Researchers at University College London (UCL) have identified a biological mechanism that helps the body bring inflammation to an end, a finding that could eventually lead to new treatments for chronic inflammatory diseases affecting millions of people. Inflammation is one of the immune system's most important defense responses. It helps the body fight infection and repair damaged tissue.
But if that response remains active for too long, it can begin to harm healthy tissue and contribute to conditions including arthritis, heart disease, and diabetes. Scientists have long known a great deal about how inflammation begins. What has been less clear is how the body decides that the danger has passed and shifts from fighting a threat to repairing the damage.
The new study, published in Nature Communications, points to a group of small fat-derived molecules called epoxy-oxylipins as part of that shutdown process. According to the researchers, these molecules act like natural brakes on the immune system. They help prevent excessive growth of intermediate monocytes,* a type of white blood cell that can support healing in the short term but may contribute to chronic inflammation if too many accumulate or remain active for too long.
To study the process directly in people, the researchers gave healthy volunteers a tiny injection of UV-killed E. coli bacteria in the forearm. Because the bacteria were no longer alive, they could not cause an infection, but they still triggered a temporary inflammatory response. That reaction produced the familiar signs of inflammation, including pain, redness, heat, and swelling, similar to what can happen after an injury or infection.
The volunteers were divided into two groups: prophylactic arm and therapeutic arm. Researchers then gave participants a drug called GSK2256294 at different stages of the inflammatory response. The drug blocks an enzyme known as soluble epoxide hydrolase (sEH).
Under normal conditions, sEH breaks down epoxy-oxylipins, so blocking the enzyme allows more of these protective molecules to remain in the body. Pain Resolved Faster and Harmful Immune Cells Fell Both approaches produced similar results. Blocking sEH increased epoxy-oxylipin levels, helped pain resolve more quickly, and sharply reduced the number of intermediate monocytes found in both the blood and tissue.
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