriodicalIF":4.4,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11658147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142857067","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":"Resolution of acute inflammation induced by monosodium urate crystals (MSU) through neutrophil extracellular trap-MSU aggregate-mediated negative signaling.","authors":"Cheng-Hsun Lu, Chieh-Yu Shen, Ko-Jen Li, Cheng-Han Wu, Yu-Hsuan Chen, Yu-Min Kuo, Song-Chou Hsieh, Chia-Li Yu","doi":"10.1186/s12950-024-00423-9","DOIUrl":"10.1186/s12950-024-00423-9","url":null,"abstract":"<p><strong>Background: </strong>Polymorphonuclear neutrophils (PMN) activation by monosodium urate crystals (MSU) is crucial to acute gouty arthritis and subsequent spontaneous remission within 7-10 days. Activated PMNs release neutrophil extracellular traps (NETs) that entrap MSU crystals, forming NET-MSU aggregates. Whether NET-MSU aggregates contribute to the resolution of acute inflammation remains to be elucidated. This study uses a cell-based approach to unveil their molecular bases.</p><p><strong>Methods: </strong>All-trans retinoic acid-differentiated HL-60 cells (dHL-60) served as surrogate PMNs. NET release from MSU-activated dHL-60 was confirmed by detecting DNA, neutrophil elastase, and citrullinated histone 3, forming large NET-MSU aggregates. NET area was measured with Fiji software after SYTOX Green staining. Released pro-inflammatory cytokines IL-8 and TNF-α, and the anti-inflammatory cytokine IL-1RA in culture supernatants were quantified to calculate the estimate inflammation score (EIS). Cellular redox state was determined by a FRET-based sensor. Expression of intracellular positive (ERK1/2) and negative (SHP-1 and SHIP-1) cytokine signaling regulators was detected by western blot. qPCR detected mRNA expressions of CISH and SOCS1-SOCS7. Flow cytometry measured neutrophil N1 (CD54) and N2 (CD182) surface markers after staining with fluorescent-conjugated antibodies.</p><p><strong>Results: </strong>Incubating dHL-60 with MSU for 4 h maximized NET-MSU aggregate formation and acute inflammation with an EIS of 11.6. Prolonging the incubation of dHL-60 + MSU to 22 h gradually raised the EIS to 19.40 without increasing NET area, due to reduced cellular redox capacity. Adding both new dHL-60 and new MSU crystals to the culture, mimicking the clinical scenario, increased NET area but conversely suppressed EIS to 1.53, indicating acute inflammation resolution. The resolution of acute inflammation following prolonged incubation was attributed to decreases in P-ERK and increases in P-SHP-1, SOCS2, SOCS3, and CISH gene expressions, which may suppress pro-inflammatory and enhance anti-inflammatory cytokine production. Moreover, the large NET-MSU aggregates facilitated N1 to N2 polarization, crucial for accelerating inflammation resolution.</p><p><strong>Conclusion: </strong>We explored the potential molecular basis for the spontaneous resolution of MSU induced acute inflammation using a cell-based model in that huge NET-MSU aggregates frustrate the transformation of newly entering PMNs to the N2 phenotype, enhancing the production of the anti-inflammatory cytokine IL-1RA.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"21 1","pages":"50"},"PeriodicalIF":4.4,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11604016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142741488","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":"Macrophage involvement in idiopathic inflammatory myopathy: pathogenic mechanisms and therapeutic prospects.","authors":"Ziqi Li, Huan Liu, Qibing Xie, Geng Yin","doi":"10.1186/s12950-024-00422-w","DOIUrl":"10.1186/s12950-024-00422-w","url":null,"abstract":"<p><p>Idiopathic inflammatory myopathies are a group of systemic autoimmune diseases characterized by chronic muscle inflammation and diverse clinical manifestations. Macrophages, pivotal components of innate immunity, are implicated in immune responses, inflammation resolution, and tissue repair. Distinct macrophage polarization states play vital roles in disease progression and resolution. Mechanistically, activated macrophages release proinflammatory cytokines, chemokines, and reactive oxygen species, perpetuating immune responses and tissue damage. Dysregulated macrophage polarization contributes to sustained inflammation. Here, we reviewed the intricate contributions of macrophages to IIM pathogenesis and explored novel therapeutic avenues. We discussed emerging strategies targeting macrophages, including receptor-based interventions and macrophage polarization modulation, for IIM treatment. This review underscores the multifaceted involvement of macrophages in IIM pathogenesis and offers insights into potential therapeutic approaches targeting these immune cells for disease management.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"21 1","pages":"48"},"PeriodicalIF":4.4,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11590228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142734763","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":"Non-ionic surfactant vesicles exert anti-inflammatory effects through inhibition of NFκB.","authors":"Jonathan McGahon, Stuart Woods, Riccardo D'Elia, Craig W Roberts","doi":"10.1186/s12950-024-00419-5","DOIUrl":"10.1186/s12950-024-00419-5","url":null,"abstract":"<p><p>Inflammation can be an unwanted consequence or cause of debilitating diseases of infectious and non-infectious aetiologies. Current anti-inflammatory medications have several deficiencies including lack of specificity and undesirable side effects. Herein, the potential of non-ionic surfactant vesicles (NISV) comprised of