In a new study, researchers reduced chronic inflammation linked to multiple sclerosis in mice using a type of lipid that mediates inflammation. Researchers found these types of mediator substances, responsible for resolving the inflammatory process when it is no longer beneficial, are minimized in people with MS. The use of these mediators could become a good strategy for the treatment of MS. 

Acute inflammation is a protective response to infection that promotes tissue regeneration after injury. Once its function has been performed, a series of mechanisms regulated by lipids acting as mediators are responsible for resolving it. An error in the resolution response results in uncontrolled inflammation that is detrimental for the tissues. In MS, the inflammation is persistent and plays a key role in the development of the disease.

A research team, led by the Institut de Neurociències at the Universitat Autònoma de Barcelona, reduced the chronic inflammation linked to MS in a mouse model of the disease, by administering one of the resolving lipid mediators of inflammation, Maresin-1. The substance exerted a therapeutic effect on mice, drastically reducing the amount of proteins promoting inflammation (cytokines), as well as the number of cells in the immune system in both the spinal cord and the blood. A continuous administration of the lipid over time also protected neurons from demyelination and improved the effects of neurological deterioration caused by the disease.

In the study, researchers looked at samples from patients with MS and from mouse models. They found there was insufficient production of Maresin-1 and other lipid mediators that end inflammation. The levels of these immunosuppressive substances, which were almost undetectable, prevented the inflammatory process from stopping.

The study, conducted in collaboration with the University of Montreal and the Universidad de La República in Uruguay, points to therapy with inflammatory-resolving mediators as an innovative and promising strategy for the treatment of MS. While the results of mouse model studies sometimes do not translate to humans and may be years away from being a marketable treatment, researchers said the next steps will be a series of tests and experiments to demonstrate the safety of the administration of this lipid, which could allow them to address possible efficacy studies in humans.

The study was published in the Journal of Neuroinflammation.