Approximately two-thirds of patients who undergo abdominal surgery will develop surgical adhesions, a type of scar tissue that is painful, harmful, and often requires additional surgery to remove. Macrophages, a type of immune cell responsible for gobbling up bacteria and other debris throughout the body, are known to contribute to wound healing. In organisms that rely completely on their innate immune systems for protection, such as sea urchins, macrophage-like cells are responsible for both scanning for pathogens and sealing up wounds. In a recent study, researchers set out to study whether macrophages in your peritoneal cavity, the part of your body that harbors your abdominal organs, could contribute to the buildup of scar tissue, such as surgical adhesions, following surgery.

The researchers developed a technique to take images and videos of peritoneal macrophages in live mice. They saw that after a small injury to the abdominal cavity, the macrophages swarmed the injury site and clumped together. This rapid macrophage aggregation resembled the response of platelets to injuries in blood vessels, and it helped the wounds heal faster.  However, the researchers showed that when this same process occurred after a large surgical wound, it caused intestinal scarring similar to that seen in patients. They also identified the specific type of receptor necessary for the aggregation. Interestingly, this same receptor is present in the macrophage-like cells in sea urchins. 

This research suggests that this wound-healing function of peritoneal macrophages has been maintained throughout evolution. Because major abdominal surgery is not something that the human immune system is evolved to respond to, the macrophage aggregation response can cause harmful tissue damage instead of promoting helpful wound healing. Importantly, the authors showed that if they depleted the peritoneal macrophages, or blocked their aggregation with a drug, they could reduce the number of surgical adhesions that form. This work represents a key step in understanding and preventing the formation of post-surgical scar tissue. 

Lead author Joel Zindel, M.D., is a surgeon and visiting Ph.D. student at the University of Calgary Cumming School of Medicine. Corresponding author Paul Kubes, Ph.D. is a Professor at the University of Calgary Cumming School of Medicine and Founding Director of the Snyder Institute for Chronic Diseases. 

Managing Correspondent: Jaclyn Long

Original Article: 

Primordial GATA6 macrophages function as extravascular platelets in sterile injury

Additional Press: 

These bacteria-gobbling immune cells help the body heal—but also cause surgical complications

Surgical adhesions: A sticky macrophage problem

Canadian scientists and Swiss surgeons discover cause of excess post-surgical scarring

Image Credit: Shutterstock ID 1261934833