Inflammation Research最新文献

MitoQ alleviates mitochondria damage in sepsis-acute lung injury in a citrate synthase dependent manner. MitoQ以柠檬酸合酶依赖的方式减轻脓毒症急性肺损伤中的线粒体损伤。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-24 DOI: 10.1007/s00011-025-02055-y

Jiaojiao Sun, Sihao Jin, Zhiqiang Wang

{"title":"MitoQ alleviates mitochondria damage in sepsis-acute lung injury in a citrate synthase dependent manner.","authors":"Jiaojiao Sun, Sihao Jin, Zhiqiang Wang","doi":"10.1007/s00011-025-02055-y","DOIUrl":"10.1007/s00011-025-02055-y","url":null,"abstract":"Sepsis is a systemic inflammatory disease caused by severe infection, involving multiple organs in the body, with the lungs being the most susceptible, leading patients to develop acute lung injury (ALI). Mitoquinone Mesylate (MitoQ) is an antioxidant specifically designed to target mitochondria, and it has anti-aging and antioxidant properties. This study aimed to investigate the protective effects of MitoQ on sepsis-induced ALI and its mechanisms. C57BL/6 mice were used to establish the cecal ligation and puncture (CLP) model of sepsis and were orally administered or not administered MitoQ for two weeks. MitoQ effectively alleviated sepsis-induced lung tissue damage, inflammatory responses, oxidative stress, and apoptosis. Furthermore, MitoQ significantly inhibited oxidative stress and mitochondrial damage in pulmonary macrophages. Mechanistically, MitoQ upregulated the mRNA and protein levels of citrate synthase (CS) in lung tissues and pulmonary macrophages. Silencing the CS gene with siRNA significantly reduced the protective effects of MitoQ against oxidative stress, inflammation, and cell apoptosis. In conclusion, MitoQ alleviates sepsis-induced ALI by preserving mitochondrial function.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"92"},"PeriodicalIF":4.8,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475062","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}

引用次数: 0

Exosomes as immunomodulators in autoimmune inflammation: implications for primary Sjögren's disease. 外泌体作为自身免疫性炎症的免疫调节剂：对原发性Sjögren病的影响。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-13 DOI: 10.1007/s00011-025-02053-0

Yanggang Hong, Siyan Chen, Xiaoyang Jiang, Jinwen Zhang, Xinyue Liang, Jiani Yao, Sheng Gao, Chunyan Hua

{"title":"Exosomes as immunomodulators in autoimmune inflammation: implications for primary Sjögren's disease.","authors":"Yanggang Hong, Siyan Chen, Xiaoyang Jiang, Jinwen Zhang, Xinyue Liang, Jiani Yao, Sheng Gao, Chunyan Hua","doi":"10.1007/s00011-025-02053-0","DOIUrl":"https://doi.org/10.1007/s00011-025-02053-0","url":null,"abstract":"Primary Sjögren's disease (pSD) is a systemic autoimmune disorder characterized by exocrine gland dysfunction and lymphocytic infiltration, leading to dry mouth and eyes. Increasing evidence implicates extracellular vesicles, particularly exosomes, as critical mediators of immune regulation in pSD. This review outlines the biogenesis, molecular composition, and immunomodulatory functions of exosomes, and summarizes their emerging roles in the pathogenesis, diagnosis, and potential treatment of pSD. Exosomes derived from immune and glandular cells carry diverse cargoes, such as miRNAs, proteins, and nucleic acids, that modulate disease-relevant immune pathways. For example, exosomal miR-BART13-3p from Epstein-Barr virus-infected B cells suppresses STIM1 and AQP5, impairing salivary gland function, while PD-L1-enriched exosomes from mesenchymal stem cells inhibit T follicular helper cell polarization via the PI3K/AKT pathway, thereby modulating B-cell activation. Additional exosomal cargoes affect Th17/Treg balance, inflammasome activation, and type I interferon signaling. We also highlight the diagnostic potential of disease-specific exosomal markers in plasma and discuss advances in preclinical studies using exosomes as therapeutic agents. However, significant challenges remain, including cargo heterogeneity, lack of standardized isolation methods, and limited clinical data, all of which hinder the translation of exosome-based therapies into clinical practice. By integrating mechanistic and translational findings, this review provides a comprehensive perspective on the immunological and clinical relevance of exosomes in pSD. These insights may guide future development of diagnostic biomarkers and targeted therapies in autoimmune diseases.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"91"},"PeriodicalIF":4.8,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144283819","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}

