Raeisi Hamideh, Azimirad Masoumeh, Schiopu Alexandru, Zarnani Amir-Hassan, Asadzadeh Aghdaei Hamid, Abdemohamadi Elham, Zali Mohammad Reza, Yadegar Abbas
Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Department of Translational Medicine, Lund University, Lund, Sweden.
Sci Rep. 2025 Apr 12;15(1):12618. doi: 10.1038/s41598-025-96211-3.
S100A8 plays a critical role in the pathogenesis of several inflammatory diseases and multiple types of cancer. Therefore, targeting the S100A8 function may alleviate the pathogenic process in various diseases. Here, specific single-chain variable fragment (scFv) antibodies targeting recombinant S100A8 (rS100A8) were selected by phage display technique and characterized using cDNA sequencing, immunoassay tests, and molecular docking. The neutralizing activity of scFvs was examined by a cell viability assay in rS100A8-treated macrophages. Furthermore, the modulatory effects of scFvs on the expression of inflammatory markers and apoptosis-related genes in macrophages and human colorectal carcinoma HT-29 cells treated with rS100A8 or dextran sulfate sodium (DSS) were assessed by RT-qPCR and flow cytometry. Based on our results, four scFvs were identified to be capable of detecting rS100A8 in the immunoassay tests. Among the selected scFvs, two clones (SA8-E6 and SA8-E12), alone or in combination, exhibited the highest blocking activity on rS100A8 and potently inhibited S100A8-induced cytotoxicity in macrophages. The use of a SA8-E6 and SA8-E12 (SA8-E6-12) cocktail inhibited the upregulation of TLR4 and RAGE, as well as inflammation and apoptosis-related genes in macrophages and HT-29 cells stimulated with rS100A8. Additionally, SA8-E6-12 exerted a significant inhibitory effect on inflammation and apoptosis induced by the S100A8/A9 complex in DSS-stimulated macrophages. We also demonstrated by molecular docking that the interaction of S100A8 with SA8-E6-12 was mainly restricted to the binding domain involved in the connection of S100A8 to TLR4. Further studies are required to explore the efficacy of these anti-S100A8 scFvs as potential therapeutic agents using in vivo models of S100A8-driven inflammatory diseases.
S100A8在多种炎症性疾病和多种类型癌症的发病机制中起关键作用。因此,靶向S100A8功能可能会减轻各种疾病的致病过程。在此,通过噬菌体展示技术筛选了靶向重组S100A8(rS100A8)的特异性单链可变片段(scFv)抗体,并利用cDNA测序、免疫测定试验和分子对接进行了表征。通过rS100A8处理的巨噬细胞的细胞活力测定来检测scFv的中和活性。此外,通过RT-qPCR和流式细胞术评估了scFv对rS100A8或硫酸葡聚糖钠(DSS)处理的巨噬细胞和人结肠直肠癌HT-29细胞中炎症标志物和凋亡相关基因表达的调节作用。基于我们的结果,在免疫测定试验中鉴定出四种scFv能够检测rS100A8。在所筛选的scFv中,两个克隆(SA8-E6和SA8-E12)单独或联合使用时,对rS100A8表现出最高的阻断活性,并有效抑制巨噬细胞中S100A8诱导的细胞毒性。使用SA8-E6和SA8-E12(SA8-E6-12)混合物可抑制rS100A8刺激的巨噬细胞和HT-29细胞中TLR4和RAGE以及炎症和凋亡相关基因的上调。此外,SA8-E6-12对DSS刺激的巨噬细胞中S100A8/A9复合物诱导的炎症和凋亡具有显著抑制作用。我们还通过分子对接证明,S100A8与SA8-E6-12的相互作用主要局限于S100A8与TLR4连接所涉及的结合域。需要进一步研究以探索这些抗S100A8 scFv作为潜在治疗剂在S100A8驱动的炎症性疾病体内模型中的疗效。