Immunological Investigations最新文献

Aflatoxin B₁ Instigated Redox Imbalance is Accompanied by Amplified Indoleamine 2,3-Dioxygenase/tryptophan Catabolism in the Spleen and Erythrocyte of Male Wistar Rats: Protective Influence of Dietary Rutin. 黄曲霉毒素B1引起的氧化还原失衡伴随着雄性Wistar大鼠脾脏和红细胞吲哚胺2,3-双加氧酶/色氨酸分解代谢的增强：饮食芦丁的保护作用

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-05-27 DOI: 10.1080/08820139.2025.2503171

Azubuike Peter Ebokaiwe, Nworie Okoro, Doris Olachi Alilonu, Euslar Nnenna Onu, Jacinta Nkechi Obimma, ChinazomMartina Eze, Olusanya Olasehinde

{"title":"Aflatoxin B1 Instigated Redox Imbalance is Accompanied by Amplified Indoleamine 2,3-Dioxygenase/tryptophan Catabolism in the Spleen and Erythrocyte of Male Wistar Rats: Protective Influence of Dietary Rutin.","authors":"Azubuike Peter Ebokaiwe, Nworie Okoro, Doris Olachi Alilonu, Euslar Nnenna Onu, Jacinta Nkechi Obimma, ChinazomMartina Eze, Olusanya Olasehinde","doi":"10.1080/08820139.2025.2503171","DOIUrl":"https://doi.org/10.1080/08820139.2025.2503171","url":null,"abstract":"Introduction: Rutin, a dietary flavonoid, exhibits anti-inflammatory, antioxidant, and immunomodulatory properties. The underlying mechanism of protection of rutin against Aflatoxin B1 (AFB1)-induced immunotoxicity is not completely elucidated. This study investigated the protective effect of rutin against Aflatoxin B1 (AFB1)-induced immunotoxicity in male Wistar rats, supported by molecular docking and dynamics simulations.Methods: Forty male Wistar rats were grouped into five: control (corn oil), AFB1 (0.75 mg/kg bwt), AFB1 (1.5 mg/kg bwt), rutin (50 mg/kg bwt), and AFB1 (1.5 mg/kg bwt) + Rutin (50 mg/kg bwt) orally for 30 days.Results: AFB1 exposure increased (p < 0.05) oxidative and inflammatory markers, altered hematological indices, and caused histological damage in the spleen and bone marrow. Elevated indoleamine 2,3-dioxygenase (IDO) activity, reduced CD4+ T cells, and unchanged tryptophan 2,3-dioxygenase (TDO) activity were also observed. Docking revealed strong binding affinities for AFB1 (-9.5 kcal/mol), rutin (-9.7 kcal/mol), and AFB1-rutin (-10.4 kcal/mol) with IDO. Rutin co-treatment restored oxidative, inflammatory, and hematological indices, mitigated histological damage, and normalized CD4+ T cells and IDO activity, as supported by computational studies.Discussion: The activities/expression of immunosuppressive indoleamine 2, 3-dioxygenase is mostly regulated by inflammation and oxidative stress. This study provides new insights into the mechanisms underlying the modulation of immunotoxicity of AFB1 by dietary rutin.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-23"},"PeriodicalIF":2.9,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

FOXM1 Enhances Transcription of S1PR1 and Promotes Pro-Inflammatory Activation of Kupffer Cells in Alcoholic Hepatitis. FOXM1增强S1PR1转录并促进酒精性肝炎Kupffer细胞的促炎激活

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-05-21 DOI: 10.1080/08820139.2025.2503167

