Immunopharmacology and Immunotoxicology最新文献

{"title":"<i>In vitro</i> anti-tumour activities of a novel recombinant immunotoxin targeting differentially overexpressed Leucine-rich repeat-containing G-protein-coupled receptor 5 in cervical cancer.","authors":"Marc Henry, Takunda Ngwegya, Nkhasi Lekena, Stefan Barth","doi":"10.1080/08923973.2025.2504904","DOIUrl":"https://doi.org/10.1080/08923973.2025.2504904","url":null,"abstract":"<p><p>Cervical cancer is the fourth most common cancer among women worldwide and is associated with infection by high-risk human papillomaviruses (HPV). In 2022, an estimated 660,000 new cases and around 350,000 deaths were recorded. The burden of this disease remains disproportionately high in low- and middle-income countries, highlighting significant disparities in access to national HPV vaccination, screening, treatment, and social and economic determinants. Leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5) is a receptor that is differentially overexpressed in various cancers, including cervical cancer and is associated with tumour progression, metastasis, and poor prognosis. Targeting LGR5 with a novel recombinant immunotoxin offers a promising therapeutic approach.ObjectiveThe study aims to develop a novel recombinant anti-LGR5 immunotoxin candidate based on a truncated form of <i>Pseudomonas</i> exotoxin A (ETA).MethodsTo develop this LGR5-specific recombinant immunotoxin, a corresponding single chain antibody fragment (αLGR5(scFv)) fused to ETA, was expressed under osmotic stress in the presence of compatible solutes in <i>Escherichia coli</i> BL21 DE3 cells. Expression was monitored by Western blot analysis facilitated by an N-terminal 10x-His tag. Purification was done using immobilized metal affinity chromatography (IMAC) and size exclusion chromatography (SEC). The recombinant immunotoxin (rIT) was assessed for cell surface binding on cervical cancer cell lines using confocal microscopy and flow cytometry. The rIT was then used in an XTT cell viability assay to assess targeted cell killing.Results and discussionUpon confirmation of full-length protein by Western blot, purified protein was used to confirm binding on LGR5-positive cervical cancer cell lines via confocal microscopy and flow cytometry using anti-His PE antibody as a secondary antibody. Selective cell-killing of this novel recombinant immunotoxin was illustrated by the dose-dependent reduction in cell viability at IC50 values in nanomolar concentrations on antigen-positive but not antigen-negative cell lines.ConclusionsIn conclusion, the rIT described is a promising candidate to treat cervical cancer, which however, would finally need to be confirmed by preclinical <i>in vivo</i> studies.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-18"},"PeriodicalIF":2.9,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077826","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":"Immune Checkpoint Inhibitors and Immunosuppressive Tumor Microenvironment: Current Challenges and Strategies to Overcome Resistance.","authors":"Gurpreet Singh Gill, Simmi Kharb, Gitanjali Goyal, Prasenjit Das, Kailash Chand Kurdia, Ruby Dhar, Subhradip Karmakar","doi":"10.1080/08923973.2025.2504906","DOIUrl":"https://doi.org/10.1080/08923973.2025.2504906","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) are shown to improve cancer treatment effectiveness by boosting the immune system of the patient. Nevertheless, the unique and highly suppressive TME poses a significant challenge, causing heterogeneity of response or resistance in a considerable number of patients. This review focuses on the evasive attributes of the TME. Immune evasion mechanism in TME include immunosuppressive cells, cytokine and chemokine signaling, metabolic alterations and overexpression of immune checkpoint molecules such as PD-1, CTLA-4, LAG-3, TIM-3, TIGIT, BTLA and their interactions within the TME. In addition, this review focuses on the overcoming resistance by targeting immunosuppressive cells, normalizing tumor blood vessels, blocking two or three checkpoints simultaneously, combining vaccines, oncolytic viruses and metabolic inhibitors with ICIs or other therapies. This review also focuses on the necessity of finding predictive markers for the stratification of patients and to check response of ICIs treatment. It remains to be made certain by new research and intelligent innovations how these discoveries of the TME and its interplay facilitate ICI treatment and change the face of cancer treatment.