Inflammation Research最新文献

{"title":"Editorial expression of concern: Monocytes and lymphocytes as active participants in the pathogenesis of experimental shock.","authors":"D Altavilla, F Squadrito, L Ammendolia, G Squadrito, G M Campo, P Canale, M Ioculano, C Musolino, A Alonci, A Sardella, G Urna, A Saitta, A P Caputi","doi":"10.1007/s00011-024-01930-4","DOIUrl":"10.1007/s00011-024-01930-4","url":null,"abstract":"","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2281"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139974","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":"Single-cell transcriptome analysis of the mouse lungs during the injury and recovery periods after lipopolysaccharide administration.","authors":"Hou-Ping Wang, Jian He, Jian-Rong He, Dan-Dan Li, He Huang, Bing Chen","doi":"10.1007/s00011-024-01951-z","DOIUrl":"10.1007/s00011-024-01951-z","url":null,"abstract":"<p><strong>Objective: </strong>This study sought to investigate the cellular and molecular alterations during the injury and recovery periods of ALI and develop effective treatments for ALI.</p><p><strong>Methods: </strong>Pulmonary histology at 1, 3, 6, and 9 days after lipopolysaccharide administration mice were assessed. An unbiased single-cell RNA sequencing was performed in alveoli tissues from injury (day 3) and recovery (day 6) mice after lipopolysaccharide administration. The roles of Fpr2 and Dpp4 in ALI were assessed.</p><p><strong>Results: </strong>The most severe lung injury occurred on day 3, followed by recovery entirely on day 9 after lipopolysaccharide administration. The numbers of Il1a⁺ neutrophils, monocytes/macrophages, and Cd4⁺ and Cd8⁺ T cells significantly increased at day 3 after LPS administration; subsequently, the number of Il1a⁺ neutrophils greatly decreased, the numbers of monocytes/macrophages and Cd4⁺ and Cd8⁺ T cells continuously increased, and the number of resident alveolar macrophages significantly increased at day 6. The interactions between monocytes/macrophages and pneumocytes during the injury period were enhanced by the Cxcl10/Dpp4 pair, and inhibiting Dpp4 improved ALI significantly, while inhibiting Fpr2 did not.</p><p><strong>Conclusions: </strong>Our results offer valuable insights into the cellular and molecular mechanisms underlying its progression and identify Dpp4 as an effective therapeutic target for ALI.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2087-2107"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390244","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":"Retraction Note: The role of nitric oxide during healing of trauma to the skeletal muscle.","authors":"Lidiane Isabel Filippin, María José Cuevas, Elena Lima, Norma Possa Marroni, Javier Gonzalez Gallego, Ricardo Machado Xavier","doi":"10.1007/s00011-024-01963-9","DOIUrl":"10.1007/s00011-024-01963-9","url":null,"abstract":"","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2279"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499587","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":"Molecular mechanism of mechanical pressure induced changes in the microenvironment of intervertebral disc degeneration.","authors":"Fei Liu, Song Chao, Lei Yang, Chaoqi Chen, Wutao Huang, Feng Chen, Zhiwei Xu","doi":"10.1007/s00011-024-01954-w","DOIUrl":"10.1007/s00011-024-01954-w","url":null,"abstract":"<p><strong>Background: </strong>Lower back pain, as a typical clinical symptom of spinal degenerative diseases, is emerging as a major social problem. According to recent researches, the primary cause of this problem is intervertebral disc degeneration (IVDD). IVDD is closely associated with factors such as age, genetics, mechanical stimulation (MS), and inadequate nutrition. In recent years, an increasing number of studies have further elucidated the relationship between MS and IVDD. However, the exact molecular mechanisms by which MS induces IVDD remain unclear, highlighting the need for in-depth exploration and study of the relationship between MS and IVDD.</p><p><strong>Methods: </strong>Search for relevant literature on IVDD and MS published from January 1, 2010, to the present in the PubMed database.</p><p><strong>Results: </strong>One of the main causes of IVDD is MS, and loading modalities have an impact on the creation of matrix metalloproteinase, the metabolism of the cellular matrix, and other biochemical processes in the intervertebral disc. Nucleus pulposus cell death induced by MS, cartilage end-plate destruction accompanied by pyroptosis, apoptosis, iron death, senescence, autophagy, oxidative stress, inflammatory response, and ECM degradation interact with one another to form a cooperative signaling network.