Ping Lu, Tianfeng Sun

{"title":"FOXM1 Enhances Transcription of S1PR1 and Promotes Pro-Inflammatory Activation of Kupffer Cells in Alcoholic Hepatitis.","authors":"Ping Lu, Tianfeng Sun","doi":"10.1080/08820139.2025.2503167","DOIUrl":"https://doi.org/10.1080/08820139.2025.2503167","url":null,"abstract":"Background: Following the bioinformatics predictions, this investigation delves into the function of FOXM1 in the phenotype of macrophages and inflammatory responses in alcoholic hepatitis (AH).Methods: A mouse model of AH was generated using the Lieber-DeCarli method, and mouse Kupffer cells (KCs) were treated with lipopolysaccharide and ethanol. Expression of FOXM1 and S1PR1 in mouse liver tissues or KCs was determined using RT-qPCR, immunofluorescence, or western blot assays. Loss- or gain-of-function assays of FOXM1 and S1PR1 were performed, followed by histopathological staining of the liver tissues, examination of the inflammatory cytokines, and assessment of macrophage phenotype.Results: FOXM1 exhibited heightened expression in the mouse liver tissues and KCs in AH models. Silencing FOXM1 reduced pathological injury, hepatic steatosis, alanine aminotransferase and aspartate aminotransferase levels, inflammatory cytokine production, and pro-inflammatory (M1) polarization markers of macrophages. This condition also alleviated M1 polarization of KCs in vitro. FOXM1 promoted transcription and expression of S1PR1 by binding to its promoter. The additional upregulation of S1PR1, in the presence of FOXM1, rescued M1 skewing of macrophages both in vitro and in vivo, thus aggravating inflammatory responses.Conclusion: This study identifies that FOXM1-mediated transcriptional upregulation of S1PR1 promotes pro-inflammatory activation of macrophages and augments liver injury in AH.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-20"},"PeriodicalIF":2.9,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Activation of NF-κB Signaling by a High-Fat and High-Sugar Diet Enhances Macrophage Polarization and Aggravates Postoperative Pain and Inflammatory Responses. 高脂高糖饮食激活NF-κB信号可增强巨噬细胞极化，加重术后疼痛和炎症反应

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-05-19 DOI: 10.1080/08820139.2025.2505900

Chenran Zhang, Ming Zhu

{"title":"Activation of NF-κB Signaling by a High-Fat and High-Sugar Diet Enhances Macrophage Polarization and Aggravates Postoperative Pain and Inflammatory Responses.","authors":"Chenran Zhang, Ming Zhu","doi":"10.1080/08820139.2025.2505900","DOIUrl":"https://doi.org/10.1080/08820139.2025.2505900","url":null,"abstract":"Objective: To investigate how a high-fat, high-sugar (HFHS) diet influences postoperative pain and inflammation, and to explore the role of NF-κB signaling and macrophage polarization.Methods: Male Sprague Dawley rats were divided into five groups: normal diet (ND), HFHS, ND + surgery (ND + S), HFHS + surgery (HFHS + S), and HFHS + surgery + NF-κB inhibitor (HFHS + S + B). After eight weeks of diet, laparotomy was performed. Pain behavior was assessed using the Rat Grimace Scale. DRG and blood samples were collected for Western blotting, ELISA, flow cytometry, and immunofluorescence.Results: HFHS combined with surgery significantly activated NF-κB signaling, shown by increased p65/IκBα phosphorylation and COX-2 upregulation. NF-κB inhibition reversed these effects and reduced pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, MCP-1) and pain scores. HFHS and surgery also increased M1 and decreased M2 macrophages; these changes were reversed by NF-κB blockade. Western blotting confirmed upregulation of iNOS and IL-6 and downregulation of Arg-1 and IL-10 under HFHS conditions.Conclusion: An HFHS diet exacerbates postoperative pain and inflammation via NF-κB activation and M1 macrophage polarization. Inhibiting NF-κB may mitigate diet-induced sensitization.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-15"},"PeriodicalIF":2.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Mechanistic Insights into HOTAIR-Driven ADAM17/NF-Κb Activation and Endothelial Dysfunction in LPS-Challenged HUVECs. hotair驱动的ADAM17/NF-Κb在lps挑战的HUVECs中激活和内皮功能障碍的机制研究

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-05-14 DOI: 10.1080/08820139.2025.2503174

Junbing He, Zixuan Shao, Zhuoji Li, Yufu He, Jingqi Zhang, Haotian Zhong, Jiekai Li, Qinghua Liu, Yiming Shao

