Inflammation最新文献_第2页

Uridine Phosphorylase 1 as a Biomarker Associated with Glycolysis in Acute Lung Injury.

IF 4.5 2区医学

Inflammation Pub Date : 2025-02-19 DOI: 10.1007/s10753-025-02270-z

Congkuan Song, Qingqing Li, Jinjin Zhang, Weidong Hu

引用次数: 0

Methamphetamine and HIV-1 Tat Synergistically Induce Microglial Pyroptosis Via Activation of the AIM2 Inflammasome.

IF 4.5 2区医学

Inflammation Pub Date : 2025-02-19 DOI: 10.1007/s10753-025-02266-9

Lin Miao, Haowei Wang, Xue Yang, Lisha Xu, Ruike Xu, Hanxin Teng, Yue Zhang, Yingjie Zhao, Genmeng Yang, Xiaofeng Zeng

{"title":"Methamphetamine and HIV-1 Tat Synergistically Induce Microglial Pyroptosis Via Activation of the AIM2 Inflammasome.","authors":"Lin Miao, Haowei Wang, Xue Yang, Lisha Xu, Ruike Xu, Hanxin Teng, Yue Zhang, Yingjie Zhao, Genmeng Yang, Xiaofeng Zeng","doi":"10.1007/s10753-025-02266-9","DOIUrl":"https://doi.org/10.1007/s10753-025-02266-9","url":null,"abstract":"Objective: Human immunodeficiency virus (HIV)-infected individuals who abuse methamphetamine (METH) exhibit more severe neurotoxicity and cognitive impairment. Pyroptosis, a programmed cell death pathway mediated by the inflammasome, has been implicated in various neurological diseases. This study aimed to elucidate the role of the AIM2 inflammasome in METH- and HIV-1 Tat-induced pyroptosis in human brain tissue and in vitro models.Methods: Postmortem brain tissue from HIV-infected individuals with a history of METH abuse was analyzed for pyroptosis markers and AIM2 inflammasome components using immunohistochemistry, immunofluorescence, and Western blotting. BV2 microglial cells were lentivirally transduced to knockdown AIM2 expression. DNA damage was assessed using Western blotting and the comet assay. Expression of pyroptosis-related proteins was evaluated by electron microscopy, Western blotting, and immunofluorescence. Cell viability was measured using the CCK8 assay.Results: Elevated levels of pyroptosis markers and AIM2 inflammasome components were observed in brain tissue from HIV-infected METH users. METH and Tat synergistically induced pyroptosis in BV2 cells in a time- and concentration-dependent manner, accompanied by DNA damage and activation of the AIM2 inflammasome. Knockdown of AIM2 significantly reduced the expression of pyroptosis-related proteins.Conclusion: METH and HIV-1 Tat proteins synergistically induce microglial pyroptosis by activating the AIM2 inflammasome through dsDNA damage. These findings suggest that targeting the AIM2 inflammasome may be a promising therapeutic strategy for HIV-associated neurocognitive disorder (HAND).","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143448941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Nrg4 Secreted by Brown Adipose Tissue Suppresses Ferroptosis of Sepsis-Induced Liver Injury.

IF 4.5 2区医学

Inflammation Pub Date : 2025-02-17 DOI: 10.1007/s10753-024-02230-z

Linqi Feng, Jun Cui, Wenlong Chen, Lei Zhu, Panpan Li, Haitao Zhou, Yang Sun, Wei Yi

引用次数: 0

Inhibition of SLC3A2 Deletion-Mediated Ferroptosis by Bone Marrow Stromal Cells to Alleviate Inflammation and Fibrosis in Diabetic Kidney Disease.

