Inflammation mediator proves promising as MS treatment

Researchers have managed to reduce chronic inflammation associated with multiple sclerosis (MS) in mice thanks to the administration of a type of lipid that mediates inflammation. The team found that these types of mediator substances, responsible for resolving the inflammatory process when it is no longer beneficial, are minimised in people with MS as well as in animal models of the disease. The use of these mediators could become a good strategy for the treatment of this autoimmune disease.

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, an autoimmune disorder in which the body’s defence cells attack the lining of the tail of neurons (myelin), the inflammation is persistent and plays a key role in the development of the disease.

A research team led by Professor Rubén López-Vales, from the Institut de Neurociències at the Universitat Autònoma de Barcelona (UAB), has now reduced the chronic inflammation associated with MS in a mice 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.

UAB researchers, working in collaboration with the Université de Montréal and the Universidad de La República, looked at samples from patients with MS and from mice models, and found that 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. López-Vales said the results, published in the Journal of Neuroinflammation, “suggest that one of the body’s mechanisms for resolving inflammation is not working properly in patients with multiple sclerosis, which could partly explain the episodes of autoimmunity they experience”.

The results also point to therapy with inflammatory-resolving mediators as an innovative and promising strategy for the treatment of MS and other autoimmune diseases. López-Vales 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.

Image credit: ©stock.adobe.com/au/freshidea

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