</p><p><strong>Conclusion: </strong>This review discusses the molecular mechanisms of the changes in the microenvironment of intervertebral discs caused by mechanical pressure, explores the interaction between mechanical pressure and IVDD, and provides new insights and approaches for the clinical prevention and treatment of IVDD.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2153-2164"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390243","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":"Macrophage activation syndrome in Sepsis: from pathogenesis to clinical management.","authors":"Shunyao Chen, Cong Zhang, Jialiu Luo, Zhiqiang Lin, Teding Chang, Liming Dong, Deng Chen, Zhao-Hui Tang","doi":"10.1007/s00011-024-01957-7","DOIUrl":"10.1007/s00011-024-01957-7","url":null,"abstract":"<p><strong>Background: </strong>Sepsis represents a significant global health and hygiene challenge. Excessive activation of macrophages in sepsis can result in certain patients displaying characteristics akin to those observed in Macrophage Activation Syndrome (MAS). MAS represents a grave immune system disorder characterized by persistent and severe inflammation within the body. In the context of sepsis, MAS presents atypically, leading some researchers to refer to it as Macrophage Activation-Like Syndrome (MALS). However, there are currently no effective treatment measures for this situation. The purpose of this article is to explore potential treatment methods for sepsis-associated MALS.</p><p><strong>Objective: </strong>The objective of this review is to synthesize the specific pathophysiological mechanisms and treatment strategies of MAS to investigate potential therapeutic approaches for sepsis-associated MALS.</p><p><strong>Method: </strong>We searched major databases (including PubMed, Web of Science, and Google Scholar etc.) for literature encompassing macrophage activation syndrome and sepsis up to Mar 2024 and combined with studies found in the reference lists of the included studies.</p><p><strong>Conclusion: </strong>We have synthesized the underlying pathophysiological mechanism of MALS in sepsis, and then summarized the diagnostic criteria and the effects of various treatment modalities utilized in patients with MAS or MALS. In both scenarios, heterogeneous treatment responses resulting from identical treatment approaches were observed. The determination of whether the patient is genuinely experiencing MALS significantly impacts the ultimate outcomes of therapeutic efficacy. In order to tackle this concern, additional clinical trials and research endeavors are imperative.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2179-2197"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464296","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":"Inhibition of neuroinflammation and neuronal damage by the selective non-steroidal ERβ agonist AC-186.","authors":"Folashade O Katola, Misturah Y Adana, Olumayokun A Olajide","doi":"10.1007/s00011-024-01952-y","DOIUrl":"10.1007/s00011-024-01952-y","url":null,"abstract":"<p><strong>Background: </strong>AC-186 (4-[4-4-Difluoro-1-(2-fluorophenyl) cyclohexyl] phenol) is a neuroprotective non-steroidal selective oestrogen receptor modulator. This study investigated whether inhibition of neuroinflammation contributed to neuroprotective activity of this compound.</p><p><strong>Methods: </strong>BV-2 microglia were treated with AC-186 (0.65-5 μM) prior to stimulation with LPS (100 ng/mL). Levels of pro-inflammatory mediators and proteins were then evaluated.</p><p><strong>Results: </strong>Treatment of LPS-activated BV-2 microglia with AC-186 resulted in significant (p < 0.05) reduction in TNFα, IL-6, NO, PGE₂, iNOS and COX-2. Further investigations showed that AC-186 decreased LPS-induced elevated levels of phospho-p65, phospho-IκBα and acetyl-p65 proteins, while blocking DNA binding and luciferase activity of NF-κB. AC-186 induced significant (p < 0.05) increase in protein expression of ERβ, while enhancing ERE luciferase activity in BV-2 cells. Effects of the compound on oestrogen signalling in the microglia was confirmed in knockdown experiments which revealed a loss of anti-inflammatory activity following transfection with ERβ siRNA. In vitro neuroprotective activity of AC-186 was demonstrated by inhibition of activated microglia-mediated damage to HT-22 neurons.</p><p><strong>Conclusions: </strong>This study established that AC-186 produces NF-κB-mediated anti-inflammatory activity, which is proposed as a contributory mechanism involved in its neuroprotective actions. It is suggested that the anti-inflammatory activity of this compound is linked to its agonist effect on ERβ.