Immunosuppressive Formulations for Immunological Defense against Traumatic Brain Injury

创伤性脑损伤 炎症 神经炎症 神经保护 医学 免疫学 神经退行性变 免疫系统 药理学 病理 精神科 疾病
作者
Kelly Lintecum,Abhirami Thumsi,K. A. Dunn,Lindsey N. 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
出处
期刊:Advanced Healthcare Materials [Wiley]
卷期号:14 (19): e2501417-e2501417 被引量:1
标识
DOI:10.1002/adhm.202501417
摘要

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.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刘的花发布了新的文献求助10
刚刚
刚刚
刚刚
亦L完成签到,获得积分20
刚刚
1秒前
阳光的雯完成签到,获得积分10
1秒前
弗拉弗拉瓦完成签到,获得积分10
1秒前
开心酬海完成签到,获得积分10
1秒前
last_champion完成签到,获得积分10
1秒前
1秒前
1秒前
朴素芝麻完成签到,获得积分10
1秒前
田様应助金元宝采纳,获得10
1秒前
Yoki发布了新的文献求助10
2秒前
李益强完成签到,获得积分10
2秒前
伶俐的万天完成签到,获得积分10
2秒前
terryok完成签到,获得积分10
2秒前
永恒完成签到,获得积分10
2秒前
2秒前
2224536完成签到,获得积分10
3秒前
Lucas应助洁净的丹南采纳,获得10
3秒前
3秒前
111发布了新的文献求助10
3秒前
sharon完成签到,获得积分10
3秒前
脑洞疼应助笨笨的梨愁采纳,获得10
3秒前
Hello应助行走的sci采纳,获得30
3秒前
3秒前
林摆摆完成签到,获得积分10
3秒前
zz发布了新的文献求助10
3秒前
4秒前
定位心海的锚完成签到,获得积分10
4秒前
4秒前
StandardR发布了新的文献求助10
4秒前
温柔的河水完成签到 ,获得积分10
4秒前
Ruby0130发布了新的文献求助10
4秒前
追光者完成签到,获得积分10
5秒前
5秒前
马里奥尝food完成签到,获得积分10
5秒前
聪明牛排完成签到,获得积分10
5秒前
orixero应助龙仔采纳,获得10
5秒前
高分求助中
Principles of Economics, 11th Edition 10000
University Physics with Modern Physics, 16th edition 10000
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Development of a Bridge Weigh-In-Motion System: A technology to convert the bridge response to the passage of traffic into data on vehicle configurations, speeds, times of travel and weights 1000
Organic Reactions, Volume 116 1000
Current concepts in cutaneous toxicity : proceedings of the Fourth Conference on Cutaneous Toxicity, Washington, D.C., May 9-11, 1979 1000
ズームレンズの光学設計に関する研究 800
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7276582
求助须知:如何正确求助?哪些是违规求助? 8897636
关于积分的说明 18814214
捐赠科研通 6949085
什么是DOI,文献DOI怎么找? 3206123
关于科研通互助平台的介绍 2377397
邀请新用户注册赠送积分活动 2180963