Immunopharmacology and Immunotoxicology最新文献

{"title":"Paulownin: a promising agent In the fight against the invasion and immune escape in triple-negative breast cancer.","authors":"Shaojie Qin, MingLiang Ning, Pei Wang, Qingyuan Liu","doi":"10.1080/08923973.2026.2716752","DOIUrl":"10.1080/08923973.2026.2716752","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer is the most prevalent malignancy among females. Paulownin has anti-tumor properties and immune-modulating activities in various cancers; however, its effects on breast cancer remain inadequately understood.</p><p><strong>Aims: </strong>This study aimed to elucidate the impact of Paulownin on breast cancer and the regulatory mechanisms.</p><p><strong>Methods: </strong>The cell viability and invasiveness were explored by CCK-8 and Transwell in MDA-MB-231 and BT549 cells. A co-culture system was established using activated CD8⁺ T cells and MDA-MB-231 or BT549 cells for 24 h. Cell apoptosis was assessed using flow cytometry. The IFN-γ level was analyzed <i>via</i> ELISA. <i>In vivo</i>, the roles of Paulownin were explored in HuPBMC-(M-NSG) mice and detected by immunohistochemistry and western blot.</p><p><strong>Results: </strong>Paulownin decreased the viability of MDA-MB-231 (IC50 = 32.54 μM) and BT549 (IC50 = 38.15 μM) cells. Paulownin reduced the levels of Ki-67 and Vimentin, increased E-cadherin expression, and impaired the invasive capabilities. Paulownin also inhibited PD-L1 expression in MDA-MB-231 and BT549 cells after co-cultured with CD8⁺ T cells. Paulownin prevented the apoptosis and elevated IFN-γ levels in CD8⁺ T cells. Additionally, Paulownin suppressed the activity of the AKT/NF-κB signaling pathway. The use of the AKT activator SC79 counteracted the effects of Paulownin on breast cancer cell growth, invasion and immune escape. <i>In vivo</i>, Paulownin inhibited tumor growth, decreased Ki-67 and Vimentin levels, increased E-cadherin, CD8 and IFN-γ levels and suppressed the AKT/NF-κB pathway activation.</p><p><strong>Conclusion: </strong>Paulownin restricted breast cancer cell proliferation, invasion, and immune escape. The mechanism may involve the inactivation of the AKT/NF-κB signaling.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"899-907"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808661","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":"Wogoniol, a novel radiolytic derivative of wogonin, programs dendritic cells for immune tolerance: suppression of T helper 1/17 and promotion of regulatory T cells.","authors":"Ha-Yeon Song, Gyeong Han Jeong, Hyoung-Woo Bai, Eui-Baek Byun","doi":"10.1080/08923973.2026.2713463","DOIUrl":"10.1080/08923973.2026.2713463","url":null,"abstract":"<p><strong>Background: </strong>Tolerogenic dendritic cells (tolDCs) play a pivotal role in maintaining immune homeostasis by driving regulatory T cell (Treg) differentiation. Modulating DC phenotypes to restore immune tolerance is a primary therapeutic goal for controlling inflammatory responses.</p><p><strong>Objectives: </strong>Here, we investigate the immunoregulatory mechanisms of wogoniol, a novel non-planar radiolytic derivative of the phytochemical wogonin featuring a C2-hydroxymethyl group, on DC-T cell crosstalk.</p><p><strong>Methods: </strong>The immunomodulatory effects of wogoniol were evaluated using lipopolysaccharide (LPS)-stimulated bone marrow-derived dendritic cells (BMDCs) and <i>in vitro</i> DC-T cell co-culture systems. Intracellular signaling mechanisms driving the DC phenotype were analyzed and validated using specific pharmacological inhibitors.