Allergologia et immunopathologia最新文献

{"title":"Hypermethylation of the <i>FOXP3</i> gene regulates Tregs immunodysregulation in chronic idiopathic thrombocytopenic purpura.","authors":"Zengsheng Wang, Tao Lang, Yan Li, Xiaoyan Zhang, Muhubair Abdur, Min Mao","doi":"10.15586/aei.v52i4.1091","DOIUrl":"10.15586/aei.v52i4.1091","url":null,"abstract":"<p><strong>Background: </strong>Chronic idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease characterized by a breakdown of immune tolerance; in ITP, the body's immune system mistakenly attacks and destroys platelets. This study aims to investigate the role and underlying mechanisms of <i>FOXP3</i> in chronic ITP.</p><p><strong>Methods: </strong>Flow cytometry was used to detect the proportion of CD4⁺CD25⁺FOXP³⁺ regulatory T cells (Tregs) in CD4⁺CD25⁺ T lymphocytes from 20 patients with chronic ITP (CITP), 20 acute ITP (AITP) controls, and 20 healthy individuals.CD4⁺CD25⁺ Treg cells were isolated from peripheral blood of patients with CITP using magnetic beads and then treated with phosphate-buffered saline solution or decitabine (a methylation inhibitor) for 48 h. The levels of interleukin-2 (IL-2), IL-10, and transforming growth factor-beta1 (TGF-β1) in the plasma and CD4⁺CD25⁺ Treg cells were assessed by Enzyme-linked-immunosorbent serologic assay and quantitative real-time polymerase chain reaction (qRT-PCR). FOXP3 level was measured by qRT-PCR and Western blot analysis. Methylation-specific PCR (MS-PCR) was adopted to detect the status of FOXP3 methylation.</p><p><strong>Results: </strong>The number of Treg cells and the contents of IL-2, IL-10, and TGF-β1 decreased in patients with CITP, compared to the AITP control group and normal group. <i>FOXP3</i> expression was reduced and <i>FOXP3</i> methylation increased in patients with CITP, compared to the AITP control group and normal group. Hypermethylation of FOXP3 promoter led to decrease in FOXP3 level in Treg cells. Inhibition of FOXP3 promoter hypermethylation promoted the secretion of IL-2, IL-10, and TGF-β1 in Treg cells.</p><p><strong>Conclusion: </strong>The number of Treg cells in CITP patients decreased, and the hypermethylation of FOXP3 promoter led to reduction of its expression in Treg cells, thus affecting the immune functioning of Treg cells.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":"52 4","pages":"30-37"},"PeriodicalIF":2.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141544424","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}

{"title":"Rhizoma coptidis can inhibit the excessive proliferation, inflammation, and transformation of lung fibroblasts into myofibroblasts.","authors":"Jie Yang, Yuting Huang, Zhimin Cui, Chang Liu, Guofang Xie","doi":"10.15586/aei.v52i4.1111","DOIUrl":"https://doi.org/10.15586/aei.v52i4.1111","url":null,"abstract":"<p><strong>Background: </strong>Pulmonary fibrosis (PF) is a chronic, progressive, and irreversible heterogeneous disease of lung interstitial tissue. To combat progression of PF, new drugs are required to be developed. Rhizoma coptidis (COP), one of the main alkaloids of Coptis chinensis, is a traditional herbal medicine used to treat various inflammatory diseases.</p><p><strong>Objective: </strong>To investigate the possible effects of Coptisine (Cop) on the growth, inflammation, as well as FMT of TNF-β1-induced HFL1 cells and uncover the mechanism.</p><p><strong>Material and methods: </strong>Human fetal lung fibroblast 1 (HFL1) was induced using 6ng/mL TGF-β1 as a model of pulmonary fibrosis. CCK-8, Brdu, and transwell assays indicated the effects on cell growth as well as motility. qPCR and the corresponding kits indicted the effects on cell inflammation. Immunoblot showed the effects on FMT and further confirmed the mechanism.</p><p><strong>Results: </strong>Coptisine inhibits excessive growth as well as motility of TNF-β1-induced HFL1 cells. It further inhibits inflammation and ROS levels in TNF-β1-induced HFL1 cells. Coptisine inhibits the FMT process of TNF-β1-induced HFL1 cells. Mechanically, coptisine promotes the Nrf2/HO-1 pathway.</p><p><strong>Conclusion: </strong>Coptisine can inhibit the excessive growth, inflammation as well as FMT of lung fibroblasts into myofibroblasts. It could serve as a promising drug of PF.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":"52 4","pages":"15-20"},"PeriodicalIF":2.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141544385","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}