{"title":"Mechanistic Insights into HOTAIR-Driven ADAM17/NF-Κb Activation and Endothelial Dysfunction in LPS-Challenged HUVECs.","authors":"Junbing He, Zixuan Shao, Zhuoji Li, Yufu He, Jingqi Zhang, Haotian Zhong, Jiekai Li, Qinghua Liu, Yiming Shao","doi":"10.1080/08820139.2025.2503174","DOIUrl":"https://doi.org/10.1080/08820139.2025.2503174","url":null,"abstract":"Introduction: HOX transcript antisense intergenic RNA (HOTAIR) has been implicated in inflammation and vascular pathology, but its role in regulation of ADAM17 and sepsis-induced endothelial injury remains unclear.Methods: LPS-treated human umbilical vein endothelial cells (HUVECs) modeled sepsis-induced endothelial injury, which were assessed via qRT-PCR, western blot and immunofluorescence. HOTAIR-knockout mice were treated with cecal ligation and perforation to establish sepsis model.Results: LPS-stimulation increased expression of HOTAIR and ADAM17 and decreased miR-326 levels in HUVECs. HOTAIR-knockdown by antisense oligonucleotides (ASOs) decreased ADAM17, TNF-α production and NF-κB activities; it also alleviated endothelial inflammation, VE-cadherin integrity damage, apoptosis and barrier dysfunction, while miR-326 inhibition reversed these effects. MiR-326 inhibited TNF-α/NF-κB via targeting ADAM17. Further experiments demonstrated recombinant TNF-α reversed the inhibitory effect of HOTAIR-ASOs on LPS-triggered TNF-α/NF-κB activation and downstream endothelial injury, which were further mitigated by NF-κB or p38 MAPK inhibitors. In-vivo experiments in HOTAIR-knockout mice confirmed the role of HOTAIR/miR-326/ADAM17 in regulating NF-κB and p38 MAPK inflammation, with improved lung injury and survival following sepsis.Discussion: The HOTAIR/miR-326/ADAM17 axis is a key regulator of inflammation, endothelial injury and barrier dysfunction during sepsis via modulation of TNF-α/NF-κB signaling, providing new insights into the mechanisms underlying endothelial injury in sepsis.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-27"},"PeriodicalIF":2.9,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

MiR-519d-3p from Placenta-Derived Exosomes Induce Immune Intolerance Regulating Immune Cells, Contributing to the Pathogenesis of Preeclampsia. 来自胎盘来源外泌体的MiR-519d-3p诱导免疫不耐受调节免疫细胞，参与子痫前期的发病机制

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-05-01 Epub Date: 2025-01-17 DOI: 10.1080/08820139.2025.2450234

Si-Qi Cao, Tu-Xiang Jiang, Ying-Ying Guo, Rong Lin, Liang Lin

{"title":"MiR-519d-3p from Placenta-Derived Exosomes Induce Immune Intolerance Regulating Immune Cells, Contributing to the Pathogenesis of Preeclampsia.","authors":"Si-Qi Cao, Tu-Xiang Jiang, Ying-Ying Guo, Rong Lin, Liang Lin","doi":"10.1080/08820139.2025.2450234","DOIUrl":"10.1080/08820139.2025.2450234","url":null,"abstract":"Background: MiR-519d-3p, also called specific placenta biomarkers, is a member of the Chromosome 19 miRNA Cluster (C19MC) with the highest concentrations of miRNAs in human placenta and maternal serum. These miRNAs are secreted by fetal trophoblast cells within extracellular vesicles (EVs) and interact with the mother's immune cells, which has been proposed to be crucial for immunological tolerance at the placental-maternal interface. A key mechanism in preeclampsia, a multifactorial, multipath hypertensive pregnancy illness, is an immunological imbalance between the mother and the fetus.Methods: Using Next Generation Sequencing, we determined that the placenta-derived Exosomes (pEXOs) of preeclamptic patients had elevated expression of miR-519. To further develop an in vitro model of trophoblast-immune cell communication, HTR-8/Svneo cells and Jurkat T cells were employed and we utilized experiments such as Western blot (WB), Real-Time Quantitative Reverse Transcription Polymerase Chain Reaction (RT-qPCR), Cell-Counting-Kit-8 (CCK-8) cell proliferation analysis, cell apoptosis analysis, and other techniques to accomplish research.Results: It was discovered that miR-519d-3p in pEXOs promoted Jurkat T cell proliferation, inhibited apoptosis, and induced Jurkat T cell differentiation toward Th17.Conclusion: MiR-519d-3p in pEXOs disrupts immune tolerance at the maternal-placental interface by encouraging Jurkat T cell proliferation, preventing Jurkat T cell apoptosis, and creating an imbalance in Th17/Treg differentiation. This likely leads to SIRS and unfavorable pregnancy complications like preeclampsia.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"522-543"},"PeriodicalIF":2.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Timosaponin A-III Alleviates Asthma-Induced Airway Inflammation, Th17 Cell Differentiation, and STAT3/RORγt Pathway. Timosaponin A-III缓解哮喘诱导的气道炎症、Th17细胞分化和STAT3/RORγt通路

