Immune cells supercharge aspirin delivery, boosting transfer up to 30-fold: Yonsei study

A research team from Yonsei University College of Medicine has developed a new drug delivery platform that significantly improves the precision and efficiency of targeting inflamed tissues by using immune cells to transport medication.

The system, which boosts aspirin delivery by up to 30 times compared to conventional methods, was published in the journal Advanced Functional Materials.

Aspirin, widely used for its anti-inflammatory and antiplatelet effects in treating cardiovascular and inflammatory diseases, typically suffers from a short duration of action due to rapid metabolism in the liver. The drug also struggles to precisely target localized inflammatory sites or vascular lesions.

To overcome these limitations, the research team, led by Professors Sung Hak-joon and Yu Seung-eun of the Department of Medical Engineering at Yonsei University College of Medicine, doctoral candidate Kim Ju-eun, and Professor Chung Se-yong of the Department of Cardiology at Severance Hospital, developed a new delivery strategy in which aspirin is loaded into spherical nanoparticles and administered via a mouse’s tail vein.

Once in the body, the nanoparticles accumulate in the spleen, an organ central to immune function where they are absorbed by monocytes, a type of white blood cell.

These monocytes then migrate toward areas of inflammation, carrying the aspirin-loaded nanoparticles to the target tissue.

At the inflamed site, the monocytes release the drug through a “handover mechanism,” producing extracellular vesicles that encapsulate the aspirin and transfer it to surrounding immune cells and platelets.

The study further revealed that the efficiency of this handover mechanism is regulated by caveolin, a protein expressed by inflammatory cells. Using live imaging, the team confirmed that caveolin expression increases in proportion to inflammation severity, enhancing the uptake of aspirin by target cells.

In experimental models involving mice with induced inflammation in muscle tissue, liver, and blood vessels, the new system demonstrated that delivery of aspirin via extracellular vesicles suppressed the inflammation marker COX-2 with 30 times greater efficiency than aspirin alone. The anti-thrombotic effect of a single intravenous dose lasted more than seven days -- compared to only two and a half hours with conventional aspirin administration.

“This study provides visual evidence of a drug delivery mechanism that becomes active in response to inflammation, representing a significant leap forward in precision therapeutics,” Professor Sung said. “Beyond conventional targeted delivery, this platform enables drugs to spread their therapeutic effects to surrounding cells, offering potential applications across a wide range of diseases, including cancer and cardiovascular disorders.”