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揭示生物活性玻璃S53P4在体外对巨噬细胞的免疫调节和代谢作用。

Unraveling the immunomodulatory and metabolic effects of bioactive glass S53P4 on macrophages in vitro.

作者信息

Kajander Karoliina, Nowak Nicole, Vaziri Negin, Vallittu Pekka K, Heino Terhi J, Määttä Jorma A

机构信息

Institute of Biomedicine, Faculty of Medicine, University of Turku, Turku, Finland.

Department of Biomaterials Science and Turku Clinical Biomaterials Centre - TCBC, Institute of Dentistry, University of Turku, Turku, Finland.

出版信息

J Mater Sci Mater Med. 2025 Jan 24;36(1):13. doi: 10.1007/s10856-025-06861-y.

Abstract

Macrophage metabolism is closely linked to their phenotype and function, which is why there is growing interest in studying the metabolic reprogramming of macrophages. Bioactive glass (BG) S53P4 is a bioactive material used especially in bone applications. Additionally, BG S53P4 has been shown to affect macrophages, but the mechanisms through which the possible immunomodulatory effects are conveyed remain unclear. According to the results presented here, the lipopolysaccharide (LPS) induced suppression in oxidative phosphorylation is rescued in macrophages cultured with BG S53P4 before the inflammatory stimulus. Additionally, BG S53P4-exposed macrophages expressed lower mRNA levels of inflammatory cytokines Il6 and Il1b, as well as demonstrated decreased activation of inflammatory interferon regulatory factor (IRF) and NF-κB pathways and nitrogen oxide secretion in response to LPS. These results did not rely on cells being in direct contact with the material as similar effects were observed in the presence of BG S53P4-conditioned medium. Our findings link the immunomodulatory properties of BG S53P4 and macrophage metabolism, which improves our understanding of the mechanisms underlying the clinical efficacy of bioactive glasses.

摘要

巨噬细胞代谢与其表型和功能密切相关,这就是为何对研究巨噬细胞的代谢重编程兴趣日增的原因。生物活性玻璃(BG)S53P4是一种特别用于骨应用的生物活性材料。此外,BG S53P4已被证明会影响巨噬细胞,但介导可能的免疫调节作用的机制仍不清楚。根据此处给出的结果,在炎性刺激之前用BG S53P4培养的巨噬细胞中,脂多糖(LPS)诱导的氧化磷酸化抑制得到挽救。此外,暴露于BG S53P4的巨噬细胞表达的炎性细胞因子Il6和Il1b的mRNA水平较低,并且对LPS的反应显示出炎性干扰素调节因子(IRF)和NF-κB途径的激活以及一氧化氮分泌减少。这些结果并不依赖于细胞与材料的直接接触,因为在BG S53P4条件培养基存在下观察到了类似的效果。我们的发现将BG S53P4的免疫调节特性与巨噬细胞代谢联系起来,这增进了我们对生物活性玻璃临床疗效潜在机制的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a778/11762225/38b2466efebb/10856_2025_6861_Fig1_HTML.jpg

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