A Study May Have Found An “Off Switch” For This Common Type Of Inflammation

by Carolyn de Lorenzo
Ashley Batz/Bustle

We’ve all heard for a while now that chronic inflammation in the body is bad news. Acne, chronic illnesses, digestive disorders, and autoimmune diseases can all be linked to an out-of-control inflammatory process. A healthy inflammatory response can help heal injured tissue and fight infection — when inflammation becomes chronic, though, it can contribute to a lot of health problems. Scientists at the Biomedical Sciences Institute at Trinity College in Dublin say they may have discovered a solution. The research team has recently discovered a molecule that may switch off inflammation-promoting macrophages — overactive immune cells which contribute to chronic illnesses like multiple sclerosis (MS) and heart disease. Quieting this overactive immune response could be a powerful way to protect your health from a slew of potential problems.

According to a recent press release, “‘Itaconate’ — a molecule derived from glucose — acts as a powerful off-switch for macrophages," potentially providing a pathway to healing inflammatory diseases like arthritis, inflammatory bowel disease, or heart disease. The study was conducted by Professor of Biochemistry at Trinity, Luke O’Neill, and Dr. Mike Murphy of the University of Cambridge. Professor O’Neill was quoted as saying that “My lab has been exploring metabolic changes in macrophages for the past six years, and we’ve come across what we think is the most important finding yet.” O’Neill further stated that “It is well known that macrophages cause inflammation, but we have just found that they can be coaxed to make a biochemical called itaconate. This functions as an important brake, or off-switch, on the macrophage, cooling the heat of inflammation in a process never before described.”

According to the National Center for Biotechnology Information (NCBI) macrophages are a type of white blood cell, and they can have a beneficial function in the body. When operating in healthy ways, they break down microbes, cancer cells, cellular debris, and other substances that can be detrimental to your health. In their optimal state, macrophages intercept pathogens, and set off the body's anti-inflammatory response to address any acute damage or injury. When this immune response becomes over-active or chronic, however, that's when trouble starts.

The discovery of itaconate is key, because, as an “off-switch” for havoc-inducing macrophages, it may play an important role in the development of new anti-inflammatory medications that can shut off the inflammatory process. Researchers also want to better understand inflammation as it relates to the development of chronic and infectious diseases. According to The Irish Times, Dr. Evanna Mills, joint lead author of the study, said that “The macrophage takes the nutrient glucose, whose day job it is to provide energy, and surprisingly turns it into itaconate. This then blocks production of inflammatory factors.” Study author Dylan Ryan added, “We’ve found that itaconate can directly modify a whole host of proteins important for inflammation [...] this reaction for the anti-inflammatory effects of itaconate.”

It’s important to remember that acute inflammation in the body is a good thing — if you sprain a muscle, for instance, inflammation is a key component to repairing that injured tissue. Inflammation is the body’s healing response to tissue damage and infection. Inflammation also plays a role in building stronger muscles with exercise — but when chronic conditions like arthritis or heart disease are present, macrophages gone awry are playing a role in that process. O’Neill said that the cause for this is unknown: “We don’t know why inflammation gets out of control,” he stated in The Irish Times report.

Researchers are hopeful that these findings will further shed light on the best ways to prevent and manage chronic illnesses. Professor O'Neill observed that "This discovery and the new research pathways it has opened up will keep us busy for some time, but we are hopeful it will one day make a difference to patients with diseases that remain difficult to treat."