IF 4.5 2区医学

Inflammation Pub Date : 2025-02-17 DOI: 10.1007/s10753-025-02261-0

Yang Fan, Ya-Ling Li, Li-Lan Huang, Ji Yang, Yue-Yuan Hou, Yi-Hua Bai

{"title":"Inhibition of SLC3A2 Deletion-Mediated Ferroptosis by Bone Marrow Stromal Cells to Alleviate Inflammation and Fibrosis in Diabetic Kidney Disease.","authors":"Yang Fan, Ya-Ling Li, Li-Lan Huang, Ji Yang, Yue-Yuan Hou, Yi-Hua Bai","doi":"10.1007/s10753-025-02261-0","DOIUrl":"https://doi.org/10.1007/s10753-025-02261-0","url":null,"abstract":"Renal fibrosis and inflammatory infiltration are common pathological features of diabetic kidney disease (DKD). Bone marrow mesenchymal stem cells (BMSCs) are recognized for their anti-fibrotic and anti-inflammatory properties. The objective of this study was to assess the effects of BMSCs on DKD and elucidate their potential mechanisms of action. To assess the role of BMSCs, a DKD model was induced in Sprague-Dawley (SD) rats using streptozotocin (STZ) combined with a high-fat diet, and a human kidney-2 (HK-2) cell damage model was established using high glucose. To investigate the mechanism of the impact of BMSCs on DKD at the genetic level, transcriptome sequencing of the treated HK-2 cells was conducted, identifying the differentially expressed gene SLC3A2, which is related to ferroptosis. A HK-2 cell damage model with SLC3A2 knockout was then constructed to assess the effects of BMSCs on ferroptosis, inflammation, and fibrosis. Also, the potential relationship between BMSCs and the mitogen-activated protein kinase (MAPK) signaling pathway was assessed. In vivo and in vitro studies demonstrated that BMSCs enhanced inflammation and fibrosis in DKD by inhibiting ferroptosis. Knockdown of SLC3A2 promoted ferroptosis, inflammation, and fibrosis, while BMSCs reversed these effects, likely through the inhibition of the MAPK signaling pathway. This research demonstrated that ferroptosis and the activation of the MAPK signaling pathway can promote the onset and progression of DKD. It revealed the therapeutic role of BMSCs in DKD treatment and proposed that SLC3A2 might serve as a potential target for DKD therapy, thereby providing a theoretical foundation for the treatment of DKD.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

SIRT5 Alleviated Eosinophilic Asthma Through ROS Inhibition and Nrf2/HO-1 Activation.

IF 4.5 2区医学

Inflammation Pub Date : 2025-02-13 DOI: 10.1007/s10753-025-02257-w

Yuwei Xie, Yingzhi He, Juan Liang, Jie Liu, Chuanghong Ke, Xiaohuan Mo, Cizheng Zeng, Sijie Wang, Xuemei Chen, Dang Ao, Jinfeng Tang, Wen Li

{"title":"SIRT5 Alleviated Eosinophilic Asthma Through ROS Inhibition and Nrf2/HO-1 Activation.","authors":"Yuwei Xie, Yingzhi He, Juan Liang, Jie Liu, Chuanghong Ke, Xiaohuan Mo, Cizheng Zeng, Sijie Wang, Xuemei Chen, Dang Ao, Jinfeng Tang, Wen Li","doi":"10.1007/s10753-025-02257-w","DOIUrl":"https://doi.org/10.1007/s10753-025-02257-w","url":null,"abstract":"Asthma is a prevalent chronic disease with high morbidity and mortality in both children and adults, imposing a burden on the physical and mental well-being of patients, as well as their families. Inhaled corticosteroids and long-acting β2 agonists are mostly used to control asthma, these therapies are not suitable for patients with severe asthma. Approximately 80% of severe uncontrolled asthma cases are classified as eosinophilic asthma (EA). Oxidative stress and inflammation play crucial roles in the pathology and development of asthma, with SIRT5 being important in the process of anti-oxidation and anti-inflammation. However, little is known about the role of SIRT5 in EA and its regulatory mechanism on substrate protein and biological function. In this study, we investigated the role of SIRT5 in ovalbumin (OVA)-induced EA mouse models and house dust mite (HDM)-induced asthmatic cell models, while exploring its potential mechanisms. We found that SIRT5 alleviated EA by inhibiting reactive oxygen species and activating Nrf2/HO-1 pathways. Interestingly, overexpression of SIRT5 attenuated the inflammatory response in EA. Taken together, these results suggest that SIRT5 may serve as a promising target for managing asthma symptoms.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143407038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Sirtuin1 Deficiency Could Exacerbate Melanocyte Apoptosis Under Endoplasmic Reticulum Stress.

IF 4.5 2区医学

Inflammation Pub Date : 2025-02-08 DOI: 10.1007/s10753-025-02255-y

Jing Zhu, Youming Guo, Lingling Luo, Xin Huang, Tianqi Wei, Baiyi Zuo, Guanying Liu, Wenbo Bu, Chengrang Li

引用次数: 0

4-octyl Itaconate Attenuates Acute Pancreatitis and Associated Lung Injury by Suppressing Ferroptosis in Mice.