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2109-2121"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365141","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":"CD90's role in vascularization and healing of rib fractures: insights from Dll4/notch regulation.","authors":"Lei Wang, Rui Hu, Pei Xu, Pengkai Gao, Bin Mo, Liya Dong, Fengqing Hu","doi":"10.1007/s00011-024-01962-w","DOIUrl":"10.1007/s00011-024-01962-w","url":null,"abstract":"<p><strong>Background: </strong>Vascularization after rib fracture is a crucial physiological process that is essential for the repair and healing of the rib. Studies have shown that CD90 plays a critical role in regulating rib fracture healing, but the underlying mechanism of its role has not been fully elucidated.</p><p><strong>Methods: </strong>CD90 adenovirus knockout mice were used to construct a rib injury model. The bone healing was observed by micro-CT. CD31/EMCN immunofluorescence staining was performed on bone tissue to observe the density of H-shaped and L-shaped blood vessels at the site of bone injury. CD31 and EMCN dual-stained single cells from the rib fracture sites were detected by flow cytometry. The periosteal stem cells transfected with CD90 or Notch1 overexpression and silencing vector were co-cultured with osteoblast MC3T3-E1 in osteogenic induction medium. Moreover, bone microvascular endothelial cells were extracted from the rib injury and co-cultured with the periosteal stem cells transfected with CD90. CCK-8 was used to detect cell viability, RT-qPCR and Western blot were used to detect Notch1, Notch2, Notch3, Notch4, CD31, HIF-1α, CD90, RUNX2, OCN and OPN expression. Alkaline phosphatase (ALP) staining and alizarin red staining were used to observe mineralized nodules. Immunofluorescence staining was used to detect the expression of Dll4, Notch, and CD90 in each group of cells. The angiogenesis experiment was conducted to observe cellular vascular formation.</p><p><strong>Results: </strong>Compared with the Adsh-NC group, the bone healing in the Adsh-CD90 group was significantly impaired, with a marked reduction in the number and volume of blood vessels at the rib fracture site, as evidenced by CD31/EMCN immunofluorescence staining, which showed a reduction in the number of H type vessels at the site of bone injury. It was found that CD90 depletion can inhibit the signaling of Dll4/Notch in the rib fracture site. Furthermore, we found that overexpression of Notch1 reverses the impairment of tubule formation in bone microvascular endothelial cells caused by CD90 suppression.r.Dll4 protein reverses the inhibitory effect of CD90 deletion on periosteal stem cells and MC3T3-E1 cell viability and osteogenesis. In the end, we found that overexpression of Notch1 and CD90 can promote angiogenesis of bone microvascular endothelial cells and Notch pathway activation.</p><p><strong>Conclusion: </strong>CD90 can affect vascular formation in mouse rib fractures, and CD90 may be regulated by Dll4/Notch.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2263-2277"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499584","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":"Immune cells mediate the causal pathway linking circulating complements to cancer: A Mendelian randomization study.","authors":"Hao Pan, Changqing Jing","doi":"10.1007/s00011-024-01955-9","DOIUrl":"10.1007/s00011-024-01955-9","url":null,"abstract":"<p><strong>Background: </strong>The role of complement in cancer remains controversial. Whether immune cells and inflammatory factors mediate the pathway from complement to cancer has not been fully elucidated.</p><p><strong>Methods: </strong>We conducted bidirectional Mendelian randomization (MR) analysis to explore the causal association between complement components and cancer. Meta-analysis was conducted to enhance the robustness of the results. We further explored the mediation roles of immune cells and inflammatory factors in these associations.</p><p><strong>Results: </strong>Our study identified causal associations between 11 complement components and 12 types of cancer. Furthermore, we identified five immune cells as potential mediators: BAFF-R on IgD + CD38- naive B cell mediated 7.434% of the increased risk for liver cancer from C3; CD4 on CD39 + activated CD4 regulatory T cell mediated 12.384% of the increased risk for biliary tract cancer from CD93; CD25 +  + CD45RA + CD4 not regulatory T cell and Basophil %CD33dim HLA DR- CD66b- mediated 7.721% and 7.986% of the increased risk of colorectal cancer from MASP1, respectively; CD45RA on resting CD4 regulatory T cell mediated 11.444% of the increased risk of skin cancer from MASP1.