{"title":"Effect of metformin on gut microbiota imbalance in patients with T2DM, and the value of probiotic supplementation.","authors":"Lu Li, Yanli Chen, Zhipeng Tang, Yan You, Yang Guo, Yong Liao","doi":"10.15586/aei.v52i4.1101","DOIUrl":"10.15586/aei.v52i4.1101","url":null,"abstract":"<p><strong>Purpose: </strong>To investigate the effect of metformin on gut microbiota imbalance in patients with type 2 diabetes mellitus (T2DM), and the value of probiotic supplementation.</p><p><strong>Methods: </strong>A total of 84 newly diagnosed T2DM patients were randomly divided into probiotics group, metformin group, and control group, with 28 patients in each group. The blood glucose control, islet function, gut microbiota, and inflammatory factors were compared between three groups.</p><p><strong>Results: </strong>After 3 months of treatment, fasting plasma glucose (FPG), 2-h postprandial plasma glucose (2-h PG), and glycosylated hemoglobin A1c (HbA1c) were evidently decreased in both probiotics and metformin groups (P < 0.05) and were lower than that in the control group prior to treatment. Besides, FPG, 2-h PG, and HbA1c were lower in the metformin group than that in the control group. FPG, 2-h PG, and HbA1c were further lower in the probiotic group than in the metformin group (P < 0.05). Fasting insulin (FINS) and islet β cell (HOMA-β) -function were dramatically increased in the same group (P < 0.05), while insulin-resistant islet β cells (HOMA-IR) were significantly lower in the same group (P < 0.05); FINS and HOMA-β were significantly higher, while HOMA-IR was significantly lower (P < 0.05) in both groups than in the control group prior to treatment. HOMA-IR was also lower in the probiotic group than in the metformin group after treatment (P < 0.05); the number of <i>lactobacilli</i> and bifidobacteria increased (P < 0.05) in both probiotic and metformin groups than in the control group prior to treatment, and the number of Enterobacteriaceae and Enterococcus was lower in the control group prior to treatment (P < 0.05). In addition, the number of <i>lactobacilli</i> and bifidobacteria was higher and the number of <i>enterobacteria</i> and <i>enterococci</i> was lower in the probiotic group than that in the metformin group after treatment, and the differences were statistically significant (P < 0.05). Lipopolysaccharide (LPS), interleukin 6 (IL-6), and C-reactive protein (CRP) levels were lower in both probiotic and metformin groups (P < 0.05). The serum LPS, IL-6, and CRP levels were lower in both probiotic and metformin groups, compared to the control group prior to the treatment (P < 0.05).</p><p><strong>Conclusion: </strong>Metformin while treating T2DM assists in improving the imbalance of gut microbiota.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":"52 4","pages":"84-90"},"PeriodicalIF":2.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141544422","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}

