Neuroinflammation involves several molecular and cellular mediators, including the activation of resident microglia and the release of inflammatory cytokines and chemokines at the injury site. Īccess to the brain from the periphery is generally regulated by the BBB, which presents a formidable obstacle for small and macromolecular cells to enter the brain. Yet, despite posing a significant threat to public health, TBI has no effective pharmacotherapy. Most of these brain injuries also result in long‐term physical, emotional, and cognitive consequences. Common pathologic consequences of TBI include hematoma, subarachnoid hemorrhage, neuroinflammation, or axonal injury. Immediately after injury, there is a breakdown of the blood‐brain barrier (BBB) and the neuroinflammatory cascade that triggers brain degeneration is activated. Traumatic brain injury (TBI) is a serious and growing health problem in the United States, accounting for approximately 2.5 million emergency room visits, 56 000 deaths per year, and more than $60 billion in direct medical expenses in palliative care and cognitive rehabilitation. In summary, the results suggest that NPs represent a promising future theranostic tool for TBI treatment. Interestingly, increased microglial proliferation, decreased macrophage infiltration, and reduced brain lesion following the NPs treatments compared to sham vehicle‐treated mice are also found. The results demonstrate selective targeting of NPs to the injured brain and increased NPs accumulation among the peripheral organs 24 h after TBI. This NP systemic delivery is visualized using advanced in vivo imaging techniques, including intravital microscopy and in vivo imaging system. Here, leukocyte‐based biomimetic NPs are fabricated as a theranostic tool to directly access inflamed regions in a TBI mouse model. Nanoparticles (NPs) have been used in multiple diseases as drug delivery tools with remarkable success due to their rapid diffusion and specificity in the target organ. Existing pharmacological drugs are unable to effectively and quickly target the brain inflamed regions, setting up a major roadblock towards effective brain trauma treatments. Traumatic brain injury (TBI) triggers both central and peripheral inflammatory responses.
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