</p><p><strong>Conclusion: </strong>This study revealed the causal relationships between complement components and certain cancers, with five immune cells as potential mediators.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2141-2152"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142345964","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":"Pentoxifylline in COVID-19 and considerations for its research in long COVID.","authors":"Ahmed Ramzi, Subhia Maya, Nadeen Balousha, Mufreh Amin, Mostafa Ramzi Shiha","doi":"10.1007/s00011-024-01942-0","DOIUrl":"10.1007/s00011-024-01942-0","url":null,"abstract":"<p><strong>Introduction: </strong>Pentoxifylline (PTX) affects most blood components and the blood vessels, potentially modulating various conditions. Due to its impact on markers linked to COVID-19 severity, research has explored PTX for acute COVID-19. Following the widespread administration of COVID-19 vaccinations, there has been a notable and consistently growing increase in research focusing on long COVID. Consequently, our examination of relevant acute COVID-19 data shall additionally be contextualized into long COVID research.</p><p><strong>Methods: </strong>Various Databases were searched until July 2024 for all primary clinical studies on Pentoxifylline (PTX) in COVID-19.</p><p><strong>Results: </strong>Studies were on acute infection with SARS-CoV-2 where PTX was an adjuvant to standard therapy for ethical and practical reasons under the circumstance. PTX generally reduced hospitalization duration and improved some inflammatory markers, but its impact on mortality was inconsistent. Adverse events were minimal. Meta-analysis revealed a significant reduction in hospitalization duration.</p><p><strong>Conclusion: </strong>This systematic review and meta-analysis suggest that adding pentoxifylline (PTX) to standard COVID-19 therapy may significantly reduce hospitalization duration and improve some inflammatory markers. However, its impact on mortality rates is inconclusive. Adverse events are minimal. PTX can be favorable as an add-on in managing acute COVID-19 and could reduce the risk of long COVID, as well as assist in managing many of its most common symptoms.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2057-2068"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499586","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":"Modulation of Plet1 expression by N-Acetylglucosamine through the IL-17 A-MAPK pathway in an imiquimod-induced psoriasis mouse model.","authors":"Balachandar Selvakumar, Bilal Rah, Jayalakshmi Jagal, Priyadarshini Sekar, Raneem Moustafa, Rakhee Kizhuvappat Ramakrishnan, Mohamed Haider, Saleh Mohamed Ibrahim, Rani Samsudin","doi":"10.1007/s00011-024-01958-6","DOIUrl":"10.1007/s00011-024-01958-6","url":null,"abstract":"<p><p>Psoriasis (Ps) is a chronic inflammatory disorder marked by skin plaque formation, driven by immune dysregulation and genetic factors. Despite the available treatments, incidence of Ps is increasing in the dermatology patients. Novel strategies are crucial due to current treatment limitations. The interleukin 17 (IL-17) pathway is pivotal in Ps pathogenesis, however the expression of its putative target gene placenta expressed transcript 1 (Plet1) remains unstudied in Ps. Considering the potential anti-inflammatory properties of N-Acetylglucosamine (GlcNAc), our study explored its role in modulating Plet1 expression in an imiquimod (IMQ)-induced Ps mouse model. Our data demonstarted a significant reduction of inflammation and Psoriasis Area and Severity Index (PASI) scores, downregulation of growth factors (GFs), IL-17 A, and MAPK expression after GlcNAc treatment. In addition, GlcNAc treatment reduced neutrophils, monocyte-dendritic cells (Mo-DC) and conventional T cells (Tcons) while increasing monocyte-macrophages (Mo-Macs) and regulatory T cells (Tregs). GlcNAc treatment also downregulated Plet1 overexpression in psoriatic mouse skin and in vitro, reduced proliferation and apoptosis in IL-17 A stimulated human dermal fibroblasts (HDF), along with IL-17 A and TGF-β mRNA expression. Together, these data suggest that, GlcNAc interferes with downstream mechanisms in IL-17 pathway and downregulating Plet1 expression, presenting a promising strategy for Ps treatment.</p>","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":" ","pages":"2217-2230"},"PeriodicalIF":4.8,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464297","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}