创伤性脑损伤免疫防御的免疫抑制制剂。

IF 9.6 2区 医学 Q1 ENGINEERING, BIOMEDICAL
Kelly Lintecum, Abhirami Thumsi, Kara Dunn, Lindsey Druschel, Sierra Chimene, David Flores Prieto, Amberlyn Simmons, Shivani Mantri, Arezoo Esrafili, Srivatsan J. Swaminathan, Mytreyi Trivedi, Shreya Anandan, Crystal Willingham, Alondra Davila, Sahil Inamdar, Joslyn L. Mangal, Abhirami P. Suresh, Niveda M. Kasthuri, Madan Mohan Chandra Sekhar Jaggarapu, Nicole Appel, Taravat Khodaei, Nathan D. Ng, Alison Sundem, Sanmoy Pathak, George Bjorklund, Jason Newbern, Jeffrey Capadona, Sarah E. Stabenfeldt, Abhinav P. Acharya
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引用次数: 0

摘要

创伤性脑损伤(TBI)和随后的神经退行性变部分是由局部和全身性慢性炎症驱动的。然而,目前的临床干预策略并不能减轻炎症后遗症,因此需要开发创新的方法来减少炎症和最大限度地减少创伤性脑损伤的有害影响。在本研究中,一种基于α -酮戊二酸(paKG)聚合物的皮下制剂,可递送糖酵解抑制剂PFK15 (PFKFB3抑制剂,糖酵解的限速步骤)、α -酮戊二酸(用于促进Krebs循环)和髓磷脂蛋白脂蛋白(PLP139-151)的肽抗原,作为TBI小鼠模型的预防性免疫抑制制剂。在体外,paKG(PFK15+PLP)制剂刺激免疫抑制性调节性T细胞的增殖并诱导T辅助-2细胞的产生。在小鼠遭受TBI前两周皮下给药,该制剂增加了TBI后第7天外周和大脑中免疫抑制巨噬细胞和树突状细胞(dc)的频率,并在TBI后28天增强了plp特异性免疫抑制细胞渗入大脑。脑损伤后28天神经炎症的免疫组织学测量改变,空间蛋白质组学显示损伤半暗带自噬增强的证据,活性制剂改善运动功能。总的来说,这些数据表明,TBI免疫抑制制剂成功地诱导了抗炎特征并减少了TBI相关的炎症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Immunosuppressive Formulations for Immunological Defense against Traumatic Brain Injury

Immunosuppressive Formulations for Immunological Defense against Traumatic Brain Injury

Immunosuppressive Formulations for Immunological Defense against Traumatic Brain Injury

Immunosuppressive Formulations for Immunological Defense against Traumatic Brain Injury

Traumatic brain injury (TBI) and subsequent neurodegeneration is partially driven by chronic inflammation both locally and systemically. Yet, current clinical intervention strategies do not mitigate inflammation sequelae necessitating the development of innovative approaches to reduce inflammation and minimize deleterious effects of TBI. Herein, a subcutaneous formulation based on polymer of alpha-ketoglutarate (paKG) delivering glycolytic inhibitor PFK15 (PFKFB3 inhibitor, a rate limiting step in glycolysis), alpha-ketoglutarate (to fuel Krebs cycle) and peptide antigen from myelin proteolipid protein (PLP139-151) is utilized as the prophylactic immunosuppressive formulation in a mouse model of TBI. In vitro, the paKG(PFK15+PLP) formulation stimulates proliferation of immunosuppressive regulatory T cells and induces generation of T helper-2 cells. When given subcutaneously in the periphery two weeks prior to mice sustaining a TBI, the formulation increases frequency of immunosuppressive macrophages and dendritic cells (DCs) in the periphery and the brain at day 7 post-TBI and by 28 days post-TBI enhanced PLP-specific immunosuppressive cells infiltrate the brain. Immunohistology measurements of neuroinflammation are altered 28 days post-TBI, spatial proteomics reveals evidence of enhanced autophagy in the injury penumbra, and the active formulation improves motor function. Overall, these data suggest that the TBI immunosuppressive formulation successfully induces an anti-inflammatory profile and decreases TBI-associated inflammation.

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来源期刊
Advanced Healthcare Materials
Advanced Healthcare Materials 工程技术-生物材料
CiteScore
14.40
自引率
3.00%
发文量
600
审稿时长
1.8 months
期刊介绍: Advanced Healthcare Materials, a distinguished member of the esteemed Advanced portfolio, has been dedicated to disseminating cutting-edge research on materials, devices, and technologies for enhancing human well-being for over ten years. As a comprehensive journal, it encompasses a wide range of disciplines such as biomaterials, biointerfaces, nanomedicine and nanotechnology, tissue engineering, and regenerative medicine.
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