Researchers have identified a biological mechanism that helps the body end inflammation, a discovery that could lead to new treatments for chronic inflammatory diseases that affect millions around the world.
Inflammation is one of the immune system's most important defense responses, helping the body fight infection and repair damaged tissue. However, if this response remains active for too long, it can begin to harm healthy tissue and contribute to conditions such as arthritis, heart disease, and diabetes.
The question that has remained unclear is how the body decides that the danger has passed, and moves from fighting the threat to repairing the damage.
The new study, conducted by a team from University College London (UCL) and published in the journal Nature Communications, points to a group of small fatty molecules called epoxy-oxylipins as part of the process of stopping inflammation.
According to the researchers, these molecules act as a natural brake for the immune system, helping to prevent the excessive growth of a type of white blood cell called "intermediate monocytes," which can support short-term healing but may contribute to chronic inflammation if they accumulate in large numbers or remain active for a long time.
To study the process directly in humans, researchers gave healthy volunteers a small injection of UV-killed E. coli bacteria into their forearms. Because the bacteria were dead, they did not cause an infection, but they did trigger a temporary inflammatory response, producing the well-known signs of inflammation, including pain, redness, heat, and swelling.
The volunteers were divided into two groups: a preventative group and a treatment group. The researchers then gave the participants a drug called GSK2256294 at different stages of the inflammatory response.
The drug works by blocking an enzyme known as soluble epoxide hydrolase (sEH). Under normal conditions, this enzyme breaks down epoxide oxylipins, so blocking it allows more of these protective molecules to remain in the body.
Both approaches produced similar results: blocking the enzyme increased levels of epoxylipins, helped relieve pain more quickly, and sharply reduced the number of mesenchymal monocytes in the blood and tissues.
The treatment did not significantly change visible signs such as redness or swelling, suggesting that the drug may have been modifying deeper immune processes even while visible symptoms remained unchanged.
The researchers then investigated how the effect works at the molecular level, where epoxylipins appear to inhibit a protein signaling pathway called p38 MAPK, which helps convert monocytes into the intermediate form associated with prolonged inflammatory activity.
Lead author Dr. Olivia Bracken from the Department of Aging, Rheumatology and Regenerative Medicine at University College London said: "Our findings reveal a natural pathway that limits the harmful expansion of immune cells and helps to calm inflammation more quickly. Targeting this mechanism could lead to safer treatments that restore immune balance without suppressing immunity overall."
Co-author Professor Derek Gilroy says: "This is the first study to map the activity of epoxylipins in humans during inflammation. By enhancing these protective lipid molecules, we can design safer treatments for diseases resulting from chronic inflammation."
The results could pave the way for clinical trials testing sEH inhibitors in chronic inflammatory conditions, including rheumatoid arthritis and cardiovascular disease.
what is your opinion on this news ?do let us know in the comments on tha comment box
if you liked this news article please share on friends & family & don't forget to follow on website & social media