引用次数: 0

The relationship between neurodevelopmental disorders (NDDs) and NLRP3 inflammasome. 神经发育障碍（ndd）与NLRP3炎性体的关系。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-03 DOI: 10.1007/s00011-025-02052-1

Abbas Shahi, Zahra Firoozi, Ghaidaa Raheem Lateef Al-Awsi, Ebrahim Mirzaei, Hojjat Shahbazi, Zahra Rezaee, Elham Mohammadisoleimani, Yaser Mansoori, Ali Moravej

{"title":"The relationship between neurodevelopmental disorders (NDDs) and NLRP3 inflammasome.","authors":"Abbas Shahi, Zahra Firoozi, Ghaidaa Raheem Lateef Al-Awsi, Ebrahim Mirzaei, Hojjat Shahbazi, Zahra Rezaee, Elham Mohammadisoleimani, Yaser Mansoori, Ali Moravej","doi":"10.1007/s00011-025-02052-1","DOIUrl":"https://doi.org/10.1007/s00011-025-02052-1","url":null,"abstract":"The brain's process of creating neural networks that affect functionality or performance is referred to as neurodevelopment. A person's capacity to learn and remember, pay attention, regulate their emotions, socialize, exercise and self-control are just a few of the cognitive and motor abilities that can be affected by abnormal brain development. Numerous neurodevelopmental diseases have been functionally related to abnormalities in innate immune signaling networks. Innate immunity is in charge of the defense of humans against pathogens and tissue damage by triggering inflammation, mainly through sensing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Some of these inflammatory processes have been shown to be mediated by large multiprotein complexes called inflammasomes which are present in cytosol and play important roles in the immune system. Due to its role in defense against infectious agents, bacteria, viruses, and fungi, NLRP3 is almost the most studied and well-known member of inflammasomes. The involvement of NLRP3 in inflammatory illnesses is evident due to the wide range of triggers and its intricate signaling pathways. In disorders with neurodevelopmental underpinnings, such as autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), schizophrenia (SCZ), obsessive compulsive disorder (OCD), bipolar disorder (BD), Tourette syndrome (TS), etc., neuroinflammation plays a significant role in their pathophysiology. For these reasons, we reviewed the roles of NLRP3 in various neurodevelopmental disorders below.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"90"},"PeriodicalIF":4.8,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208452","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}

引用次数: 0

Successful treatment of refractory erythrodermic pemphigus foliaceus with low-dose rituximab and intravenous immunoglobulin. 小剂量利妥昔单抗联合静脉注射免疫球蛋白成功治疗难治性红皮病性天疱疮。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-06-03 DOI: 10.1007/s00011-025-02059-8

Jiawen Zhang, Chengfeng Zhang, Zhongyi Xu, Jun Liang, Qinyuan Zhu

引用次数: 0

OptiStack classifier: optimized stacking framework with ensemble feature engineering for enhanced cardiovascular risk prediction. OptiStack分类器：采用集成特征工程优化的叠加框架，增强心血管风险预测。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-05-31 DOI: 10.1007/s00011-025-02039-y

M Dhilsath Fathima, S P Raja, K Jayanthi, R Hariharan

{"title":"OptiStack classifier: optimized stacking framework with ensemble feature engineering for enhanced cardiovascular risk prediction.","authors":"M Dhilsath Fathima, S P Raja, K Jayanthi, R Hariharan","doi":"10.1007/s00011-025-02039-y","DOIUrl":"https://doi.org/10.1007/s00011-025-02039-y","url":null,"abstract":"Background: Cardiovascular diseases (CVD) are a leading cause of morbidity and mortality globally, highlighting the urgent need for accurate risk prediction to improve early intervention and management. Traditional models have difficulty capturing the complex interactions between risk factors, which limits their predictive power.Objective: This paper proposes the OptiStack Classifier, an optimized stacking framework developed to enhance CVD risk prediction through ensemble feature engineering and machine learning techniques.Methods: The model uses dimensionality reduction and ensemble feature engineering methods, including polynomial expansion, binning and domain-specific feature transformation, to improve data representation. Principal Component Analysis (PCA) is used to dimensionality reduction, improving computational efficiency. A stacking framework integrates multiple machine learning algorithms as base learners, with Logistic Regression acting as the meta-classifier. Bayesian Optimization is applied for hyperparameter tuning, further boosting predictive performance.Results: The proposed model shows significant improvements in predicting CVD risk, helping with early diagnosis and prevention, which can lead to better health outcomes for patients.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"88"},"PeriodicalIF":4.8,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191732","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}

