Some immune cells normally maintain chronic inflammation. Boosting the body's own fat molecules reduces the activity of these cells, thus accelerating pain relief without affecting the immune response

 

Some immune cells normally maintain chronic inflammation. Boosting the body's own fat molecules reduces the activity of these cells, thus accelerating pain relief without affecting the immune response

Scientists at University College London have demonstrated that the human body possesses a mechanism to curb inflammation. Epoxyoxylipin molecules—small molecules derived from lipids—play a pivotal role in this process, inhibiting the growth of monocytes, immune cells that actively accumulate during inflammation and contribute to its chronicization. When epoxyoxylipin levels rise, the immune system transitions more rapidly from a defensive to a healing phase.

The researchers tested this mechanism on healthy volunteers, inducing short-term inflammation in participants by injecting UV-inactivated E. coli bacteria into the skin of their forearms. Typical responses included pain, redness, localized warmth, and swelling.

Some volunteers received GSK2256294, a drug that inhibits the soluble epoxide hydrolase enzyme, which normally breaks down epoxy oxylipins. The drug was administered either before the onset of inflammation or four hours after the onset of symptoms. The results showed that in both cases, the level of protective lipid molecules increased, pain decreased more rapidly, and the number of monocytes in the blood and tissues declined significantly. In contrast, redness and swelling remained largely unchanged, indicating continued normal immune response.

Further experiments have shown that one epoxy oxylipinate, 12,13-EpOME, inhibits the p38 MAPK signaling pathway, an important molecular mechanism that promotes inflammatory behavior in monocytes. This effect has been confirmed both in vitro and in human volunteers.


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