Archivum Immunologiae et Therapiae Experimentalis最新文献

{"title":"Herd-Trained Immunity: A Hidden Component of Population-Level Innate Immunity.","authors":"Janusz Marcinkiewicz","doi":"10.2478/aite-2026-0017","DOIUrl":"https://doi.org/10.2478/aite-2026-0017","url":null,"abstract":"","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148293370","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":"<i>Saccharomyces cerevisiae</i> β-Glucan Training Induces a Nonclassical PGE₂-^High/NO-^Low Macrophage Phenotype in Response to <i>Pseudomonas aeruginosa</i> Exopolysaccharide.","authors":"Marta Ciszek-Lenda, Grzegorz Majka, Maciej Suski, Sabina Górska, Edyta Golińska, Izabela Siemińska, Rafał Olszanecki, Magdalena Strus, Janusz Marcinkiewicz","doi":"10.2478/aite-2026-0014","DOIUrl":"10.2478/aite-2026-0014","url":null,"abstract":"<p><p>Exopolysaccharide (EPS), a major constituent of <i>Pseudomonas aeruginosa</i> biofilms, protects bacteria from M1-macrophage-mediated clearance while promoting chronic inflammation. This study investigated how <i>Saccharomyces cerevisiae</i> β-glucan (BG)-induced macrophage training reshapes subsequent inflammatory and antimicrobial responses to EPS. Peritoneal macrophages from C57BL/6 mice were trained <i>in vitro</i> with BG and subsequently stimulated with EPS purified from a clinical <i>P. aeruginosa</i> isolate obtained from a patient with severe cystic fibrosis. Cytokines, prostaglandin E₂ (PGE₂), and nitric oxide (NO) were quantified, and global proteomic profiling was performed. BG training amplified EPS-induced secretion of TNF-α, IL-6, and additional pro-inflammatory mediators. Trained macrophages also showed markedly increased PGE₂ production, minimal NO release, and reduced phagocytic activity. Proteomic analyzes confirmed upregulation of PGE₂-biosynthetic enzymes and suppression of inducible NO synthase, along with enhanced expression of antimicrobial and immunoregulatory factors, including platelet factor 4, antileucoproteinase, C1q components, and selected chemokines. These data reveal a previously uncharacterized macrophage state-neither M1 nor M2-emerging specifically from BG training and defined by high PGE₂ and low NO production in response to EPS. <i>S. cerevisiae</i> BG training reprograms EPS-stimulated macrophages toward a distinct, non-classical trained-immunity phenotype characterized by elevated PGE₂ and suppressed NO production. This newly defined phenotype represents a novel form of trained immunity and highlights the dual proinflammatory and immunoregulatory roles of macrophage-derived PGE₂. These findings suggest that targeted macrophage reprogramming may offer a promising therapeutic strategy for mitigating <i>P. aeruginosa</i> biofilm-driven chronic inflammation, including in cystic fibrosis.</p>","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136704","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":"Salvianolic Acid C Activates the AMPK Pathway to Inhibit Ferroptosis and Alleviate Cardiomyocyte Injury after Acute Myocardial Infarction.","authors":"Yanping Zeng, Lin Chen, Zhenhua Qian, Weixing Ma, Cheng Ma, Yan Wang, Guanfeng Zhu","doi":"10.2478/aite-2026-0015","DOIUrl":"10.2478/aite-2026-0015","url":null,"abstract":"<p><p>Myocardial infarction (MI) is one of the leading causes of death worldwide and results in substantial harm to human health and family well-being. Salvianolic acid C (SAC), a bioactive compound isolated from <i>Salvia miltiorrhiza</i> Bge., exhibits anti-oxidant, anti-inflammatory, and anti-apoptotic capacities. However, the protective effects of SAC against MI-induced cardiomyocyte injury and the underlying molecular mechanisms, particularly its role in ferroptosis and AMPK signaling, remain unclear. Infarct size in rat hearts was assessed through triphenyltetrazolium chloride (TTC) staining. Myocardial tissue damage was examined through hematoxylin-eosin (HE) staining. The mRNA and protein levels of inflammatory cytokines, including Interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, were measured by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Apoptosis in myocardial tissues was evaluated through the terminal deoxynucleotide transferase-mediated dUTP nick end-labeling (TUNEL) assay. Protein expression levels were determined by Western blot. The results demonstrated that SAC significantly reduced infarct size in MI rats. Inflammation and cardiomyocyte apoptosis were markedly increased in the MI group, but these impacts were neutralized after SAC treatment. In addition, SAC effectively suppressed ferroptosis in MI rats. Mechanistically, SAC activates the AMPK pathway. Finally, SAC was shown to alleviate oxygen-glucose deprivation (OGD)-induced cardiomyocyte injury by activating the AMPK pathway. This study is the first to demonstrate that SAC activates the AMPK pathway to inhibit ferroptosis and alleviate cardiomyocyte injury after acute MI. These findings suggest that SAC may present a promising therapeutic candidate for the treatment of MI.