Implanted medical devices often arise the body’s immune system, which motivates the formation of scar tissue (fibrosis) around the intruder, causing serious issues for the patients whose implants are rejected. Immunosuppressants are often used to prevent this reaction, but they end up compromising the patient in other ways.
Scientists from MIT and Boston Children’s Hospital have now identified a molecule, called colony stimulating factor-1 receptor (CSF1R), which is involved in chemical signaling that leads to scar formation around rejected objects. Inhibiting the activity of this molecule in rodents and non-human primates led to their bodies no longer forming scar tissue around commonly used implantable materials such as ceramics, polymers, and hydrogels. Moreover, the activity of white blood cells to do things like producing reactive oxygen species, wound healing, and killing bacteria through ingestion is not compromised following inhibition of CSF1R.
Hopefully this research will lead to a practical and routine way of suppressing scar formation in implants made from a variety of materials. It may lead to devices currently only used externally, such as glucose sensors, to one day reside within the body for years at a time.
Image: The immune system often builds up a wall of dense scar tissue around implanted medical devices, a process known as fibrosis. The cell shown in blue represents a macrophage that has been blocked from initiating fibrosis. Credit: Felice Frankel