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-45"},"PeriodicalIF":2.9,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077827","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":"Dapagliflozin alleviates thioacetamide induced-liver fibrosis in rats via controlling the Nrf2/HO-1 and TLR4/TGF-β1/PI3K signaling pathways.","authors":"Nourhan Hussien Hassan, Gehan M Kamel, Hany M Fayed, Reda M S Korany, Amer Ramadan","doi":"10.1080/08923973.2025.2496661","DOIUrl":"https://doi.org/10.1080/08923973.2025.2496661","url":null,"abstract":"<p><strong>Objectives: </strong>Because liver fibrosis causes several insults that can result in death, it is regarded as an epidemic health issue. As \"an inhibitor of the sodium-glucose cotransporter-2 (SGLT2),\" Dapagliflozin (Dapa) is one of the newest anti-diabetic drugs used to treat type 2 diabetes mellitus. Dapa's antioxidant, anti-inflammatory, and antifibrotic properties produced positive impacts in numerous human and animal models. Due to Dapa's previously documented properties, we planned this investigation to elucidate the protective function of Dapa in male rat liver fibrosis caused by thioacetamide (TAA) as well as the expected pathways.</p><p><strong>Methods: </strong>There were four groups of 24 rats: a control group, a TAA group that received (100 mg/kg b.wt intraperitoneally twice a week for 6 weeks), \"TAA + Dapa\" groups that given oral Dapa at (1 and 2 mg/kg b.wt. for 4 weeks in addition to TAA injections).</p><p><strong>Results: </strong>It was shown that TAA injections increased toll-like receptor 4 (TLR4) (509.6%), tumor necrosis factor (TNF-<i>α</i>) (298.8%), alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), interleukin-6 (IL-6) (330.9%), phosphotidylinositol-3-kinase (PI3K) (428.9% %), and transforming growth factor-beta (TGF-<i>β</i>1) (416.6%) levels. All of these markers were considerably reduced by Dapa treatment. In addition, reduced glutathione (GSH), nuclear factor erythroid 2-related factor 2 (Nrf2) (79%), albumin, Heme-oxygenase 1 (HO-1) (69%), and superoxide dismutase (SOD) were all decreased after TAA injection; however, they were restored by Dapa administration. The Dapa-treated groups had higher Nrf2 and HO-1 gene expressions, based on the results of PCR. Biochemical outcomes were validated by histopathological results. Immunohistopathological study revealed that DAPA treatment decreased caspase-3 and alpha-smooth Muscle Actin (<i>α</i>SMA) expression.</p><p><strong>Conclusion: </strong>Due to its interactions with the Nrf2/HO-1 and TLR4 pathways, our research showed that Dapa had antioxidant and anti-inflammatory qualities against TAA-induced liver fibrosis.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-14"},"PeriodicalIF":2.9,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998874","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":"Therapeutic effect of nintedanib in orbital fibroblasts in patients with Graves' orbitopathy.","authors":"Hyun Young Park, Soo Hyun Choi, JaeSang Ko, Jin Sook Yoon","doi":"10.1080/08923973.2025.2491554","DOIUrl":"https://doi.org/10.1080/08923973.2025.2491554","url":null,"abstract":"<p><strong>Background: </strong>Nintedanib is a potent antifibrotic angiokinase inhibitor approved for various fibrotic lung diseases. Potential therapeutic efficacy of nintedanib in various inflammatory diseases is under investigation. In this study, we investigated the therapeutic effect of nintedanib on adipogenesis and fibrosis in orbital fibroblasts in patients with Graves' orbitopathy (GO).</p><p><strong>Methods: </strong>Primary orbital fibroblasts were cultured from orbital connective tissue of patients with GO and healthy controls. The cells were pretreated with nintedanib before stimulation with either interleukin (IL)-1β, transforming growth factor (TGF)-β, insulin-like growth factor-1, or IL-11. Fibrosis-related and intracellular signaling protein expressions were assessed using western blotting. Hyaluronan and procollagen concentrations were quantified using enzyme-linked immunosorbent assay. Adipogenesis was quantified by Oil Red O staining and the levels of adipogenic transcription factors were determined by Western blot.</p><p><strong>Results: </strong>TGF-β-induced fibronectin and collagen 1/3 protein expression was abrogated by nintedanib treatment. Nintedanib decreased the phosphorylation of signal transducer and activator of transcription 3, SMAD 2/3, Akt, c-Jun N-terminal kinase, and extracellular regulated protein kinase. Exposure to nintedanib hindered adipocyte differentiation and expression of adipogenic transcription factors, including peroxisome proliferator-activated receptor γ, CCAAT/enhancer-binding protein α/β, adipocyte protein 2, adiponectin, and leptin. Additionally, nintedanib reduced hyaluronan and procollagen secretion.