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-05-01 Epub Date: 2025-01-16 DOI: 10.1080/08820139.2025.2450239

Lijie Wang, Jiabo Yuan, Ruiqi Zhao, Congyao Wang, Zhuying Li

{"title":"Timosaponin A-III Alleviates Asthma-Induced Airway Inflammation, Th17 Cell Differentiation, and STAT3/RORγt Pathway.","authors":"Lijie Wang, Jiabo Yuan, Ruiqi Zhao, Congyao Wang, Zhuying Li","doi":"10.1080/08820139.2025.2450239","DOIUrl":"10.1080/08820139.2025.2450239","url":null,"abstract":"Introduction: T helper 17 (Th17) cells have a significant effect in the pathogenesis of asthma, and signal transducer and activator of transcription 3 (STAT3) pathway activation is critical for Th17 cell differentiation. Timosaponin A-III (TA3) was reported to inhibit the STAT3 pathway. Here, we investigated whether TA3 improved asthma by inhibiting the STAT3 pathway.Methods: Ovalbumin (OVA)-induced asthma murine models were developed, and TA3 (10 or 20 mg/kg) was gavage daily during OVA challenge. Murine naïve CD4+T cells were triggered for Th17 differentiation, and TA3 (5 or 10 μM) was used to treat cells during induction of Th17 differentiation.Results: In vivo experiments showed that TA3 decreased airway inflammation, goblet cell and smooth muscle hyperplasia, α-smooth muscle actin and collagen deposition, Th17 differentiation, and STAT3/RORγt signaling activation in mice exposed to OVA. The inhibitory effect of TA3 on STAT3/RORγt signaling activation was also observed in in vitro experiments. Compared to positive control static (a specific inhibitor of STAT3), TA3 had a similar effect on Th17 differentiation.Discussion: These findings indicate that TA3 may ameliorate Th17 cell differentiation by suppressing STAT3/RORγt signaling. Our data provide evidence of the potential benefits of TA3 for the treatment of asthma.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"544-559"},"PeriodicalIF":2.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Hirsutella sinensis Fungus Promotes CD8⁺ T Cell-Mediated Anti-Tumor Immunity by Affecting Tumor-Associated Macrophages-Derived CCRL2. 毛杆菌真菌通过影响肿瘤相关巨噬细胞衍生的CCRL2促进CD8+ T细胞介导的抗肿瘤免疫

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-05-01 Epub Date: 2025-01-17 DOI: 10.1080/08820139.2025.2450246

