New Nanomedicine Resolves Inflammation, Promotes Tissue Healing
The world of medicine just got a lot smaller.
A team of researchers have developed biodegradable nanoparticles that are capable of delivering inflammation-resolving drugs to sites of tissue injury.
The nanomedicine, which was successfully tested on lab mice, has the potential to treat a vast array of human diseases characterized by inflammation, such as atherosclerosis
One way the human body protects itself against infection or injury is through acute inflammation. Ideally the inflammation will promote the clearance of pathogens or damaged tissue and the body will then go on to heal itself back to normal states. However, in many conditions, including heart disease, arthritis, and neurodegenerative diseases, the inflammatory process never resolves, leading to tissue damage.
"A variety of medications can be used to control inflammation. Such treatments, however, usually have significant side effects and dampen the positive aspects of the inflammatory response," said Dr. Ira Tabas, one of the study's senior co-authors.
For the new nanomedicine, researchers first took advantage of a 24-amino-acid peptide, Ac2-26, which is derived from a naturally occurring protein mediator of inflammation resolution called annexin A1. Second, rather than simply inject the "naked" peptide into injured mice, they packaged the peptide into nanoparticles that are able to target drugs to sites of tissue injury.
The nanoparticles were given this ability through the addition of two components: one that gives them stealth-like properties, enabling them to avoid detection and clearance by white blood cells and the liver; and a second that gives them the ability to target collagen IV, a protein found at sites of tissue injury.
Each nanoparticle is less than 100 nanometers in diameter, or 1/100,000th the diameter of a human hair.
"These targeted polymeric nanoparticles are capable at very small doses of stopping neutrophils, the most abundant form of white blood cells, from infiltrating sites of disease or injury," said co-lead author Nazila Kamaly. "This action stops the neutrophils from secreting further signaling molecules that can lead to a constant hyper-inflammatory state and further disease complications."
Researchers from Columbia University Medical Center, Brigham and Women's Hospital, Mount Sinai School of Medicine and Massachusetts Institute of Technology completed the study, which was published Monday in the online edition of Proceedings of the National Academy of Sciences.
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