IF 4.5 2区医学

Inflammation Pub Date : 2025-02-07 DOI: 10.1007/s10753-025-02256-x

Shimin Lu, Yang Gong, Pengzhan He, Mingming Qi, Weiguo Dong

{"title":"4-octyl Itaconate Attenuates Acute Pancreatitis and Associated Lung Injury by Suppressing Ferroptosis in Mice.","authors":"Shimin Lu, Yang Gong, Pengzhan He, Mingming Qi, Weiguo Dong","doi":"10.1007/s10753-025-02256-x","DOIUrl":"https://doi.org/10.1007/s10753-025-02256-x","url":null,"abstract":"Acute pancreatitis (AP) is a common gastrointestinal emergency requiring hospitalization. In recent years, several studies have demonstrated a role for 4-octyl itaconate (4-OI) in anti-inflammatory and oxidative stress injury. However, the potential effects of 4-OI in AP have not been investigated. Caerulein and LPS were used to induce experimental AP models in mice and AR42J cells and then studied by histopathology, biochemical, and molecular analysis. Ferroptosis inhibitor ferrostatin-1 effectively improves pancreatic injury and reduces lipid peroxidation products in experimental AP mice. 4-OI treatment significantly alleviated pancreatic and AP-associated lung injury and inflammation in experimental AP mice by inhibiting ferroptosis. The ferroptosis activator Erastin blocked the protective effect of 4-OI against pancreatic injury in AP, validating that 4-OI alleviates pancreatitis injury through ferroptosis. In vitro experiments further confirmed that 4-OI treatment ameliorated AP-induced pancreatic injury by inhibiting ferroptosis. Our study, for the first time, found that 4-OI ameliorates AP and AP-related lung injury by inhibiting ferroptosis in experimental AP mice, providing a new therapeutic target for alleviating AP.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Therapeutic Efficacy of Intermittent Ketogenesis in Modulating Adenosine Metabolism, Immune Response, and Seizure Severity in Refractory Temporal Lobe Epilepsy: A Pilot Human Study.

IF 4.5 2区医学

Inflammation Pub Date : 2025-02-07 DOI: 10.1007/s10753-025-02264-x

Seyyed Hossein Khatami, Parsa Alehossein, Sajad Ehtiati, Tayebe Zarei, Farzaneh Salmani, Sadegh Bagherzadeh, Mohammad Razmafrooz, Masoumeh Rajabibazl, Aram Halimi, Mohammad Reza Shahmohammadi, Morteza Faghih Jouibari, Abbas Tafakhori, Saeed Karima

{"title":"Therapeutic Efficacy of Intermittent Ketogenesis in Modulating Adenosine Metabolism, Immune Response, and Seizure Severity in Refractory Temporal Lobe Epilepsy: A Pilot Human Study.","authors":"Seyyed Hossein Khatami, Parsa Alehossein, Sajad Ehtiati, Tayebe Zarei, Farzaneh Salmani, Sadegh Bagherzadeh, Mohammad Razmafrooz, Masoumeh Rajabibazl, Aram Halimi, Mohammad Reza Shahmohammadi, Morteza Faghih Jouibari, Abbas Tafakhori, Saeed Karima","doi":"10.1007/s10753-025-02264-x","DOIUrl":"https://doi.org/10.1007/s10753-025-02264-x","url":null,"abstract":"Temporal lobe epilepsy (TLE) is a common neurological disorder characterized by recurrent seizures originating in the temporal lobe, often affecting patients' physical, cognitive, and social well-being. Despite the availability of antiseizure medication (ASMs), approximately 30% of TLE patients exhibit drug-resistant seizures, emphasizing the need for alternative therapeutic approaches. Ketogenic diets, known for their anticonvulsant effects, have shown promise in managing drug-resistant epilepsy. However, their demanding high-fat, low-carbohydrate regimens pose significant adherence challenges. Medium-chain triglyceride (MCT) offers a viable alternative by inducing ketosis periodically without the need for continuous dietary restrictions. This study evaluated seizure severity, biochemical markers, and immune-related factors in TLE patients. The intervention group received neuro-Capridin caprylate and caprate (n-CAP), while the control group did not. Significant findings included increased plasma ATP and adenosine levels in the treatment group, along with higher expression of ADORA1 and CD73 and reduced expression of ADK. Corresponding protein changes were observed, with increased CD73 and decreased ADK levels. Caprylate and Caprate also elevated regulatory T cells and reduced proinflammatory cytokines (TNF-α, IL-6, IL-1β). These changes were associated with significant reductions in seizure severity and frequency. Intermittent ketogenesis through the consumption of Caprylate and Caprate effectively reduced seizures and improved immune and metabolic markers in drug-resistant TLE patients. These findings highlight its potential as a complementary therapy, warranting further exploration of its long-term impact and underlying molecular mechanisms.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

NOX4 Regulates NLRP3 by Inhibiting the Ubiquitination of LRRC8A to Promote Ferroptosis in Nucleus Pulposus Cells.