</p><p><strong>Conclusions: </strong>Nintedanib suppressed profibrotic protein production, adipogenesis, and hyaluronan production in <i>in vitro</i>. These findings indicate the potential therapeutic efficacy of nintedanib in GO management.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-13"},"PeriodicalIF":2.9,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006880","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":"Mavorixafor: a CXCR4 antagonist for WHIM syndrome.","authors":"Canyu Chen, Bo Xu, Weiyi Li, Jixiang Chen, Zunbo He, Jiecan Zhou","doi":"10.1080/08923973.2025.2491551","DOIUrl":"https://doi.org/10.1080/08923973.2025.2491551","url":null,"abstract":"<p><strong>Background: </strong>WHIM syndrome is a rare primary immune deficiency and chronic neutropenia caused by overactivation of the C-X-C motif chemokine receptor 4/C-X-C motif chemokine ligand 12 (CXCR4/CXCL12) signaling pathway. On April 26th, 2024, Xolremdi (mavorixafor) capsules received its approval from US FDA, is the first targeted treatment specifically for patients aged ≥12 years with WHIM syndrome. Mavorixafor, as a selective CXCR4 antagonist, is able to increase the number of mature neutrophils and lymphocytes in the blood.</p><p><strong>Objective: </strong>This review is to describe the pharmacological properties of mavorixafor and evaluate its clinical efficacy and safety profile.</p><p><strong>Methods: </strong>A literature search was conducted using keywords mavorixafor, XOLREMDI, AMD070, AMD11070, X4P-001, WHIM Syndrome, and CXCR4/CXCL12 on Web of Science, Google Scholar, and PubMed. Drug information was obtained from the FDA website.</p><p><strong>Results: </strong>In the pivotal 52-week phase III trial, time above absolute neutrophil count threshold (TAT_ANC) values in the mavorixafor group were higher than those in the placebo group at 4 different time points (15.04 h vs 2.75 h; <i>p</i> < 0.0001), and mavorixafor group had lower infection frequency, severity and duration. The most common adverse events are thrombocytopenia, pityriasis, rash, rhinitis, epistaxis, vomiting, and dizziness.</p><p><strong>Conclusion: </strong>Mavorixafor 400mg daily effectively increases WBC count, reduces disease symptoms and infection burden in WHIM syndrome patients ≥12 years. Future clinical programs will continue to evaluate the safety and efficacy of mavorixafor in patients with chronic neutropenic disease.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-7"},"PeriodicalIF":2.9,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144002951","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":"Pro-inflammatory effects of all-trans retinoic acid in experimental acute inflammation - insights into eosinophil and neutrophil dynamics.","authors":"Bruno Marques Vieira, Daniela Masid-de-Brito, Lucas Everton Simões, Francisco Leonardo da Silva Medeiro, Juliana Macedo Monte Vianna Pires, Maria Ignez Capella Gaspar-Elsas, Pedro Paulo Xavier-Elsas","doi":"10.1080/08923973.2025.2489402","DOIUrl":"https://doi.org/10.1080/08923973.2025.2489402","url":null,"abstract":"<p><strong>Context: </strong>All-trans retinoic acid (ATRA), a metabolite of vitamin A, regulates embryogenesis, regeneration, hematopoiesis, differentiation, and apoptosis. It also exerts immunomodulatory effects and is used in inflammatory disease models.</p><p><strong>Objective: </strong>This study aimed to investigate the paradoxical pro-inflammatory effects of ATRA on eosinophil and neutrophil recruitment and activation.</p><p><strong>Materials and methods: </strong>We used thioglycolate- and zymosan-induced peritonitis models in mice to evaluate leukocyte recruitment following ATRA treatment. The roles of inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF), and the 5-lipoxygenase (5-LO) pathway were assessed using genetically deficient mice and pharmacological inhibitors.</p><p><strong>Results and discussion: </strong>ATRA increased total leukocyte, eosinophil, and neutrophil counts in peritoneal exudates, enhancing the response to both thioglycolate and zymosan. The effects were microenvironment-dependent and likely mediated by local release of pro-inflammatory cytokines and chemokines. iNOS was required for eosinophil recruitment, while TNF contributed to both eosinophil and neutrophil recruitment. The 5-LO pathway was essential for eosinophil involvement. These findings suggest that ATRA can paradoxically enhance inflammation by modulating innate immune cell responses.</p><p><strong>Conclusions: </strong>ATRA promotes inflammation through iNOS, TNF, and 5-LO-dependent pathways, revealing complex mechanisms of immune modulation with potential relevance for inflammatory disease management.