A Neutrophil Hijacking Nanoplatform Reprograming NETosis for Targeted Microglia Polarizing Mediated Ischemic Stroke Treatment.
Na YinWenya WangFei PeiYuzhen ZhaoChanghua LiuMingming GuoKaixiang ZhangZhenzhong ZhangJinjin ShiYun ZhangZhi-Hao WangJunjie LiuPublished in: Advanced science (Weinheim, Baden-Wurttemberg, Germany) (2024)
Precise and efficient regulation of microglia is vital for ischemic stroke therapy and prognosis. The infiltration of neutrophils into the brain provides opportunities for regulatory drugs across the blood-brain barrier, while hindered by neutrophil extracellular traps (NETs) and targeted delivery of intracerebral drugs to microglia. This study reports an efficient neutrophil hijacking nanoplatform (referred to as APTS) for targeted A151 (a telomerase repeat sequence) delivery to microglia without the generation of NETs. In the middle cerebral artery occlusion (MCAO) mouse model, the delivery efficiency to ischemic stroke tissues increases by fourfold. APTS dramatically reduces the formation of NETs by 2.2-fold via reprogramming NETosis to apoptosis in neutrophils via a reactive oxygen species scavenging-mediated citrullinated histone 3 inhibition pathway. Noteworthy, A151 within neutrophils is repackaged into apoptotic bodies following the death pattern reprogramming, which, when engulfed by microglia, polarizes microglia to an anti-inflammatory M2 phenotype. After four times treatment, the cerebral infarction area in the APTS group decreases by 5.1-fold. Thus, APTS provides a feasible, efficient, and practical drug delivery approach for reshaping the immune microenvironment and treating brain disorders in the central nervous system.
Keyphrases
- inflammatory response
- neuropathic pain
- cancer therapy
- drug delivery
- middle cerebral artery
- mouse model
- atrial fibrillation
- reactive oxygen species
- photodynamic therapy
- white matter
- oxidative stress
- cell death
- gene expression
- stem cells
- drug release
- resting state
- spinal cord injury
- internal carotid artery
- transcription factor
- dna methylation
- endoplasmic reticulum stress
- combination therapy
- mesenchymal stem cells
- cerebral ischemia
- multiple sclerosis
- cell therapy
- amino acid
- brain injury
- blood brain barrier
- cell proliferation