Immunity, Inflammation and Disease最新文献

{"title":"Active Compounds, Targets, and Mechanisms of Salvia miltiorrhiza Bunge in Treating Interstitial Cystitis/Bladder Pain Syndrome","authors":"Liang Wang,&nbsp;Bei Yu,&nbsp;YaRong Wang,&nbsp;Xi Qu,&nbsp;Wei Tang","doi":"10.1002/iid3.70173","DOIUrl":"https://doi.org/10.1002/iid3.70173","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To investigate the active compounds, molecular targets, and biological mechanisms of <i>Salvia miltiorrhiza</i> Bunge (SM) in treating interstitial cystitis/bladder pain syndrome (IC/BPS) through network pharmacology and a cyclophosphamide-induced cystitis model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A network pharmacology approach was used to assess the effects of SM and luteolin in IC/BPS. Female C57BL/6 mice were divided into four groups: CON, CON + Luteolin, CYP, and CYP + Luteolin, with luteolin (100 mg/kg) administered for CYP-induced cystitis. Histological and molecular analyses, including H&amp;E staining, TUNEL, ELISA, Western blot, and urodynamics, were performed to explore the mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Network pharmacology showed 65 active ingredients and 148 potential targets of SM in the treatment of IC/BPS, of which luteolin had the highest potential. TP53, AKT1, CCND1, EGFR, and ERBB2 are the core targets, and PI3K-Akt and p53 are important signaling pathways for luteolin in the treatment of IC/BPS. Compared with the CYP group, the CYP + Luteolin group showed significantly lower bladder tissue scores; reduced expression of malondialdehyde, inflammatory factors (IL-18, IL-1β, IL-6), and apoptosis-related proteins (cleaved-Caspase-3, Bax, cleaved-Caspase-8); significantly increased expression of total SOD and glutathione; and improved bladder function. Animal experiments have shown that luteolin can block the activation of the PI3K-Akt and p53 signaling pathways.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>SM has a variety of potentially active components for the treatment of IC/BPS, of which luteolin has the highest potential. Luteolin can inhibit inflammation, oxidative stress, and apoptosis through the p53 and PI3K-Akt signaling pathways and plays a role in treating IC/PBS.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70173","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143826959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Oxaliplatin Activates P53/miR-34a/Survivin Axis in Inhibiting the Progression of Gastric Cancer Cells","authors":"","doi":"10.1002/iid3.70191","DOIUrl":"https://doi.org/10.1002/iid3.70191","url":null,"abstract":"<p><b>RETRACTION</b>: Q. Guo, X.-Y. Wang, Y.-C. Zhai, Y.-W. Dong, and Q.-S. He, “Oxaliplatin Activates P53/miR-34a/Survivin Axis in Inhibiting the Progression of Gastric Cancer Cells,” <i>Immunity, Inflammation and Disease</i> 12, no. 9 (2024): e70004, https://doi.org/10.1002/iid3.70004.</p><p>The above article, published online on 10 September 2024 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Marc Veldhoen; and John Wiley &amp; Sons Ltd. The retraction has been agreed upon due to insufficient information included within the methodology, which prevents accurate reproduction of the study. Furthermore, there are concerns that the beta actin bands included in Figure 3a do not originate from the same gel as the other bands shown in this figure. Finally, the cell line used in this study was reported to be contaminated. The authors were contacted for comment and supporting data, but they did not respond. The editors consider the results and conclusions unreliable. The authors were informed of the retraction.</p>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70191","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: LncRNA TUG1 Relieves Renal Mesangial Cell Injury by Modulating the miR-153-3p/Bcl-2 Axis in Lupus Nephritis","authors":"","doi":"10.1002/iid3.70193","DOIUrl":"https://doi.org/10.1002/iid3.70193","url":null,"abstract":"<p><b>RETRACTION:</b> L. Liu, Y. Zhang and L. Zhong, “LncRNA TUG1 Relieves Renal Mesangial Cell Injury by Modulating the miR-153-3p/Bcl-2 Axis in Lupus Nephritis,” <i>Immunity, Inflammation and Disease</i> 11, no. 4 (2023): e811, https://doi.org/10.1002/iid3.811.