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-10"},"PeriodicalIF":2.9,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063540","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":"Evaluating the impact of amitriptyline on Nitric Oxide signaling in rat models of neuropathic pain.","authors":"Hamid Reza Mohammadi, Zahra Haghighatian, Behrouz Beiranvand, Peyman Amanolahi Baharvand, Amin Hasanvand","doi":"10.1080/08923973.2025.2481870","DOIUrl":"https://doi.org/10.1080/08923973.2025.2481870","url":null,"abstract":"<p><strong>Introduction: </strong>Nitric oxide (NO) plays a crucial role in the induction of neuropathic pain by stimulating the production of inflammatory cytokines. Additionally, research indicates that amitriptyline can inhibit nitric oxide production. In this study, we examined the inhibitory role of the nitric oxide signaling pathway through the administration of amitriptyline in the treatment of neuropathic pain.</p><p><strong>Methods: </strong>Forty rats were randomly assigned to five groups, with eight animals in each group: (1) Sham-operated, (2) Chronic constriction injury (CCI), (3) CCI plus amitriptyline, (4) CCI plus amitriptyline and L-arginine, and (5) CCI plus amitriptyline and L-NAME. Behavioral tests, including thermal hyperalgesia, cold allodynia, and mechanical allodynia, were conducted on the fourth, seventh, and fourteenth days following CCI induction. On the final day, spinal cord samples were collected to assess the levels of inflammatory cytokines. Additionally, the sciatic nerve was isolated on the same day for histological examination.</p><p><strong>Results: </strong>The results indicated that the administration of amitriptyline can reduce levels of inflammatory cytokines and improve symptoms of neuropathic pain. It should be noted that the simultaneous use of L-NAME and amitriptyline increases the therapeutic impacts of amitriptyline. However, the beneficial effects of amitriptyline are reduced by the nitric oxide stimulation induced by L-arginine.</p><p><strong>Conclusion: </strong>It was determined that one of the mechanisms by which amitriptyline ameliorates neuropathic pain is the inhibition of the nitric oxide signaling pathway. In this study, this effect was associated with a reduction in the release of inflammatory cytokines and a decrease in inflammation surrounding the nerve.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-9"},"PeriodicalIF":2.9,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772239","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":"Zerumbone modulates the expression of inflammatory mediators and antioxidant enzymes in TNF-α-stimulated human periodontal ligament cells.","authors":"Risa Okamoto, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Keiichi Hosaka","doi":"10.1080/08923973.2024.2445724","DOIUrl":"10.1080/08923973.2024.2445724","url":null,"abstract":"<p><strong>Objectives: </strong>Periodontal disease is a chronic inflammatory disease caused by periodontopathogenic bacteria, and its progression leads to periodontal tissue destruction and tooth loss. Zerumbone is a bioactive substance found in ginger (<i>Zingiber zerumbet</i>) and is known to have bioactive effects such as anticancer effects, but there have been no attempts to use it for periodontitis treatment. In addition, there have been no reports examining its effects on periodontal tissue component cells. In this experiment, we aimed to determine whether zerumbone affects the production of inflammatory mediators induced by tumor necrosis factor (TNF)-α in human periodontal ligament cells (HPDLCs), including its effects on signaling pathways.</p><p><strong>Methods: </strong>HPDLCs were stimulated by TNF-α (10 ng/ml) with or without zerumbone (6.25, 12.5, or 25 µM). Cytokine production in supernatant was determined using ELISA. Activation of signal transduction pathways and intracellular protein expression were investigated using the western blot analysis.</p><p><strong>Results: </strong>Zerumbone significantly suppressed TNF-α-induced production of CC chemokine ligand 2 (CCL2), CCL20, CXC chemokine ligand 10 (CXCL10), and interleukin-6 (IL-6) in HPDLCs. In addition, zerumbone decreased intercellular adhesion molecule-1 (ICAM-1) and cyclooxygenase-2 (COX-2) expression in TNF-α-stimulated HPDLCs. Furthermore, zerumbone suppressed activation of nuclear factor (NF)-κB and signal transducer and activator of transcription 3 (STAT3) pathways in TNF-α-treated HPDLCs. Finally, zerumbone enhanced the production of heme oxygenase-1 (HO-1), an antioxidant enzyme, in HPDLCs.</p><p><strong>Conclusion: </strong>These results suggest that zerumbone suppressed the production of several inflammatory mediators by inhibiting the NF-κB and STAT3 pathways in HPDLCs.