</p><p><strong>Results: </strong>In LPS-stimulated bone marrow-derived dendritic cells (BMDCs), the parent wogonin acted as a nonspecific inhibitor, suppressing both pro- (TNF-α and IL-12p70) and anti-inflammatory (IL-10) cytokines. In contrast, wogoniol induced a stable tolDC phenotype, suppressing TNF-α and IL-12p70 while significantly upregulating the anti-inflammatory cytokine IL-10 and immunosuppressive molecule PD-L1. Mechanistically, wogoniol suppressed JNK phosphorylation while activating p38 and STAT3. Pharmacological inhibition confirmed that these pathways are essential for the observed tolerogenic phenotype. In subsequent DC-T cell co-cultures, wogoniol-treated DCs potently suppressed Th1 (T-bet/IFN-γ) and Th17 (RORγt/IL-17A) differentiation while strongly promoting the induction of CD4⁺CD25⁺Foxp3⁺ regulatory T cells (Tregs) to a level comparable to dexamethasone.</p><p><strong>Conclusions: </strong>Wogoniol exhibits a potent immune skewing mechanism absent in its parent compound, programming DCs to suppress pathogenic Th1/Th17 responses while actively inducing Foxp3⁺ Tregs. These findings establish wogoniol as a promising new pharmacological candidate for inducing immune tolerance.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"882-898"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758718","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":"Correction.","authors":"","doi":"10.1080/08923973.2026.2696627","DOIUrl":"10.1080/08923973.2026.2696627","url":null,"abstract":"","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"908-909"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148360467","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":"Immuno-regulatory effects of hydroxychloroquine in experimental autoimmune thyroiditis.","authors":"Chao-Wen Cheng, Wen-Fang Fang, Yea-Mey Yang, Yuan-Hung Wang, Jiunn-Diann Lin","doi":"10.1080/08923973.2026.2692421","DOIUrl":"10.1080/08923973.2026.2692421","url":null,"abstract":"<p><strong>Background: </strong>Hydroxychloroquine (HCQ) is a commonly used immunomodulatory drug in various autoimmune diseases; however, its role in autoimmune thyroid diseases (AITDs) remains unclear.</p><p><strong>Objective: </strong>This study aimed to evaluate the potential effects of HCQ in autoimmune thyroiditis using both naïve and experimental autoimmune thyroiditis (EAT) mouse models.</p><p><strong>Materials and methods: </strong>Mice were administered HCQ <i>via</i> drinking water. Plasma levels of free thyroxine (FT4), anti-thyroglobulin antibody (ATA), B-cell activating factor (BAFF), and interferon-α (IFN-α), along with thyroid histopathology, were assessed. Thyroid tissues were subjected to next-generation sequencing (NGS), followed by over-representation analysis (ORA) and gene set enrichment analysis (GSEA) for functional enrichment evaluation.</p><p><strong>Results: </strong>In EAT mice, HCQ treatment did not significantly affect FT4 or ATA levels, nor did it alter thyroid histological features. However, HCQ reduced human thyroglobulin stimulated splenocyte metabolic activity and plasma BAFF levels, indicating a systemic immunomodulatory effect. NGS of thyroid tissues revealed widespread upregulation of immune and inflammatory genes in EAT mice, which were partially attenuated by HCQ. GSEA also confirmed downregulation of immune-related pathways, including IL-6-JAK-STAT3 signaling and allograft rejection. No significant changes were observed in naïve mice treated with HCQ.</p><p><strong>Conclusions: </strong>In the context of autoimmune thyroiditis, HCQ showed preliminary immunomodulatory effects on certain immunological markers without recovering histological damage in the short term. Further long-term and mechanistic studies are warranted to clarify HCQ's therapeutic potential in autoimmune thyroiditis.