引用次数: 0

Interleukin-37 modulates microglial phenotype and inhibits inflammatory response via the MyD88/NF-κB pathway in lipopolysaccharide-induced neuroinflammation. 在脂多糖诱导的神经炎症中，白细胞介素-37通过MyD88/NF-κB通路调节小胶质细胞表型并抑制炎症反应。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-05-29 DOI: 10.1007/s00011-025-02048-x

Jingwen Zhang, Muhammad Abid Hayat, Yu Si, Tao Guo, Yinying Ni, Qian Wang, Yancheng Hong, Yudie Cao, Sijia He, Zijuan Weng, Fengmei Li, Hao Zuo, Xin Sun, Bo Chen, Jiabo Hu

{"title":"Interleukin-37 modulates microglial phenotype and inhibits inflammatory response via the MyD88/NF-κB pathway in lipopolysaccharide-induced neuroinflammation.","authors":"Jingwen Zhang, Muhammad Abid Hayat, Yu Si, Tao Guo, Yinying Ni, Qian Wang, Yancheng Hong, Yudie Cao, Sijia He, Zijuan Weng, Fengmei Li, Hao Zuo, Xin Sun, Bo Chen, Jiabo Hu","doi":"10.1007/s00011-025-02048-x","DOIUrl":"https://doi.org/10.1007/s00011-025-02048-x","url":null,"abstract":"Objective: Interleukin-37 (IL-37), an anti-inflammatory cytokine within the interleukin-1 (IL-1) family, exhibits immunomodulatory properties. Here we evaluate the effects of IL-37 on microglia in neuroinflammation and its potential mechanisms.Methods: C57BL/6 mice were injected intraperitoneally with 1 µg of recombinant human IL-37 protein (rhIL-37), and 24 h later with lipopolysaccharide (LPS) (5 mg/kg) to induce neuroinflammation. After 2-h pretreatment of BV2 cells with rhIL-37 (100 ng/mL), an in vitro model was established by treating with LPS (100 ng/mL). Mice were assessed for behavioral tests, and neuronal damage was evaluated by Nissl staining and hematoxylin and eosin staining. The expression of Iba1, CD86, CD206, and NF-κB were detected by immunofluorescence staining, and inflammatory mediators and pathway proteins were evaluated by ELISA, qRT-PCR, and Western blot.Results: IL-37 significantly ameliorated LPS-induced behavioral deficits and protected mice from inflammatory injury. In vitro experiments suggested that IL-37 modulates polarization of microglia from M1 to M2 phenotype, along with reducing pro-inflammatory cytokine production. Moreover, IL-37 attenuated the production of NF-κB and MyD88.Conclusions: IL-37 regulates microglia against neuroinflammatory responses by blocking the MyD88/NF-κB pathway and shows for the first time how IL-37 influences the phenotype of microglia, suggesting a potential therapeutic target for neuroinflammation.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"87"},"PeriodicalIF":4.8,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173613","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}

引用次数: 0

Aldosterone induces renal lymphangiogenesis through macrophage-lymphatic endothelial cell transformation and Inhibition by esaxerenone. 醛固酮通过巨噬细胞-淋巴内皮细胞转化诱导肾淋巴管生成，并通过艾赛酮的抑制诱导。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-05-24 DOI: 10.1007/s00011-025-02044-1

Haixia Guo, Ziqian Liu, Ruyan Lv, Boya Zhang, Panpan Qiang, Xuan Wang, Yi Chang, Fan Yang, Tatsuo Shimosawa, Qingyou Xu, Yunzhao Xiong