</p><p>The above article, published online on 12 April 2023 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Marc Veldhoen; and John Wiley &amp; Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party. The investigation revealed that the LPS+miR-153-3p inhibitor flow cytometry plot presented in Figure 6B has been found duplicated in another article by a different author group representing different scientific conditions. The authors provided an explanation and some data but this was not deemed sufficient. The editors have lost confidence in the data presented and consider the conclusions to be compromised. The authors disagree with the retraction.</p>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70193","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Expression and Significant Roles of the lncRNA NEAT1/miR-493-5p/Rab27A Axis in Ulcerative Colitis","authors":"","doi":"10.1002/iid3.70192","DOIUrl":"https://doi.org/10.1002/iid3.70192","url":null,"abstract":"<p><b>RETRACTION:</b> H. Wang, J. Teng, M. Wang, Y. Zhang, X. Liu and Z. Liu, “Expression and Significant Roles of the lncRNA NEAT1/miR-493-5p/Rab27A Axis in Ulcerative Colitis,” <i>Immunity, Inflammation and Disease</i> 11, no. 5 (2023): e814, https://doi.org/10.1002/iid3.814.</p><p>The above article, published online on 16 May 2023 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Marc Veldhoen; and John Wiley &amp; Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party. The investigation revealed that the LPS+lncRNA NEAT1-sRNA+inhibitor control flow cytometry plot and parts of the LPS plot presented in Figure 5E have been published in other articles representing different scientific contexts. The authors provided an explanation and some data, but this was not deemed sufficient. The editors have lost confidence in the data presented and consider the conclusions to be compromised.</p>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70192","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: MicroRNA-425-3p Inhibits Myocardial Inflammation and Cardiomyocyte Apoptosis in Mice With Viral Myocarditis Through Targeting TGF-β1","authors":"","doi":"10.1002/iid3.70190","DOIUrl":"https://doi.org/10.1002/iid3.70190","url":null,"abstract":"<p><b>RETRACTION</b>: J. Li, J. Tu, H. Gao and L. Tang “MicroRNA-425-3p Inhibits Myocardial Inflammation and Cardiomyocyte Apoptosis in Mice With Viral Myocarditis Through Targeting TGF-β1,” <i>Immunity, Inflammation and Disease</i> 9, no. 1 (2021): 288–298, https://doi.org/10.1002/iid3.392.</p><p>The above article, published online on 17 December 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Marc Veldhoen; and John Wiley &amp; Sons Ltd. The retraction has been agreed following an investigation into concerns raised by a third party. The investigation revealed inappropriate duplication of the control and CVB3 images presented in Figure 6A. Additionally, the CVB3 + miR-425-3p mimic image shown in Figure 6A was previously published in another article in a different scientific context. Lastly, evidence of undisclosed splicing was observed in the western blots shown in Figures 5F, 6C and 6E. The authors were invited to comment and provide their raw data, but they were unable to supply any data or an explanation. The editors consider the results and conclusion reported in this article unreliable. The authors were informed of the retraction.</p>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70190","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered Circulating Cytokine Profile Among mRNA-Vaccinated Young Adults: A Year-Long Follow-Up Study","authors":"Amani Alghamdi,&nbsp;Syed Danish Hussain,&nbsp;Kaiser Wani,&nbsp;Shaun Sabico,&nbsp;Abdullah M. Alnaami,&nbsp;Osama Emam Amer,&nbsp;Nasser M. Al-Daghri","doi":"10.1002/iid3.70194","DOIUrl":"https://doi.org/10.1002/iid3.70194","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Objectives&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;This longitudinal study aimed to assess the impact of COVID-19 vaccination on cytokine profile.