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"739-748"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148316919","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":"Expression of Concern: First identification of Toll-like receptor-4 in avian brain: evolution of lipopolysaccharide recognition and inflammation-dependent responses.","authors":"","doi":"10.1080/08923973.2026.2704357","DOIUrl":"10.1080/08923973.2026.2704357","url":null,"abstract":"","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"910"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535856","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":"Ivabradine alleviates the cisplatin-induced cardiotoxicity in rats through regulating the crosstalk between MLCP/PKG, MEK/ERK pathways and miRNA-34a levels.","authors":"Nayef A Aldabaan, Basel A Abdel-Wahab, Ehab A M El-Shoura, Saad Misfer Alqahtani, Marwa B Bakir, Hebatallah M Saad, Zainab Mohammed Mahmoud Omar, Dalia Zaafar","doi":"10.1080/08923973.2026.2713465","DOIUrl":"10.1080/08923973.2026.2713465","url":null,"abstract":"<p><strong>Background: </strong>Ivabradine (IVA), a broad-spectrum hyperpolarization-activated cyclic nucleotide-gated (HCN) channel inhibitor, improves cardiac function in cardiovascular diseases and may protect against drug-induced cardiotoxicity. This study investigated the cardioprotective effects of IVA against cisplatin (Cis)-induced cardiac injury and explored the underlying molecular mechanisms.</p><p><strong>Methods: </strong>Rats received IVA (5 mg/kg, orally) for 28 consecutive days and Cis (7.5 mg/kg, intraperitoneally) on day 5. Cardiac oxidative stress biomarkers, inflammatory cytokines, histopathological alterations, and molecular signaling pathways were evaluated using biochemical assays, H&E staining, western blotting, PCR, and immunohistopathology.</p><p><strong>Results: </strong>IVA markedly improved cardiac histoarchitecture and attenuated Cis-induced pathological alterations. It exerted antioxidant and anti-inflammatory effects by reducing malondialdehyde (MDA), NADPH oxidase, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 levels, while increasing superoxide dismutase (SOD), IL-10, and endothelial nitric oxide synthase (eNOS). IVA downregulated cAMP response element-binding protein (CREB), extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase kinase (MEK), protein kinase C-epsilon (PKCε), and microRNA-34a (miRNA-34a), while upregulating protein kinase G (PKG), myosin light chain phosphatase (MLCP), and rapidly accelerated fibrosarcoma-1 (Raf-1). Furthermore, IVA enhanced cardiac cell survival, as evidenced by increased B-cell lymphoma 2 (Bcl-2) expression and reduced caspase-3 immunostaining.</p><p><strong>Conclusion: </strong>IVA significantly attenuates Cis-induced cardiotoxicity through antioxidant, anti-inflammatory, anti-apoptotic, and miRNA-34a-mediated mechanisms involving multiple cardioprotective signaling pathways.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"857-869"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663822","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":"Mastoparan, a wasp venom-derived peptide, promotes healing in <i>Candida albicans</i>-infected wounds through antifungal and anti-inflammatory mechanisms.","authors":"Basma H Amin, Alaa M Elsharkawy, Rania A Galhom, Magda H Rady, Dina M Aboraya, Alsayed E Mekky, Eman E Helal, Hossam A Abdelsamed, Mohammed Yosri, Asmaa Amer","doi":"10.1080/08923973.2026.2705916","DOIUrl":"10.1080/08923973.2026.2705916","url":null,"abstract":"<p><strong>Background: </strong><i>Candida albicans-</i>infected wounds are difficult to treat due to delayed healing, excessive inflammation, and oxidative stress. Mastoparan, a bioactive peptide with antimicrobial and immunomodulatory properties, was investigated for its potential to enhance wound healing and antifungal activity. This study evaluated its effects on oxidative stress, inflammation, and the expression of <i>TGF-β1, VEGF, NF-κB,</i> and <i>COL1A1 in a C. albicans-</i>infected wound model, compared with ketoconazole.