Medical devices implanted in the body for drug delivery, sensing, or tissue regeneration usually come under fire from the host’s immune system. Defense cells work to isolate material they consider foreign to the body, building up a wall of dense scar tissue around the devices, which eventually become unable to perform their functions. Researchers have identified a signaling molecule that is key to this process of fibrosis, and they have shown that blocking the molecule prevents the scar tissue from forming. The findings could help scientists extend the lifespan of many types of implantable medical devices.

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)

The team found that cells called macrophages are necessary for fibrosis to occur, and that when those cells are missing, scar tissue does not form around implanted devices. The researchers identified a signaling molecule that appears to help macrophage precursors known as monocytes differentiate into mature macrophages, which then initiate fibrosis. They discovered that if they blocked the cell surface receptors for this molecule, known as CSF1, they could prevent implant-induced fibrosis from occurring.

Implantable devices whose functions can be disrupted by fibrosis include glucose sensors for diabetics, pacemakers, and other devices that need to interact with surrounding tissue. The researchers are working on ways to deliver the CSF1R-blocking drug along with various types of implantable devices. This targeted approach holds the potential to be safer than widespread suppression of the immune system.