{"title":"Frequency of <i>Euroglyphus maynei</i> sensitization in respiratory allergies: a real-life study with bioinformatic analysis and geographical exploration of allergen prevalence.","authors":"Stefano Palazzo, Alessandro Cinquantasei, Concetta De Chirico, Marco Zurlo, Vincenzo Aresta, Nada Chaoul, Marcello Albanesi","doi":"10.15586/aei.v52i4.1089","DOIUrl":"https://doi.org/10.15586/aei.v52i4.1089","url":null,"abstract":"<p><strong>Background: </strong><i>Dermatophagoides pteronyssinus</i> and <i>Dermatophagoides farinae</i> belong to the family <i>Pyroglyphidae</i> (subfamily: \"Dermatophagoidinae\") and have the respective allergenic proteins of Der p1, Der p2, and Der p23 and Der f1 and Der f2. <i>Euroglyphus maynei</i>, belongs to the family <i>Pyroglyphidae</i> (subfamily: \"Pyroglyphinae\") and its main allergenic protein is Eur m1, a source of sensitization. Sensitization to <i>D. pteronyssinus</i> and <i>D. farinae</i> is assessed through skin tests, while sensitization to <i>E. maynei</i> is assessed less frequently.</p><p><strong>Objective: </strong>This experimental work aims to analyze the prevalence of sensitization to <i>E. maynei</i> in patients with respiratory allergies treated at M. Albanesi Allergy and Immunology Unit in Bari, Italy, and the sequence homology of major allergenic proteins of <i>E. maynei</i> with <i>D. farinae</i> and <i>D. pteronyssinus</i> was analyzed.</p><p><strong>Methods: </strong>In this real-life study, 65 patients were enrolled. In particular, patients with respiratory allergy were subjected to skin prick tests for common respiratory allergens, including <i>Euroglyphus maynei</i>. The sequence homology analysis was performed between the major allergenic proteins of <i>E. maynei</i> and those of <i>D. pteronyssinus</i> and <i>D. farinae</i>.</p><p><strong>Results: </strong>Sensitization to <i>E. maynei</i> accounts for 41.5% of patients. All patients with <i>E. maynei</i> sensitization had concomitant sensitization to <i>D. farinae</i> and <i>D. pteronyssinus</i>. The analysis of sequence homology of Der p1 and Der f1 proteins with the sequence of Eur m1 protein demonstrated an identity of 84.4% and 86%, respectively.</p><p><strong>Conclusions: </strong>Nearly 50% of house dust mites-sensitized patients have a concomitant sensitization to <i>E. maynei</i>. The cross-sensitization could be due to Der f1, Der p1, and Eur m1 similarity.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":"52 4","pages":"1-8"},"PeriodicalIF":2.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141544423","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}

{"title":"Knockdown of GNL3 inhibits LUAD cell growth by regulating Wnt-β-catenin pathway.","authors":"Guihong Dai, Yuejun Sun","doi":"10.15586/aei.v52i4.1117","DOIUrl":"10.15586/aei.v52i4.1117","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD) is a leading cause of tumor-associated mortality, and it is needed to find new target to combat this disease. Guanine nucleotide-binding -protein-like 3 (GNL3) mediates cell proliferation and apoptosis in several cancers, but its role in LUAD remains unclear.</p><p><strong>Objective: </strong>To explore the expression and function of Guanine nucleotide-binding protein-like 3 (GNL3) in lung adenocarcinoma (LUAD) and its potential mechanism in inhibiting the growth of LUAD cells.</p><p><strong>Methods: </strong>We evaluated the expression of GNL3 in LUAD tissues and its association with patient prognosis using databases and immunohistochemistry. Cell proliferation was assessed by CCK-8 assay as well as colony formation, while apoptosis was evaluated by FCM. The effect of GNL3 knockdown on the Wnt/β-catenin axis was investigated by Immunoblot analysis.</p><p><strong>Results: </strong>GNL3 is overexpressed in LUAD tissues and is correlated with poor prognosis. Knockdown of GNL3 significantly inhibited the growth as well as induced apoptosis in A549 as well as H1299 cells. Furthermore, we found that the inhibitory effect of GNL3 knockdown on LUAD cell growth is associated with the downregulation of the Wnt/β-catenin axis.</p><p><strong>Conclusion: </strong>GNL3 is key in the progression of LUAD by metiating Wnt/β-catenin axis. Targeting GNL3 may represent a novel therapeutic method for LUAD treatment.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":"52 4","pages":"46-52"},"PeriodicalIF":2.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141544382","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}

{"title":"Methotrexate might become the sole treatment option for leukemia following the occurrence of Stevens-Johnson syndrome.","authors":"Carolina Sanchez Aranda, Katherine Maciel Costa Silvestre, Kamila da Silva Marques, Maria Lucia Lee, Dirceu Solé","doi":"10.15586/aei.v52i4.983","DOIUrl":"https://doi.org/10.15586/aei.v52i4.983","url":null,"abstract":"<p><strong>Introduction: </strong>Severe cutaneous adverse reactions (SCARs) arising from drug interactions can carry life-threatening implications and result in lasting effects. SCARs can be triggered by various factors, with trimethoprim/sulfamethoxazole identified as a primary culprit. Anticonvulsants and antineoplastic agents have been noted as secondary triggers. Notably, antineoplastics linked to SCARs include immunomodulatory agents. The higher mortality rates among cancer patients with SCARs underscore the significance of comprehending cancer--specific risk factors. Our objective is to present the case of a boy with acute lymphocytic leukemia (ALL) who developed Stevens-Johnson syndrome (SJS) following MTX treatment.</p><p><strong>Case report: </strong>We present the case of a three-year-old male patient diagnosed with ALL who developed Stevens-Johnson syndrome (SJS) subsequent to the administration of MTX, following the \"BFM 2009\" protocol. He had undergone intrathecal MTX administration on six previous occasions. Our patient received IVIG at a dose of 2g/kg along with steroids, resulting in partial clinical improvement after 21 days. An innovative protocol was developed, involving IVIG before MTX infusion and dexamethasone before MTXi, with folinic acid rescue. Intravenous immunoglobulin (IVIG) mitigates SJS/TEN via type IV hypersensitivity down-regulation and apoptosis curbing.</p><p><strong>Conclusion: </strong>As far as we know, the prophylactic use of IVIG to counteract SCARs in a pediatric leukemia patient represents uncharted territory. Moreover, research into the immune system dynamics within these patients and the preservation of indispensable treatments should involve allergist-immunologists as part of the multidisciplinary team attending to neoplastic conditions.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":"52 4","pages":"81-83"},"PeriodicalIF":2.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141544383","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}