monopalmityol glycerol, dicetyl phosphate and cholesterol) as an anti-inflammatory drug and their mode of action is investigated. NISV were able to inhibit LPS-induced IL-6 from BMD macrophages. The individual components of NISV, monopalmityol glycerol, dicetyl phosphate and cholesterol did not affect LPS induced IL-6 levels, proving that formulation of NISV is essential for their anti-inflammatory effects. Transcriptomic analyses showed NISV mediated down-regulation of transcripts for inflammatory mediators in LPS stimulated macrophages. Notably, NISV downregulate NF-κB transcripts in LPS stimulated macrophages. Measurement of inflammatory mediators by cytometric bead array validated a number of transcriptomic findings as NISV were found to inhibit LPS induced IL-6, IL-12, and multiple chemokines. Further investigation demonstrated that NISV inhibited Poly(I:C) or Pam3csk4 induced inflammatory mediators. This indicates that the effects of NISV are distal to both MyD88 and TRIF signalling. Overall, the data generated highlights the potential of NISV as an anti-inflammatory therapeutic.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"21 1","pages":"49"},"PeriodicalIF":4.4,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11590361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142734765","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":"Carvacrol alleviates LPS-induced myocardial dysfunction by inhibiting the TLR4/MyD88/NF-κB and NLRP3 inflammasome in cardiomyocytes.","authors":"Lu Xu, Xu Yang, Xiao-Ting Liu, Xia-Yun Li, Han-Zhao Zhu, Yan-Hua Xie, Si-Wang Wang, Yao Li, Ye Zhao","doi":"10.1186/s12950-024-00411-z","DOIUrl":"10.1186/s12950-024-00411-z","url":null,"abstract":"<p><strong>Background: </strong>Sepsis-induced myocardial dysfunction (SIMD) may contribute to the poor prognosis of septic patients. Carvacrol (2-methyl-5-isopropyl phenol), a phenolic monoterpene compound extracted from various aromatic plants and fragrance essential oils, has multiple beneficial effects such as antibacterial, anti-inflammatory, and antioxidant properties. These attributes make it potentially useful for treating many diseases. This study aims to investigate the effects of CAR on LPS-induced myocardial dysfunction and explore the underlying mechanism.</p><p><strong>Results: </strong>H9c2 cells were stimulated with 10 µg/ml LPS for 12 h, and c57BL/6 mice were intraperitoneally injected with 10 mg/kg LPS to establish a septic-myocardial injury model. Our results showed that CAR could improve cardiac function, significantly reduce serum levels of inflammatory cytokines (including TNF-α, IL-1β, and IL-6), decrease oxidative stress, and inhibit cardiomyocyte apoptosis in LPS-injured mice. Additionally, CAR significantly downregulated the expression of TLR4, MyD88, and NF-κB in LPS-injured mice and H9c2 cells. It also inhibited the upregulation of inflammasome components (such as NLRP3, GSDMD, and IL-1β) in H9c2 cells triggered by LPS.</p><p><strong>Conclusion: </strong>Taken together, CAR exhibited potential cardioprotective effects against sepsis, which may be mainly attributed to the TLR4/MyD88/NF-κB pathway and the NLRP3 inflammasome.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"21 1","pages":"47"},"PeriodicalIF":4.4,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11568595/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142645185","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":"Unveiling the hidden world of transfer RNA-derived small RNAs in inflammation.","authors":"Peiru Qiu, Qi Jiang, Haojun Song","doi":"10.1186/s12950-024-00418-6","DOIUrl":"10.1186/s12950-024-00418-6","url":null,"abstract":"<p><p>Transfer RNA-derived small RNAs (tsRNAs) are a newly discovered class of small noncoding RNAs (sncRNAs) that include tRNA-derived stress-induced RNAs (tiRNAs) and tRNA-derived fragments (tRFs). Following the development of high-throughput sequencing technology, an increasing number of tsRNAs have been discovered with vital functions in different physiological and pathophysiological processes. Extensive research has revealed that tsRNAs are involved in various diseases, such as cancers, autoimmune illnesses and other diseases. This review focuses on the role and significance of tsRNAs in inflammation, such as the regulation of substances including inflammatory inducers, inflammatory cells and inflammatory factors, which contribute to the pathogenesis of inflammation-related diseases. Moreover, we discuss in-depth the molecular pathogenic mechanisms of tsRNAs in inflammation-related diseases through different signaling pathways and assess their clinical value, providing new perspectives for the exploration of tsRNA functions and inflammation-related diseases.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"21 1","pages":"46"},"PeriodicalIF":4.4,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11556027/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142633546","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":"Correction: Sodium butyrate alleviates R97-116 peptide-induced myasthenia gravis in mice by improving the gut microbiota and modulating immune response.","authors":"Jing Sun, Juanjuan Chen, Qinfang Xie, Mengjiao Sun, Wenjing Zhang, Hongxia Wang, Ning Liu, Qi Wang, Manxia Wang","doi":"10.1186/s12950-024-00408-8","DOIUrl":"https://doi.org/10.1186/s12950-024-00408-8","url":null,"abstract":"","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"21 1","pages":"45"},"PeriodicalIF":4.4,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11552367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142633545","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}