</p>","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147959451","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":"Di-Chimeric Cell Therapy Derived From Hematopoietic and Mesenchymal Stem Cells Promotes Immune Tolerance and Extends Vascularized Composite Allograft Survival.","authors":"Maria Siemionow, Safak Halil Uygur, Katarzyna Stawarz, Lucile Chambily, Katarzyna Budzynska, Weronika Radecka","doi":"10.2478/aite-2026-0013","DOIUrl":"10.2478/aite-2026-0013","url":null,"abstract":"<p><p>Chimerism-based strategies remain promising for tolerance induction in solid organ and vascularized composite allograft (VCA) transplantation. This study aimed to develop a novel, less toxic chimeric cell therapy to prolong allograft survival and reduce the need for lifelong immunosuppression. Di-chimeric cells (DCC) were created via polyethylene glycol (PEG)-mediated <i>ex vivo</i> fusion of allogeneic hematopoietic stem cells (HSC) and mesenchymal stem cells (MSC) derived from August Copenhagen Irish (ACI) and Lewis rats. Twenty-four fully major histocompatibility complex (MHC)-mismatched groin flap VCAs were transplanted from ACI rat major histocompatibility complex (rat MHC) (RT1^a) donors to Lewis (RT1¹) recipients under a 7-day immunosuppressive protocol of anti-αβTCR antibody and tacrolimus, combined with four different cell therapies of <i>n</i> = 6/group: Group 1, saline control; Group 2, MSC; Group 3, HSC/HSC DCC; and Group 4, HSC/MSC DCC. DCC were delivered via the intraosseous injection. DCC phenotype was confirmed by flow cytometry (FC). Graft rejection was evaluated macroscopically. A single DCC dose significantly prolonged VCA survival, with the best results in Group 4 (94 ± 1.65 days), followed by Group 3 (66 ± 1.24 days), Group 2 (45.5 ± 4.08 days), and Group 1 (38 ± 4.29 days). This study confirmed immunomodulatory and tolerogenic properties of DCC, supporting VCA transplantation.</p>","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147653488","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":"BDH2 Inhibits Lung Adenocarcinoma Metastasis by Promoting Ferroptosis.","authors":"Qiao Yang, Lin Tian, Xiaodong Chen, Xiong Mei, Yongli Nie, Jun Chen","doi":"10.2478/aite-2026-0012","DOIUrl":"10.2478/aite-2026-0012","url":null,"abstract":"<p><p>To investigate the role of 3-hydroxybutyrate dehydrogenase 2 (BDH2) in regulating ferroptosis and its impact on the metastasis of lung adenocarcinoma (LUAD). Expression levels of BDH2 were modulated in LUAD cell lines (A549, PC9) using pcDNA-BDH2 plasmid transfection. Cell motility was assessed by Transwell assays, while ferroptosis-associated markers, including Fe²⁺, malondialdehyde (MDA), lipid reactive oxygen species (ROS), ACSL4, and GPX4, were evaluated by biochemical assays, flow cytometry, and Western blotting. The involvement of the Nrf2/HO-1 signaling axis was analyzed by Western blotting and RT-qPCR. Furthermore, a xenograft mouse model was established to confirm the effect of BDH2 on tumor progression and metastasis <i>in vivo</i>. Overexpression of BDH2 significantly inhibited LUAD cell migration and invasion. BDH2 upregulation enhanced ferroptosis, effects that were reversed by the ferroptosis inhibitor Fer-1. Mechanistically, BDH2 suppressed the activation of the Nrf2/HO-1 pathway, thereby enhancing sensitivity to ferroptosis. <i>In vivo</i>, BDH2 overexpression markedly reduced tumor growth and metastasis in nude mice, while inhibition of ferroptosis attenuated these effects. BDH2 suppresses metastasis in LAUD by promoting ferroptosis via suppression of the Nrf2/HO-1 pathway, highlighting BDH2 as a potential therapeutic target for LUAD.