Kaixiang Zhao, Yan Ma, Jing Luo, Yanhui Xu, Qiyang Shou, Hao Jiang, Xinhai Zhu

{"title":"Hirsutella sinensis Fungus Promotes CD8+ T Cell-Mediated Anti-Tumor Immunity by Affecting Tumor-Associated Macrophages-Derived CCRL2.","authors":"Kaixiang Zhao, Yan Ma, Jing Luo, Yanhui Xu, Qiyang Shou, Hao Jiang, Xinhai Zhu","doi":"10.1080/08820139.2025.2450246","DOIUrl":"10.1080/08820139.2025.2450246","url":null,"abstract":"Introduction: Hirsutella sinensis fungus (HSF)is an artificial substitute for Cordyceps sinensis and has shown promising therapeutic effects in various diseases including cancer. Previous studies have demonstrated that HSF can affect macrophage polarization and activate systemic immune response. In our preliminary experiments, we validated that HSF inhibited the proliferation of lung cancer (LC) cells, but the underlying mechanism is elusive. We intended to explore the mechanism of HSF in promoting anti-tumor immunity.Methods: In vivo experiments were performed to confirm inhibitory effect of HSF on LC growth, and sequencing results revealed abnormal expression of CCRL2. Knockdown and overexpression of CCRL2 were conducted to investigate its effect on macrophage polarization, and co-culture with T cells was to assay the impact of HSF+CCRL2 on CD8+ T cell activation by flow cytometry.Results: Overexpression of CCRL2 promoted macrophage polarization toward M1 and activated the proliferation and effector function of CD8+ T cells. HSF promoted CCRL2 expression and affected M1 polarization via CCRL2, which in turn affected CD8+ T cell-mediated anti-tumor immunity.Discussion: Our study demonstrated that HSF promoted macrophage M1 polarization and activated CD8+ T cells via CCRL2, thereby inhibiting the progression of LC.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"573-588"},"PeriodicalIF":2.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Innovative Approaches to Psoriasis: Small Molecules Targeting Key Signaling Pathways. 银屑病的创新方法：靶向关键信号通路的小分子。

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-05-01 Epub Date: 2025-01-17 DOI: 10.1080/08820139.2025.2449960

Meeral Gosia, Gaurav Doshi, Siddhi Bagwe Parab, Angel Godad

{"title":"Innovative Approaches to Psoriasis: Small Molecules Targeting Key Signaling Pathways.","authors":"Meeral Gosia, Gaurav Doshi, Siddhi Bagwe Parab, Angel Godad","doi":"10.1080/08820139.2025.2449960","DOIUrl":"10.1080/08820139.2025.2449960","url":null,"abstract":"Background: Psoriasis (Pso) is a chronic, immune-mediated dermatological condition characterized by dysregulated inflammatory responses and the hyperproliferation of keratinocytes. Biologics, which target specific cytokines such as IL-17 and IL-23, have revolutionized the management by addressing key drivers of its pathophysiology. Despite their efficacy, biologics are not without limitations, including the need for intermittent administration and ongoing monitoring. In contrast, small molecules offer a promising alternative by selectively inhibiting key signaling pathways that modulate pro-inflammatory cytokines involved in the inflammatory cascade.Methods and results: This review suggests a new therapeutic strategy for Pso treatment, emphasizing the intricate relationships between small molecules and important signaling pathways involved in the pathophysiology of skin conditions. Improving treatment outcomes and reducing the side effects associated with conventional medicines, this review aims to better understand how tailored small-molecule inhibitors might efficiently control these pathways. This creative approach promotes the creation of individualized treatment plans that can greatly enhance the quality of life of patients with Psoby utilizing the knowledge gathered from recent developments in signaling pathway research.Conclusion: This review delves into the molecular mechanisms underlying Pso and explores how small molecules can be harnessed to enhance treatment outcomes, presenting a new paradigm for managing this chronic skin disorder.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"457-493"},"PeriodicalIF":2.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 Mechanism of Baicalin in the Treatment of Mycoplasma Pneumoniae Pneumonia by Regulating NLRP3/Caspase-1 Signaling Pathway. 黄芩苷通过调节NLRP3/Caspase-1信号通路治疗肺炎支原体肺炎的机制

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-05-01 Epub Date: 2025-01-09 DOI: 10.1080/08820139.2025.2450244