</p><p><strong>Materials and methods: </strong>The antifungal activity of mastoparan was assessed <i>in vitro</i> using inhibition zone analysis and MIC determination against <i>C. albicans</i>. For comparison, ketoconazole was tested at 10 µg/mL <i>in vitro</i> and as a 2% topical formulation <i>in vivo. In vivo</i> wound healing was evaluated using two MIC-informed doses of mastoparan (7.8 and 15.6 mg/kg/day) administered topically once daily in non-infected and infected rat wound models, in comparison with ketoconazole. Eight groups were studied (<i>n</i> = 12/group): untreated control, wounded untreated, wounded + mastoparan (two doses), infected untreated, infected + mastoparan (two doses), and infected + ketoconazole (reference). Treatments were applied for 14 days. Wound healing, histology, ultrastructure, oxidative stress, inflammation, and gene expression analyzed.</p><p><strong>Results: </strong>Mastoparan showed strong antifungal activity and dose-dependently enhanced infected wound healing by accelerating wound closure, reducing fungal burden, improving tissue integrity, decreasing oxidative stress and inflammation, and promoting wound-healing<i>-</i>related gene expression, with the greatest effects observed at 15.6 mg/kg/day.</p><p><strong>Conclusions: </strong>Mastoparan exerts potent antifungal activity and accelerates wound healing through coordinated antioxidant, anti-inflammatory, and pro-regenerative mechanisms, supporting its potential as a therapeutic alternative to conventional antifungal agents.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"830-843"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548836","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":"Quinic acid attenuates cisplatin-induced acute kidney injury by modulating inflammatory cytokines, oxidative stress, apoptosis, and the Nrf2/HO-1/NQO1 pathway in rats.","authors":"Mehdi Goudarzi, Zohreh Lamoochi, Susan Sabbagh, Amir Mohammad Zamani, Abdolah Mousavi Salehi","doi":"10.1080/08923973.2026.2705914","DOIUrl":"10.1080/08923973.2026.2705914","url":null,"abstract":"<p><strong>Background: </strong>The nephrotoxicity induced by cisplatin (Cis) is mediated by oxidative stress, inflammation, and apoptosis, which limit the clinical utility of this commonly used chemotherapeutic drug. Natural polyphenolic compounds such as quinic acid (QA) have cytoprotective and antioxidant properties. This study evaluated the protective effect of QA against cisplatin-induced acute kidney injury (AKI) in rats and its impact on the associated oxidative, inflammatory, apoptotic, and Nrf2/HO-1/NQO1 pathways.</p><p><strong>Methods: </strong>Forty male Wistar rats were randomly divided into five groups (<i>n</i> = 8): Control, Cis (7.5 mg/kg, i.p.), Cis + QA was administered orally at doses of 25, 50, or 100 mg/kg once daily for 14 days before the cisplatin challenge. Biochemical markers (BUN, creatinine, KIM-1, NGAL), oxidative stress indices (MDA, NO, GSH, TAC, SOD, CAT, GPx), inflammatory cytokines (TNF-α, IL-1β), apoptotic gene expression (Bax, Bcl-2, caspase-3), and Nrf2 pathway proteins (Nrf2, HO-1, NQO1) were assessed. Renal histopathology was evaluated using blinded scoring.</p><p><strong>Results: </strong>Cisplatin caused severe renal dysfunction, oxidative imbalance, inflammation, and apoptosis, along with the suppression of Nrf2/HO-1/NQO1 signaling. QA, particularly at doses of 50 and 100 mg/kg, significantly improved serum renal markers, restored antioxidant capacity, reduced MDA and NO levels, downregulated TNF-α and IL-1β, modulated apoptotic gene expression toward cell survival, and enhanced Nrf2-pathway protein levels. Histological injury scores were significantly lower in groups treated with QA.</p><p><strong>Conclusions: </strong>The antioxidant, anti-inflammatory, anti-apoptotic, and Nrf2-pathway-modulating properties of quinic acid markedly attenuate cisplatin-induced AKI. Further mechanistic and translational research on QA to evaluate its potential as a nephroprotective adjunct is warranted.