IF 4.5 2区医学

Inflammation Pub Date : 2025-02-06 DOI: 10.1007/s10753-025-02253-0

Feng Zhang, Di Cui, Zhaodong Wang, Yifei Li, Kangkang Wang, Haitao Lu, Haiyang Yu, Wei Jiao, Xilong Cui

{"title":"NOX4 Regulates NLRP3 by Inhibiting the Ubiquitination of LRRC8A to Promote Ferroptosis in Nucleus Pulposus Cells.","authors":"Feng Zhang, Di Cui, Zhaodong Wang, Yifei Li, Kangkang Wang, Haitao Lu, Haiyang Yu, Wei Jiao, Xilong Cui","doi":"10.1007/s10753-025-02253-0","DOIUrl":"https://doi.org/10.1007/s10753-025-02253-0","url":null,"abstract":"Intervertebral disc degeneration (IDD) is a significant contributor to low back pain, imposing a considerable socioeconomic burden. Ferroptosis, a novel form of cell death driven by iron and characterized by the accumulation of reactive oxygen species (ROS), has been associated with the progression of IDD. Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) has been widely recognized as a pivotal factor promoting ferroptosis across various diseases; however, its precise role in the pathogenesis of IDD remains incompletely understood. Our experimental findings demonstrated a marked upregulation of NOX4 in degenerated cells, accompanied by elevated ROS levels and a diminished mitochondrial membrane potential, indicating the participation of ferroptosis. Furthermore, the expression of the critical regulatory factor GPX4 was reduced, while ACSL4 levels were significantly increased, further corroborating the involvement of ferroptosis. Functional loss and gain experiments revealed that NOX4 overexpression augmented ferroptosis and ROS production while promoting the secretion of inflammatory cytokines. Subsequent studies indicated that the knockdown of NOX4 could reverse tert-butyl hydroperoxide (TBHP)-induced ferroptosis. Mass spectrometry analysis identified leucine-rich repeat-containing 8A (LRRC8A) as an interacting protein of NOX4, and further validation confirmed that they co-regulate Nod-like receptor pyrin domain-3 (NLRP3) activation through their interaction. Utilizing a rat model of intervertebral disc degeneration, we further corroborated the role of NOX4 in IDD. This study provides theoretical support for the potential application of NOX4-targeting drugs in the treatment of IDD.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Prenatal Inflammation Reprograms Hypothalamic-Pituitary-Gonadal Axis Development in Female Rats.

IF 4.5 2区医学

Inflammation Pub Date : 2025-02-05 DOI: 10.1007/s10753-025-02243-2

Vasilina Ignatiuk, Viktoriya Sharova, Liudmila Zakharova

{"title":"Prenatal Inflammation Reprograms Hypothalamic-Pituitary-Gonadal Axis Development in Female Rats.","authors":"Vasilina Ignatiuk, Viktoriya Sharova, Liudmila Zakharova","doi":"10.1007/s10753-025-02243-2","DOIUrl":"https://doi.org/10.1007/s10753-025-02243-2","url":null,"abstract":"The hypothalamic-pituitary-gonadal (HPG) axis development during critical periods of ontogenesis can be disrupted by stress factors, including in particular maternal immune activation by infectious agents. Bacterial lipopolysaccharide (LPS, E.coli) exposure induces inflammation accompanied by proinflammatory cytokine release. The resulting elevated cytokine levels may lead to a disruption of epigenetic mechanisms regulating HPG axis development and to a reduced fertility in the offspring. This study focused on the long-term effects of prenatal LPS exposure on HPG axis development in female rats and the modulation of such effects by anti-inflammatory drugs: polyclonal IgG and monoclonal anti-IL6-receptor antibodies. LPS exposure on embryonic day 12 led to a decrease in the number of synaptic inputs on gonadotropin-releasing-hormone-producing neurons in the hypothalamus, high levels of follicular atresia, and suppressed steroidogenesis in the ovaries of adult female offspring. IgG treatment or IL6 receptor blockade by monoclonal antibodies 40 minutes after LPS exposure prevented these long-term negative effects of LPS. The data obtained suggest that IL6 is involved in the regulation of HPG axis development.","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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