</p>","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147653404","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":"<i>Fusobacterium nucleatum</i> Promotes Bladder Cancer Development Through lncRNA <i>IDH1-AS1</i>-Mediated Autophagy.","authors":"JunJie Hu, BiYan Li, XiaoYuan Xu, ShuYing Lin, Shui Xu, YueJun Chen, GaoYin Tong","doi":"10.2478/aite-2026-0011","DOIUrl":"10.2478/aite-2026-0011","url":null,"abstract":"<p><p>Bladder cancer is a prevalent malignancy with a high recurrence rate, necessitating the identification of novel molecular targets for diagnosis and therapy. Recent studies have highlighted the role of long noncoding RNAs (lncRNAs) in cancer progression. This study aims to investigate the role of the lncRNA <i>IDH1-AS1</i> in bladder cancer, focusing on its effects on tumor growth, cell proliferation, and autophagy-related protein expression. We utilized both <i>in vivo</i> and <i>in vitro</i> models to assess the impact of <i>IDH1-AS1</i> overexpression and knockdown. Tumor growth was evaluated in nude mice model of bladder cancer, while cell proliferation was measured using the EDU assay. Protein expression levels of Beclin1, <i>P62</i>, and LC3 were determined by Western Blot analysis. Gene expression of <i>IDH1-AS1</i> was quantified using quantitative polymerase chain reaction (qPCR). Overexpression of <i>IDH1-AS1</i> in nude mice model of bladder cancer led to a significant increase in tumor volume and weight, whereas knockdown of <i>IDH1-AS1</i> resulted in a substantial decrease in tumor size. <i>In vitro</i>, <i>IDH1-AS1</i> overexpression significantly enhanced cell proliferation, while its knockdown reduced proliferation. Western Blot analysis revealed that <i>IDH1-AS1</i> overexpression increased the levels of autophagy-related proteins Beclin1 and LC3, and decreased <i>P62</i> protein levels, with contrary effects observed upon <i>IDH1-AS1</i> knockdown. qPCR confirmed successful modulation of <i>IDH1-AS1</i> expression in experimental groups. Our findings indicate that <i>IDH1-AS1</i> promotes tumor growth and cell proliferation in bladder cancer, potentially through the regulation of autophagy-related proteins. These results suggest that <i>IDH1-AS1</i> could serve as a novel biomarker and therapeutic target for bladder cancer.</p>","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147760607","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":"Bowel-Associated Dermatosis and Arthritis Syndrome (BADAS) - A Literature Review With Diagnostic and Therapeutic Implications and a Report of Two Cases of BADAS Associated With Inflammatory Bowel Disease.","authors":"Raman Nitskovich, Aleksandra Jóźwik, Piotr Sobolewski, Paweł Głuszak, Dagmara S Mahadea, Irena Walecka","doi":"10.2478/aite-2026-0010","DOIUrl":"10.2478/aite-2026-0010","url":null,"abstract":"<p><p>Bowel-associated dermatosis-arthritis syndrome (BADAS) is a rare neutrophilic dermatosis characterized by recurrent erythematous macules, papules or vesicopustules accompanied by fever, malaise, arthralgia and peripheral arthritis. Although originally described after intestinal bypass procedures, BA-DAS is increasingly recognized in inflammatory bowel disease (IBD), yet remains underdiagnosed and lacks practical guidance. We reviewed published IBD-associated BADAS cases to define clinical patterns and therapeutic options, and report two additional cases managed by an interdisciplinary team. Across the literature, 21 IBD-associated BADAS cases were identified, with a female predominance (65%) and a mean age at onset of 36.7 years; pediatric presentations accounted for 17%. Ulcerative colitis (12 cases) and Crohn's disease (10 cases) were the most frequent underlying conditions. BADAS was often diagnosed concurrently with IBD, indicating that the combination of cutaneous eruptions, joint inflammation and systemic symptoms should prompt gastrointestinal evaluation. Frequently reported abnormalities included leukocytosis, anemia and elevated inflammatory markers, and skin histopathology typically showed a neutrophilic dermatosis often with leukocytoclastic vasculitis. Case 1 (30-year-old woman with ulcerative colitis) achieved sustained remission with antibiotics, corticosteroid taper, cyclosporine induction and azathioprine maintenance. Case 2 (67-year-old man with Crohn's disease) responded to antibiotics followed by infliximab, with resolution of skin, joint and intestinal activity. We propose a pragmatic management approach integrating antibiotics, optimization of IBD therapy and early use of biologics (preferably anti-TNF) in severe or steroid-refractory disease.