{"title":"Study on the Association between Cesarean Section Birth and Asthma Risk in the Pediatric Population of the Health Area of Palencia between 1993 and 2020.","authors":"Jesús Rodríguez Calleja, Eva María Jiménez Hernández, Alba Macías Panedas, José Fernando Soltero Carracedo, Carla González García, María Paz Barrio Alonso, María Teresa Cantero Tejedor, José Elviro Fernández Alonso","doi":"10.15586/aei.v52i4.1084","DOIUrl":"10.15586/aei.v52i4.1084","url":null,"abstract":"<p><strong>Introduction and objectives: </strong>Both asthma prevalence and the percentage of cesarean sections have increased in parallel in recent years. Research studies suggest an increased risk of developing atopic diseases and asthma after cesarean section birth compared to vaginal delivery. The main objective of this study is to analyze the risk of asthma admission after cesarean section birth compared to vaginal delivery in the pediatric population.</p><p><strong>Population and methods: </strong>Retrospective observational analytical case-control study from 1993 to 2020. The cases include all admitted patients to our health area hospital, for patients aged 7 to 16 diagnosed with asthma. For each case, a control without a diagnosis of asthma is selected with the same age, and that has also caused an episode of admission.</p><p><strong>Results: </strong>A total of 290 admission episodes with a diagnosis of asthma were obtained, caused by 155 patients. Out of these, 145 cases with documented delivery types were selected. For cases, 155 controls were selected. The historical proportion of cesarean sections in the asthmatic group is 18.6%, compared to 14.2% in the non-asthmatic group. There is a statistically non-significant difference of 4.4% more cesarean sections in the asthmatic group compared to the control group.</p><p><strong>Discussion: </strong>We have not demonstrated a statistically significant association between being born by cesarean section and an increased risk of asthma admission. Based on this finding, we cannot conclude that there is an association between being born by cesarean section and a higher risk of suffering from asthma, unlike what has been postulated in other research studies.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":"52 4","pages":"68-72"},"PeriodicalIF":2.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141544386","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}

{"title":"Chloroquine regulates the lipopolysaccharide-induced inflammatory response in RAW264.7 cells.","authors":"Natsuki Ota, Shoya Endo, Kouki Honma, Kuninori Iwayama, Hiroshi Yamashita, Ryosuke Tatsunami, Keisuke Sato","doi":"10.15586/aei.v52i4.1083","DOIUrl":"https://doi.org/10.15586/aei.v52i4.1083","url":null,"abstract":"<p><strong>Introduction and objectives: </strong>Macrophage-induced inflammation plays a key role in defense against injury and harmful pathogens. Autophagy and the inflammatory response are associated; however, the relationship between the autophagy pathway and lipopolysaccharide (LPS)- induced inflammatory responses remains unknown. We aimed to determine the effect of autophagy on the LPS-induced myeloid differentiation factor 88 (MyD88)/nuclear transcription factor kB (NF-kB) pathway-mediated inflammatory response in RAW264.7 cells.</p><p><strong>Materials and methods: </strong>To determine the effect of autophagy on the LPS-induced inflammatory response, using various in vitro assays, we determined the effect of autophagy inhibitors and inducers on the inflammatory response in RAW264.7 cells.</p><p><strong>Results: </strong>Chloroquine (CQ), an autophagy inhibitor, suppressed pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor α (TNFα) in LPS-stimulated RAW264.7 cells. CQ also affected inflammatory mediators such as myeloid differentiation factor 88 and NF-kB in LPS-stimulated RAW264.7 cells.</p><p><strong>Conclusion: </strong>This study demonstrated that CQ regulates the LPS-induced inflammatory response in RAW264.7 cells. We propose that targeting the regulation of pro-inflammatory cytokine levels and inflammatory mediators using CQ is a promising therapeutic approach for preventing inflammatory injury. CQ serves as a potential therapeutic target for treating various inflammatory diseases.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":"52 4","pages":"97-103"},"PeriodicalIF":2.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141544418","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}