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;A total of 84 Saudi subjects (57.1% females) with mean age of 27.2 ± 12.3 participated in this longitudinal study. Anthropometric data and fasting blood samples were obtained at baseline and after final vaccination, with an average follow-up duration of 14.1 ± 3.6 months for adolescents and 13.3 ± 3.0 months for adults, calculated from the first dose of vaccination. Assessment of cytokine profiles was done using commercially available assays.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;After follow-up, a significant increase in weight and body mass index was observed overall (&lt;i&gt;p&lt;/i&gt; = 0.003 and &lt;i&gt;p&lt;/i&gt; = 0.002, respectively). Postvaccination, significant increases were observed in several cytokines, including basic fibroblast growth factor 2 (&lt;i&gt;p&lt;/i&gt; &lt; 0.001), interferon gamma (IFNγ) (&lt;i&gt;p&lt;/i&gt; = 0.005), interleukin-1 beta (IL1β) (&lt;i&gt;p&lt;/i&gt; &lt; 0.001), IL4 (&lt;i&gt;p&lt;/i&gt; &lt; 0.001), IL6 (&lt;i&gt;p&lt;/i&gt; = 0.003), IL7 (&lt;i&gt;p&lt;/i&gt; = 0.001), IL17E (&lt;i&gt;p&lt;/i&gt; &lt; 0.001), monocyte chemoattractant protein-1 (MCP1) (&lt;i&gt;p&lt;/i&gt; = 0.03), MCP3 (&lt;i&gt;p&lt;/i&gt; = 0.001), tumor necrosis factor alpha (TNFα) (&lt;i&gt;p&lt;/i&gt; &lt; 0.001), and VEGFA (&lt;i&gt;p&lt;/i&gt; &lt; 0.001). A significant reduction was observed only in macrophage colony-stimulating factor (&lt;i&gt;p&lt;/i&gt; &lt; 0.001). When adjusted for age, epidermal growth factor (EGF), IL4, IL6, MCP3, TNFα, and vascular endothelial growth factor (VEGFA) remained statistically significant. Gender-based analysis revealed that men experienced greater increases in IL6 (&lt;i&gt;p&lt;/i&gt; = 0.008), IL4 (&lt;i&gt;p&lt;/i&gt; = 0.04), and TNFα (&lt;i&gt;p&lt;/i&gt; = 0.015) compared to women. Age-based analysis showed that older participants had more pronounced increases in EGF (&lt;i&gt;p&lt;/i&gt; = 0.011), IL6 (&lt;i&gt;p&lt;/i&gt; = 0.029), MCP1 (&lt;i&gt;p&lt;/i&gt; = 0.042), and TNFα (&lt;i&gt;p&lt;/i&gt; = 0.017), while younger participants had a greater increase in VEGFA (&lt;i&gt;p&lt;/i&gt; = 0.025).&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusions&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;The findings of this study indicated that COVID-19 vaccination resulted in an increase in cytokine levels, which signifies the persistence of the humoral immune response to messenger RNA (mRNA) vaccines. This effect may be attributed to the persistent production of spike protein and highly inflammatory nature of mRNA–lipid nanoparticle. Additionally, the results suggested differences in cytokine levels based on gender and age. Notably, the cytokine profile remains favorably altered in young adults who receiv","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70194","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143801877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Inflammation and Hearing Loss: Key Biomarkers and Subgroup Differences by Gender and BMI in a National Cohort","authors":"Zhe Peng,&nbsp;Chun-li Zhao,&nbsp;Guo-peng Wang,&nbsp;Qian Wu,&nbsp;Shu-sheng Gong","doi":"10.1002/iid3.70188","DOIUrl":"https://doi.org/10.1002/iid3.70188","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Hearing loss (HL) significantly impacts quality of life and economic status worldwide. Chronic inflammation is suggested to influence hearing, yet the connection with inflammation-related indexes in the general population is not well understood.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This cross-sectional study analyzed data from 7231 adults from six cycles (2005–2012 and 2015–2018) of the National Health and Nutrition Examination Survey (NHANES). It examined the correlation between systemic immune-inflammatory biomarkers (NLR, SII, PLR, and LMR) and auditory threshold shifts/HL using multivariable logistic regression models. Smooth curve fitting visualized the association, and log-likelihood ratio tests determined the existence of thresholds in biomarker effects, supplemented by subgroup analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>After adjustments, significant associations were found for low-frequency HL with ln-transformed NLR (OR = 1.29, 95% CI: 1.06–1.56, <i>p</i> = 0.0116), ln-SII (OR = 1.31, 95% CI: 1.08–1.59, <i>p</i> = 0.0065), and ln-LMR (OR = 0.74, 95% CI: 0.60–0.91, <i>p</i> = 0.00043). For high-frequency HL, similar patterns were observed for ln-SII (OR = 1.25, 95% CI: 1.05–1.48, <i>p</i> = 0.0105) and ln-LMR (OR = 0.76, 95% CI: 0.64–0.90, <i>p</i> = 0.007); however, the association with ln-NLR did not reach statistical significance (OR = 1.18, 95% CI: 1.00–1.40, <i>p</i> = 0.0562). NLR and SII positively correlated with HL, while LMR showed a negative correlation. No significant association was noted with PLR. Dose–response relationships were observed, particularly between LMR and all categorized frequencies of HL and between SII and high-frequency HL. Subgroup analyses indicated that NLR and SII are risk factors for HL in healthy BMI males, with LMR being more protective in males, the elderly, and diabetics.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Systemic inflammation-related indexes, especially SII, are predictive of both high- and low-frequency HL, highlighting the role of inflammatory homeostasis in hearing health. LMR may offer protective effects, particularly in specific subgroups. These findings suggest potential targets for HL treatment by regulating inflammation, warranting further investigation into their clinical application.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70188","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143801557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantitative Proteomic Analysis Indicates That Pggt1b Deficiency Promotes Cytokine Secretion in Resiquimod-Stimulated Bone Marrow-Derived Macrophages via the NF-κB Pathway","authors":"Shanshan Yu,&nbsp;Xuecui Wei,&nbsp;Fangyuan Long,&nbsp;Heng Gu,&nbsp;Zhimin Hao","doi":"10.1002/iid3.70185","DOIUrl":"https://doi.org/10.1002/iid3.70185","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Psoriasis is a systemic inflammatory skin disease mediated by the innate and adaptive immune systems. Recent studies have indicated that macrophages may contribute to the pathogenesis of psoriasis. However, the role of macrophage protein geranylgeranyl transferase type-1β subunit (PGGT1B) in psoriasis is unclear. In this study, we aimed to establish how a reduction in Pggt1b expression in monocytes influences the onset and progression of psoriasis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Myeloid cell-specific Pggt1b knockout mice were generated, and their bone marrow-derived macrophages (BMDMs) were stimulated with resiquimod (R848) to mimic the psoriatic immune microenvironment. The proteomic analysis enabled us to identify 17 differentially expressed proteins associated with Pggt1b deficiency in the psoriasis macrophage model (folded change ≥ 1.3 and <i>p</i> &lt; 0.05). Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment was performed. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blot assays were used to verify the differentially expressed proteins and signaling pathways. Finally, an enzyme-linked immunosorbent assay was used to verify the expression of the key inflammatory cytokine interleukin (IL)-1β.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In total, six proteins (Dlgap5, Fas, Fnta, Nlrp3, Cd14, and Ticam2) were identified as hub proteins. Furthermore, we found that Pggt1b might mediate R848-induced inflammation via the small G-proteins Rac1 or Cdc42. We found that Pggt1b positively regulates pro-inflammatory responses in R848-stimulated BMDMs via the NF-κB signaling pathway.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study clarified that PGGT1B affected the synthesis of inflammatory cytokines via NF-κB pathway and provided insights into the mechanisms underlying immune responses and inflammation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70185","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Farnesoid X Receptor Regulated Sepsis-Induced Abnormal Bile Acid Metabolism via the Fibroblast Growth Factor 15/Fibroblast Growth Factor Receptor 4 Pathway","authors":"Ziyang Zhou,&nbsp;Dan Xu,&nbsp;Liou Huang,&nbsp;Yuhui Cui,&nbsp;Hui Chen,&nbsp;Jianguo Tang","doi":"10.1002/iid3.70155","DOIUrl":"https://doi.org/10.1002/iid3.70155","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The study aims to investigate the mechanism of Farnesoid X receptor (FXR) activation in sepsis-induced abnormal bile acid metabolism and the metabolism status of each bile acid type.