{"title":"Aldosterone induces renal lymphangiogenesis through macrophage-lymphatic endothelial cell transformation and Inhibition by esaxerenone.","authors":"Haixia Guo, Ziqian Liu, Ruyan Lv, Boya Zhang, Panpan Qiang, Xuan Wang, Yi Chang, Fan Yang, Tatsuo Shimosawa, Qingyou Xu, Yunzhao Xiong","doi":"10.1007/s00011-025-02044-1","DOIUrl":"https://doi.org/10.1007/s00011-025-02044-1","url":null,"abstract":"Objective and design: Inflammation plays a crucial role in the occurrence and development of renal fibrosis. Lymphatic vessels have emerged as new hotspots in the domain of inflammation. Recent studies have revealed that macrophages are involved in lymphangiogenesis through direct and indirect mechanisms. However, the underlying mechanisms of macrophage transdifferentiation into lymphatic endothelial cells (LECs) are still poorly understood.Methods: In vivo, thirty male Wistar rats were randomly divided into a sham group, an aldosterone group and an aldosterone + esaxerenone group. In vitro, Raw 264.7 cells and bone marrow-derived macrophages (BMDMs) were used. H&E, Masson, western blotting, immunohistochemistry, immunofluorescence, flow cytometry, and BMDM tube formation assays were used to assess renal fibrosis and lymphangiogenesis in a rat model of aldosterone-induced renal injury.Results: In this study, we observed pathological renal fibrosis and lymphangiogenesis in 12-week-old rats after aldosterone infusion. In addition, the treatment of rats with esaxerenone, a mineralocorticoid receptor blocker (MRB), significantly reduced renal lymphangiogenesis and fibrosis. Interestingly, we found that aldosterone can activate MR to stimulate macrophages to secrete vascular endothelial growth factor C (VEGF-C) and promote lymphatic angiogenesis.Conclusions: Our data suggest that renal fibrosis occurs in aldosterone-treated rats and that inflammation-induced macrophage transdifferentiation into LECs occurs during this process and that MRB attenuates renal fibrosis and lymphangiogenesis due to inflammatory injury.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"85"},"PeriodicalIF":4.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142374","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}

引用次数: 0

Melatonin inhibits salivary gland epithelial cell ferroptosis via the NRF2/HO-1/GPX4 signaling pathway in primary Sjögren's syndrome. 褪黑素通过NRF2/HO-1/GPX4信号通路抑制原发性Sjögren综合征唾液腺上皮细胞铁下垂。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-05-24 DOI: 10.1007/s00011-025-02047-y

Xiuhong Weng, Simin Wang, Qing Wang, Mingbo Wei, Bo Cheng

{"title":"Melatonin inhibits salivary gland epithelial cell ferroptosis via the NRF2/HO-1/GPX4 signaling pathway in primary Sjögren's syndrome.","authors":"Xiuhong Weng, Simin Wang, Qing Wang, Mingbo Wei, Bo Cheng","doi":"10.1007/s00011-025-02047-y","DOIUrl":"https://doi.org/10.1007/s00011-025-02047-y","url":null,"abstract":"Background: Primary Sjögren's syndrome (pSS) is an autoimmune disease characterized by xerostomia and autoimmune sialadenitis. Interferon-γ (IFN-γ) induces ferroptosis in salivary gland epithelial cells (SGECs), leading to salivary gland (SG) hypofunction. We previously demonstrated the beneficial effects of melatonin (MLT) in alleviating SG dysfunction and inflammation in a pSS animal model. However, the precise underlying mechanism remains unclear.Methods: Female NOD/ltj and ICR mice were used as the pSS mouse model and control group, respectively. MLT was administered via intraperitoneal injection to NOD/ltj mice to detect its effect on ferroptosis in SGs. Primary human SGECs and A253 cells were treated with IFN-γand ferroptosis inducers, with or without MLT.Results: Exogenous MLT alleviated pathological SG alterations and promoted saliva production through inhibiting SGEC ferroptosis. MLT inhibited SGEC ferroptosis induced by IFN-γ and ferroptosis inducers via nuclear factor erythroid 2-related factor 2/heme oxygenase-1/glutathione peroxidase 4 (NRF2/HO-1/GPX4) pathway activation. Moreover, MLT suppressed the nuclear factor-kappa B (NF-κB) pathway, which is triggered by ferroptosis in SGECs. Nevertheless, ML385-mediated NRF2 inhibition abrogated the antiferroptotic protective effects of MLT on SGECs.Conclusions: MLT inhibits SGEC ferroptosis through NRF2/HO-1/GPX4 pathway activation and thus attenuates ferroptosis-triggered NF-κB activity. Melatonin represents a potential therapeutic approach for pSS owing to its capacity to regulate ferroptosis.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"84"},"PeriodicalIF":4.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142403","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}

引用次数: 0

Influence of homocysteine on regulating immunothrombosis: mechanisms and therapeutic potential in management of infections. 同型半胱氨酸对调节免疫血栓形成的影响：感染管理的机制和治疗潜力。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-05-24 DOI: 10.1007/s00011-025-02045-0