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"819-829"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578604","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":"Clinical characteristics, treatment, and prognosis of ixekizumab-induced inflammatory bowel disease.","authors":"Yong Pan, Wei Sun, Chunjiang Wang","doi":"10.1080/08923973.2026.2702335","DOIUrl":"10.1080/08923973.2026.2702335","url":null,"abstract":"<p><strong>Background: </strong>To explore the clinical characteristics of ixekizumab-induced inflammatory bowel disease (IBD) and provide references for prevention, diagnosis, and treatment.</p><p><strong>Methods: </strong>Clinical reports of ixekizumab-induced IBD published on December 31, 2025, were collected for retrospective analysis.</p><p><strong>Results: </strong>A total of 30 patients were enrolled, with a median age of 47.5 years (range 21, 81). The median time of IBD onset was 4 months (range 0.25, 24). Abdominal pain (80.0%), diarrhea (56.7%), hematochezia (30.0%), bloody diarrhea (26.7%), weight loss (26.7%), and fever (23.3%) were the main symptoms. Colonoscopy can reveal ulcers (80.0%), loss of vascular pattern (26.7%), erythema (26.7%), friability (26.7%), colitis (23.3%), and bleeding (20.0%). After discontinuing ixekizumab and receiving systemic steroids (70.0%), anti-TNF therapy (53.3%), and mesalazine treatment, most patients experienced symptom improvement.</p><p><strong>Conclusion: </strong>Ixekizumab was associated with exacerbation or new-onset IBD within the first six months. Gastrointestinal symptoms and a family history of IBD should be ruled out before ixekizumab is administered. During the treatment with ixekizumab, the patient's gastrointestinal symptoms should be closely monitored.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"779-785"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148420916","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":"Immunomodulatory activity of phenylephrine on LPS stimulated macrophages.","authors":"Esra Aydemir, Sude Yasemin Uran, Nur Ekimci Gürcan, Ayse Zehra Aroğuz, Furkan Ayaz","doi":"10.1080/08923973.2026.2702339","DOIUrl":"10.1080/08923973.2026.2702339","url":null,"abstract":"<p><strong>Background: </strong>Phenylephrine (PE) acts as a sympathomimetic vasoconstrictor frequently utilized to alleviate nasal blockage <i>via</i> the activation of α-1-adrenergic receptors. This study primarily sought to investigate the drug's potential to influence immune system responses.</p><p><strong>Methods: </strong>The effect of phenylephrine was analyzed by comparing cytokine production levels in LPS-stimulated and unstimulated J774.1 macrophages. The changes in concentrations of IL-6, TNF-α, IL-12p40, and GM-CSF induced by phenylephrine were measured by ELISA.</p><p><strong>Results: </strong>PE exhibited no intrinsic pro-inflammatory activity, as basal levels of TNF-α, IL-12p40, IL-6, and GM-CSF remained at or near detection limits in PE-only groups. In LPS-stimulated cultures, PE significantly attenuated the inflammatory response across multiple pathways, though the inhibitory patterns varied by cytokine. PE induced a robust, non-dose-dependent inhibition, reducing levels by 40-45% across all concentrations (<i>P</i> < 0.05). A significant dose-dependent suppression was observed, with the maximal dose (10 µg/mL) reducing levels from 9,258 pg/mL to 5,802 pg/mL (<i>P</i> < 0.05). Inhibition followed a non-monotonic trend; concentrations of 1 and 10 µg/mL significantly lowered IL-6 (<i>P</i> < 0.05), while the intermediate 5 µg/mL dose yielded no significant effect. PE mediated modulation was restricted, with significant inhibition occurring only at the highest concentration (10 µg/mL; <i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>The results indicate that phenylephrine influences inflammatory cytokine production and may have potential clinical relevance regarding immune responses and inflammatory diseases.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"760-766"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148430208","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}