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"176-181"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921577","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":"Efficacy and safety of ibuprofen and naproxen in the treatment of oligoarticular juvenile idiopathic arthritis: bi-national cohort study.","authors":"Orly Ohana, Itay Marmor, Rina Ferguson, Yoel Levinsky, Shiri Rubin, Kevin Baszis, Rotem Tal, Liora Harel, Orit Peled, Gil Amarilyo","doi":"10.1080/08923973.2024.2421523","DOIUrl":"10.1080/08923973.2024.2421523","url":null,"abstract":"<p><strong>Objectives: </strong>Juvenile idiopathic arthritis (JIA) is the most common rheumatic disease in children. Nonsteroidal anti-inflammatory drugs (NSAIDs) and intra-articular corticosteroid injections are first-line therapy for oligoarticular JIA. NSAIDs Adverse events (AEs) include gastrointestinal ulcers/bleeding and impaired renal function. The most prescribed NSAIDs for oligoarticular JIA are ibuprofen and naproxen. However, direct comparison between these drugs is lacking. We aimed to compare the efficacy and safety of ibuprofen versus naproxen for oligoarticular JIA.</p><p><strong>Methods: </strong>This is a bi-national retrospective study of oligoarticular JIA patients treated with either ibuprofen or naproxen as first-line therapy. Efficacy was defined as patients that achieved complete response (no evidence for arthritis). Safety was assessed by the occurrence of adverse events during follow-up.</p><p><strong>Results: </strong>Of 164 patients, 103 were treated in the Israeli group and 61 in the US group. The study population had a mean age of 4.49 ± 3.55 years, with F:M ratio of ∼2.5:1. No significant difference was found in drug efficacy [Complete response was observed in 15% of the ibuprofen group <i>vs</i>. 17.3% in naproxen group (<i>p</i> = 0.7)]. Treatment duration > 28 days was associated with significantly higher odds for complete response (<i>p</i> = 0.021). For safety, 12 AEs were associated with naproxen, whereas no AEs were associated with ibuprofen (<i>p</i> = 0.004). Treatment was discontinued in all AEs cases.</p><p><strong>Conclusions: </strong>Ibuprofen and naproxen showed similar albeit low efficacy which emphasizes their role as bridging therapy until IACI is achieved. However, ibuprofen showed better safety profile naproxen and therefore should be considered as first-line therapy.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"141-146"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142948211","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 biological treatment on the thiol/disulfide parameters in patients with axial spondyloarthritis.","authors":"Semra Fırat, Şükran Erten, Serdar Can Güven, Sezen Tutar, Yüksel Maraş, Salim Neşelioğlu, Selçuk Akan, Ahmet Kor, Berkan Armağan, Kevser Orhan, İsmail Doğan, Orhan Küçükşahin, Özcan Erel","doi":"10.1080/08923973.2025.2469211","DOIUrl":"10.1080/08923973.2025.2469211","url":null,"abstract":"<p><strong>Objective: </strong>Aim of this study is to compare the thiol/disulfide variables before treatment, at the 3^rd and 6^th months of biologic treatment in patients with axSpA.</p><p><strong>Materials & methods: </strong>Consecutive patients with axial spondyloarthritis to whom biologic treatment was initiated in our clinic were enrolled upon consent. Demographics, clinical characteristics, laboratory parameters and treatment agents were collected. Disease activity scores and thiol-disulfide balance parameters were recorded at baseline and 3^rd, 6^th months of treatment. Statistical analyses were performed in all patients and in subgroups of ankylosing spondylitis and non-radiographic axial spondyloarthritis patients.</p><p><strong>Results: </strong>In all patients, total thiol levels were significantly increased at 6^th month in comparison to baseline values (470.5 ± 74.7 vs 491.9 ± 69.6, <i>p</i> = 0.047). Native thiol levels were increased at 6^th month close to significance (438.9 ± 70.4 vs 458.8 ± 63.7, <i>p</i> = 0.060). Moderately strong negative correlations were observed between native thiol levels and disease activity parameters (BASDAI: <i>p</i> = 0,019; ASDAS-CRP: <i>p</i> = 0,035; ASDAS-ESR: <i>p</i> = 0,030), and between total thiol levels and disease activity parameters (BASDAI: <i>p</i> = 0,031; ASDAS-CRP: <i>p</i> = 0,020; ASDAS-ESR: <i>p</i> = 0,026) at 6^th month evaluation.</p><p><strong>Discussion & conclusions: </strong>Our results demonstrated oxidative stress reducing effect of biologics in axSpA patients parallel to suppression of disease activity at 6^th month of the treatment.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"228-233"},"PeriodicalIF":2.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467899","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}