Aswathy S Nair, Lloyd Tauro, Harshit B Joshi, Arnab Makhal, Teddy Sobczak, Julien Goret, Antoine Dewitte, Srinivas Kaveri, Harinath Chakrapani, Maria Mamani Matsuda, Manjunath B Joshi

{"title":"Influence of homocysteine on regulating immunothrombosis: mechanisms and therapeutic potential in management of infections.","authors":"Aswathy S Nair, Lloyd Tauro, Harshit B Joshi, Arnab Makhal, Teddy Sobczak, Julien Goret, Antoine Dewitte, Srinivas Kaveri, Harinath Chakrapani, Maria Mamani Matsuda, Manjunath B Joshi","doi":"10.1007/s00011-025-02045-0","DOIUrl":"10.1007/s00011-025-02045-0","url":null,"abstract":"Mechanisms controlling innate immune responses and coagulation are interdependent, evolutionarily entangled and make a complex network to form immuno-thrombosis axis which is an integral part of host-defence response. During infections, immunothrombosis generates intravascular scaffold enabling recognition, trap and destruction of pathogens facilitating tissue integrity. However, the accompanying dysregulation fosters into pathologies associated with thrombosis and regulates severity, morbidity and mortality in infections. Several extrinsic and intrinsic factors such as (epi)genetic mechanisms, age, metabolism and lifestyle regulate immunothrombosis during infections. Mounting evidence demonstrates that homocysteine, a metabolic intermediate of methionine synthesis pathway activate cells participating in immuno-thrombosis such as neutrophils, platelets, monocytes and endothelial cells. Interestingly, multiple infections are significantly associated with perturbed homocysteine metabolism. In the present review, we describe mechanistic insights into how homocysteine drives immuno-thrombotic crosstalk that generate a vicious cycle of inflammation and coagulation that fuels organ failure during infections with an emphasis on sepsis, COVID-19, and other infectious diseases caused by parasites, viral, and bacterial pathogens. Subsequently, we discuss therapeutic strategies targeting homocysteine metabolism that may improve clinical outcomes in infections.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"86"},"PeriodicalIF":4.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142378","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}

引用次数: 0

Lung contusion drives lung injury by modifying miRNA cargo in alveolar small extracellular vesicles. 肺挫伤通过改变肺泡小细胞外囊泡中的miRNA货物驱动肺损伤。

IF 4.8 3区医学

Inflammation Research Pub Date : 2025-05-24 DOI: 10.1007/s00011-025-02051-2

Keita Nakatsutsumi, Dong Jun Park, Wooil Choi, William Johnston, Katie Pool, Jenny Kezios, Raul Coimbra, Brian P Eliceiri, Todd W Costantini

{"title":"Lung contusion drives lung injury by modifying miRNA cargo in alveolar small extracellular vesicles.","authors":"Keita Nakatsutsumi, Dong Jun Park, Wooil Choi, William Johnston, Katie Pool, Jenny Kezios, Raul Coimbra, Brian P Eliceiri, Todd W Costantini","doi":"10.1007/s00011-025-02051-2","DOIUrl":"10.1007/s00011-025-02051-2","url":null,"abstract":"Objective: To evaluate the micro-RNA (miRNA) cargo of alveolar small extracellular vesicles (sEVs) after lung contusion (LC), which can contribute to the development of trauma-related acute lung injury (ALI).Methods: A mouse model of LC was conducted with a controlled cortical impact device. Bronchoalveolar lavage fluid (BAL) was collected 24 h post-injury and sEVs were purified using size exclusion chromatography. sEVs characteristics and miRNA cargo were analyzed with vesicle flow cytometry and sequencing. Macrophages were treated with BAL sEVs in vitro to assess their pro-inflammatory effect.Results: LC increased lung permeability and caused ALI histologically. LC increased the number of sEVs in the BAL and altered their miRNA cargo. BAL sEVs collected after LC increased pro-inflammatory cytokine release from macrophages.Conclusion: LC increased the mobilization of sEVs to the alveolar space and modified their miRNA cargo that might contribute to the development of ALI by activating the immune response in macrophages.","PeriodicalId":13550,"journal":{"name":"Inflammation Research","volume":"74 1","pages":"83"},"PeriodicalIF":4.8,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142402","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}

引用次数: 0