</p>","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146776118","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":"Mechanism of RBM15 in Regulating PD-L1-Mediated Immune Escape in Ovarian Cancer Through the JAK2/STAT3/STAT5 Pathway.","authors":"Chengju Zhang, Tiantian Feng, Hu Wang, Deng He, Xi Wang, Shangqi Ni, Yuesong Wang","doi":"10.2478/aite-2026-0009","DOIUrl":"10.2478/aite-2026-0009","url":null,"abstract":"<p><p>This paper elucidates the role of RNA-binding motif protein 15 (RBM15) in programmed death-ligand 1 (PD-L1)-mediated immune escape in ovarian cancer (OC), providing a novel immunotherapeutic strategy. RBM15/circFGFR3/JAK2/STAT3/STAT5 expression was assessed. OC cell progression was analyzed. OC cells were co-cultured with CD8⁺ T cells. The m6A enrichment on circRNA fibroblast growth factor receptor 3 (circFGFR3) was determined. The expression of p-JAK2, p-STAT3, and p-STAT5 was investigated. The bindings of circFGFR3 to EIF4A3 and EIF4A3 to JAK2, STAT3, or STAT5 were analyzed. In conclusion, RBM15 promotes PD-L1-mediated immune escape and accelerates OC progression by upregulating circFGFR3 expression through m6A modification and activating the Janus kinase-signal transducer and activator of transcription (JAK/STAT) pathway.</p>","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146177528","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":"Neuronal Transdifferentiation in Humans: Protocols for Monocytes Conversion into Neuronal-Like Cells with Small Molecules.","authors":"Kornelia Jankowska, Saeid Ghavami, Jolanta Hybiak, Marek J Łos","doi":"10.2478/aite-2026-0008","DOIUrl":"10.2478/aite-2026-0008","url":null,"abstract":"<p><p>Neurodegenerative diseases, such as Parkinson's, Alzheimer's, and Huntington's, are major causes of disability. Current treatments are mostly symptomatic, due to a limited understanding of the disease mechanisms and the brain's poor regenerative capacity. Neuronal transdifferentiation offers a promising solution. Existing protocols are often inefficient, invasive, or time-consuming, and expensive. Furthermore, they mostly rely on nucleic acids as transdifferentiation-inducers, hence this carries risks of insertion mutagenesis. In this study, monocytes were isolated from buffy coats and cultured under four protocols using different small-molecule combinations. Two protocols successfully generated TUJ1⁺ MAP2⁺ SYP⁺ cells. Transdifferentiation is achievable through cheap and efficient chemical induction.</p>","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146046073","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":"Significance of the LL-37 Peptide Delivered from Human Cathelicidin in the Pathogenesis, Treatment, and Diagnosis of Sepsis.","authors":"Angelika Mańkowska, Paulina Paprocka, Grzegorz Król, Agata Lesiak, Jakub Spałek, Ewelina Piktel, Sławomir Okła, Piotr Bijak, Wiesława Niklińska, Bonita Durnaś, Robert Bucki","doi":"10.2478/aite-2025-0025","DOIUrl":"https://doi.org/10.2478/aite-2025-0025","url":null,"abstract":"<p><p>Antimicrobial peptides, which function as the first line of host immune defense, have recently been identified as important immunomodulators of inflammation, and are involved as regulatory molecules in infections, including sepsis. Treatment of sepsis is very complex and remains largely challenging and sometimes ineffective. This creates a need to develop new therapeutic strategies focusing not only on the elimination of sepsis-causing microorganisms, which can be achieved with antibiotics, but also on the control of the immune system and its overactive response resulting in increased vascular endothelial permeability. One approach to develop new treatments for patients with sepsis is to better understand the pleiotropic function of the human LL-37 peptide that originates from the human cathelicidin antibacterial protein (h-CAP18). An increasing number of studies indicate high dynamics of changes in LL-37 concentration in the blood during sepsis. Additionally, in animal models, administration of exogenous LL-37 peptide to mice with experimentally induced sepsis increases their survival. It can therefore be assumed that knowledge of the molecular mechanism of cathelicidin LL-37 action, as well as the synthesis of its stable analogs, will result in progress in the diagnosis and therapy of sepsis.</p>","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"73 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074226","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}