{"title":"Deciphering the mechanism of cimifugin in mitigating LPS-induced neuroinflammation in BV-2 cells.","authors":"Zhang Bu, Shan Xu, Feng Xu","doi":"10.15586/aei.v52i4.1107","DOIUrl":"https://doi.org/10.15586/aei.v52i4.1107","url":null,"abstract":"<p><strong>Purpose: </strong>Sepsis often triggers a systemic inflammatory response leading to multi-organ dysfunction, with complex and not fully understood pathogenesis. This study investigates the therapeutic effects of cimifugin on BV-2 cells under sepsis-induced stress conditions.</p><p><strong>Methods: </strong>We utilized a BV-2 microglial cell model treated with lipopolysaccharide (LPS) to mimic sepsis. Assessments included cellular vitality, inflammatory cytokine quantification (6 interleukin [6IL]-1β, interleukin 6 [IL-6], and tumor necrosis factor-α [TNF-α]) via enzyme-linked-immunosorbent serologic assay, and analysis of mRNA expression using real-time polymerase chain reaction. Oxidative stress and mitochondrial function were also evaluated to understand the cellular effects of cimifugin.</p><p><strong>Results: </strong>Cimifugin significantly attenuated LPS-induced inflammatory responses, oxidative stress, and mitochondrial dysfunction. It enhanced cell viability and modulated the secretion and gene expression of inflammatory cytokines IL-1β, IL-6, and TNF-α. Notably, cimifugin activated the deacetylase sirtuin 1-nuclear factor erythroid 2-related factor 2 pathway, contributing to its protective effects against mitochondrial damage.</p><p><strong>Conclusion: </strong>Cimifugin demonstrates the potential of being an effective treatment for sepsis--induced neuroinflammation, warranting further investigation.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":"52 4","pages":"38-45"},"PeriodicalIF":2.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141544421","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}

{"title":"Jolkinolide B attenuates allergic airway inflammation and airway remodeling in asthmatic mice.","authors":"Haiyan Lin, Chao Xu, Jintong Ge, Hua Wu, Qi Wang","doi":"10.15586/aei.v52i4.1126","DOIUrl":"https://doi.org/10.15586/aei.v52i4.1126","url":null,"abstract":"<p><p>Asthma is a widely prevalent chronic disease that brings great suffering to patients and may result in death if it turns severe. Jolkinolide B (JB) is one diterpenoid component separated from the dried roots of Euphorbia fischeriana Steud (Euphorbiaceae), and has anti--inflammatory, antioxidative, and antitumor properties. However, the detailed regulatory role and associated regulatory mechanism in the progression of asthma remain elusive. In this work, it was demonstrated that the extensive infiltration of bronchial inflammatory cells and the thickening of airway wall were observed in ovalbumin (OVA)-induced mice, but these impacts were reversed by JB (10 mg/kg) treatment, indicating that JB relieved the provocative symptoms in OVA-induced asthma mice. In addition, JB can control OVA-triggered lung function and pulmonary resistance. Moreover, JB attenuated OVA-evoked inflammation by lowering the levels of interleukin (IL)-4, IL-5, and IL-13. Besides, the activated nuclear factor kappa B (NF-κB) and transforming growth factor-beta-mothers against decapentaplegic homolog 3 (TGFβ/smad3) pathways in OVA-induced mice are rescued by JB treatment. In conclusion, it was disclosed that JB reduced allergic airway inflammation and airway remodeling in asthmatic mice by modulating the NF-κB and TGFβ/smad3 pathways. This work could offer new opinions on JB for lessening progression of asthma.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":"52 4","pages":"91-96"},"PeriodicalIF":2.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141544381","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}