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This peritoneal macrophage can protect the abdomen or trigger a serious surgical side effect.
Microscopy Dennis Kunkel / Scientific source
By Mitch Leslie
Abdominal surgery is bad enough. But every year, hundreds of thousands of patients undergo follow-up operations to cut up the resulting internal scar tissue, causing problems like pain and bowel blockages. Now, researchers have found that normally protective immune cells called macrophages can cause this scar tissue to build up, offering a possible strategy to thwart it.
This post-surgical scarring “is a huge problem,” explains cell biologist and immunologist Daniel McVicar of the National Cancer Institute, who did not participate in the work. The study, he says, “targets the cellular mechanism of how this happens.”
University of Calgary immunologist Paul Kubes and colleagues accidentally discovered the link between macrophages and abdominal scar tissue buildup. They were investigating the roles of cells in the fluid-filled peritoneal cavity, which houses organs such as the liver and intestines. Macrophages there, like those elsewhere in the body, engulf bacteria and other microbial invaders. But 5 years ago, researchers found that peritoneal cells also appeared to promote healing from organ damage.
For the new study, Kubes’ team has developed a way to spy on living mouse cells. The researchers stretched the middle of the abdomen between the stomach muscles of the animals to create a bulge much like a hernia. Scientists were able to observe cell activity through a translucent band of tissue in this part of the abdomen.
The team then used a laser to cause a small burn to the abdominal wall. The macrophages clustered around the damaged area – hundreds of them arrived within minutes – and formed a hood. “We thought they might be like ants crawling on organs,” until the cells found the site where they were needed, says Kubes.
Instead, peritoneal cells drift off and attach themselves to injured tissue as they pass. Their “ go-with-the-flow ” style makes them different from typical macrophages, which focus on their targets, and more like platelets, the shards of cells that cluster together at wounds to produce blood clots. By assembling, macrophages speed up recovery, the team reports today in Science. When the researchers gave the mice a molecule that prevents cells from coming together, their wounds healed about 50% slower.
“This is a clear and cool example of the role of macrophages in healing wounds,” says immunologist David Mosser of the University of Maryland, College Park, who was unrelated to the study.
But macrophages apparently cannot cope with the severe tissue trauma caused by the surgery. When the team performed abdominal surgery on the mice, the cells arrived at the incision site, piled up in huge clumps and intertwined with hard protein fibers. This process resulted in structures that resemble peritoneal adhesions, girdles of scar tissue that can be painful and sometimes fatal.
In humans, most peritoneal adhesions result from surgery and their removal is the motivation for approximately 300,000 operations each year in the United States. “I suspect that adhesions are an inappropriate response” from macrophages, Kubes says. He and his team are now working with medicinal chemists to develop drugs that interfere with their training.
However, Gwendalyn Randolph, an immunologist at Washington University St. Louis School of Medicine, says she remains “very skeptical” that the team has nailed down the mechanism of how these macrophages heal and heal. harm. To confirm the role of immune cells, she argues, researchers need to test whether adhesions are reduced in genetically engineered mice that lack the cells. Still, she says, the study could provide a boost by getting researchers to think more about this surgical complication.
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