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The sepsis mouse model was developed via lipopolysaccharide intraperitoneal injection and confirmed via hematoxylin and eosin (H&amp;E) staining. FXR agonist activated the FXR/fibroblast growth factor (FGF)15/FGFR pathway via quantitative real-time polymerase chain reaction and Western blot. Consequently, metabolomics and bioinformatics analysis were conducted to identify the alterations in each kind of bile acid content following FXR agonist/inhibitor intervention.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The H&amp;E staining indicated that FXR activation alleviates the liver injury of the sepsis mouse model. The increased FGF15 and FXFR expression levels and decreased CYP7A1 demonstrated FXR/FGF15/FGFR pathway activation following FXR agonist treatment. Furthermore, total bile acid, interleukin (IL)-6, and tumor necrosis factor-α concentrations were downregulated after FXR activation, whereas IL-10 concentration was upregulated, indicating the alleviated effect of FXR agonist in sepsis. Consequently, metabolomics and bioinformatics analysis determined that T-a-MCA were downregulated in both FXR agonist and inhibitor groups, whereas six bile acid types were altered in the control group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>FXR activation was crucial in alleviating sepsis-induced hepatic injury and cholestasis through the FGF15/FGFR signaling pathway, and FXR may act as a potential preventive and intervention target of sepsis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70155","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current Advancements in Serum Protein Biomarkers for Hepatitis B Virus-Associated Hepatocyte Remodeling and Hepatocellular Carcinoma","authors":"Adane Adugna,&nbsp;Gashaw Azanaw Amare,&nbsp;Mohammed Jemal","doi":"10.1002/iid3.70171","DOIUrl":"https://doi.org/10.1002/iid3.70171","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Hepatitis B virus (HBV)-related liver cancer is the third most common cause of cancer-related death globally. Hepatocyte remodeling, also known as hepatocyte transformation and immortalization, and hepatocellular carcinoma (HCC), are brought on by persistent inflammation caused by HBV in the host hepatocytes. One of the main concerns in the perspective of HBV-induced hepatocyte remodeling and liver cancer is accurately identifying cancer stages to maximize early screening and detection. Biological signatures have a significant impact on solving this problem.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This review article aimed to discuss the novel serum protein biomarkers for HBV-induced hepatocyte remodeling and HCC.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The information was collected from various peer-reviewed journals through electronic searches utilizing various search engines, including PubMed, Google Scholar, HINARI, and Cochrane Library from 2017 to 2024. Keywords for searches included “serum protein biomarkers in HBV-HCC,” “blood-based biomarkers in HBV-HCC,” and “viral biomarkers for HBV-HCC.”</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Recently, novel protein signatures have been discovered for the early diagnosis, treatment, and prognosis of HBV-induced hepatic cell remodeling and HCC from proteomic data sets. We have discussed the recent literature on the clinical utility of the protein signatures for the diagnosis and forecasting of HBV-associated hepatocyte remodeling and HCC, including golgi protein 73 (GP73), glypican-3 (GPC3), midkine (MDK), des-γ-carboxy-prothrombin (DCP), von Willebrand factor (vWF), pentraxin 3 (PTX3), pseudouridine synthases 7 (PUSs 7), squamous cell carcinoma antigen (SCCA), and osteopontin (OPN).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>All these protein markers also exhibit the survival of HBV-related HCC patients, the proliferation, migration, antiapoptosis, mitogenesis, transformation, and angiogenesis of HBV-infected hepatocytes.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70171","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}