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
{"title":"创伤性脑损伤免疫防御的免疫抑制制剂。","authors":"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","doi":"10.1002/adhm.202501417","DOIUrl":null,"url":null,"abstract":"<p>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.</p>","PeriodicalId":113,"journal":{"name":"Advanced Healthcare Materials","volume":"14 19","pages":""},"PeriodicalIF":9.6000,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/adhm.202501417","citationCount":"0","resultStr":"{\"title\":\"Immunosuppressive Formulations for Immunological Defense against Traumatic Brain Injury\",\"authors\":\"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\",\"doi\":\"10.1002/adhm.202501417\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>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.</p>\",\"PeriodicalId\":113,\"journal\":{\"name\":\"Advanced Healthcare Materials\",\"volume\":\"14 19\",\"pages\":\"\"},\"PeriodicalIF\":9.6000,\"publicationDate\":\"2025-05-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1002/adhm.202501417\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Advanced Healthcare Materials\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://advanced.onlinelibrary.wiley.com/doi/10.1002/adhm.202501417\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ENGINEERING, BIOMEDICAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advanced Healthcare Materials","FirstCategoryId":"5","ListUrlMain":"https://advanced.onlinelibrary.wiley.com/doi/10.1002/adhm.202501417","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENGINEERING, BIOMEDICAL","Score":null,"Total":0}
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.
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.