Dan Song, Wenfeng Wei, Jie Zhang, Lu Zhang, Weiming Wang, Jinhai Huo

{"title":"The Mechanism of Baicalin in the Treatment of Mycoplasma Pneumoniae Pneumonia by Regulating NLRP3/Caspase-1 Signaling Pathway.","authors":"Dan Song, Wenfeng Wei, Jie Zhang, Lu Zhang, Weiming Wang, Jinhai Huo","doi":"10.1080/08820139.2025.2450244","DOIUrl":"10.1080/08820139.2025.2450244","url":null,"abstract":"Objective: This study investigated the mechanism of baicalin (BIA) attenuating the inflammatory response and lung injury in mycoplasma pneumoniae pneumonia (MPP) mice.Methods: MPP mouse models were established and then treated with BIA, azithromycin, or NLRP3 inflammasome activator. Lung wet-to-dry weight (W/D) ratio were weighed. Serum levels of MP-IgM, C-reactive protein (CRP) and bronchoalveolar lavage fluid (BALF) protein were detected by kits, NLRP3/Caspase-1 pathway-related protein levels by Western blot, and IL-1β, IL-18, IL-6 and TNF-α levels by ELISA. HE staining was performed to detect lung injury.Results: MPP mice showed elevated mouse lung W/D ratio, upregulated serum MP-IgM and CRP levels and BALF protein, and enhanced IL-6 and TNF-α levels, which were reversed by BIA or azithromycin treatment, suggesting that BIA attenuated pulmonary inflammatory response in MPP mice. The lung tissue of MPP mice showed upregulated NLRP3, cleaved Caspase-1,Caspase-1, GSDMD-N and GSDMD levels and raised IL-1β and IL-18 levels, and changes were annulled by BIA or azithromycin treatment, suggesting that BIA inhibited the NLRP3/Caspase-1 pathway activation. NLRP3/Caspase-1 pathway activation partially abrogated the alleviative effect of BIA on the pulmonary inflammatory response of MPP mice.Conclusion: BIA mitigates inflammatory response and lung injury in MPP mice by inhibiting NLRP3/Caspase-1 pathway activation.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"560-572"},"PeriodicalIF":2.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142948205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Immunomodulatory Effects of Pterocarpanquinone LQB-118 in Murine Peritoneal Macrophages. pterocarpan醌LQB-118对小鼠腹腔巨噬细胞的免疫调节作用。

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-05-01 Epub Date: 2025-01-08 DOI: 10.1080/08820139.2025.2449949

Éssia de Almeida Lima, Luiz Henrique Agra Cavalcante-Silva, Deyse Cristina Madruga Carvalho, Mariana Mendonça Soares, Anna Beatriz Araujo Medeiros, Chaquip Daher Netto, Paulo Roberto Ribeiro Costa, Sandra Rodrigues-Mascarenhas

{"title":"Immunomodulatory Effects of Pterocarpanquinone LQB-118 in Murine Peritoneal Macrophages.","authors":"Éssia de Almeida Lima, Luiz Henrique Agra Cavalcante-Silva, Deyse Cristina Madruga Carvalho, Mariana Mendonça Soares, Anna Beatriz Araujo Medeiros, Chaquip Daher Netto, Paulo Roberto Ribeiro Costa, Sandra Rodrigues-Mascarenhas","doi":"10.1080/08820139.2025.2449949","DOIUrl":"10.1080/08820139.2025.2449949","url":null,"abstract":"Background: Phagocytosis is an important function of macrophages. However, when it's dysregulated, it could compromise homeostasis. Thus, this study aimed to assess the inhibitory activity of pterocarpanquinone LQB 118 on murine macrophage phagocytosis.Methods: We used peritoneal macrophages isolated from mice to evaluate the impact of LQB 118 (5 μM) on the modulation of phagocytic activity and possible action mechanism related: IL-12 (by ELISA), NO (by Griess reaction),ROS production (by flow cytometry), and intracellular signaling proteins (iNOS, P-Akt, P-mTOR, NF-κB, and P-NF-κB) (by flow cytometry).The macrophages were stimulated with zymosan to assess both phagocytic activity and flow cytometry assays.Results: Treatment with LQB 118 resulted in a reduction in the phagocytosis of zymosan particles by macrophages. This effect could potentially be attributed to LQB's inhibition of IL-12 production and mTOR/NF-κB signaling. Furthermore, LQB 118 decreased the levels of ROS and NO without interfering with iNOS and Akt activation.Conclusion: These findings show the anti-phagocytic activity of LQB 118 on macrophage, highlighting the potential of this compound as a candidate for modulating macrophage-driven inflammation.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"494-505"},"PeriodicalIF":2.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142948123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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