New multiple sclerosis treatment reduces chronic inflammation

multiple sclerosis treatment
© iStock/Md Saiful Islam Khan

A team of international researchers has identified a potential new multiple sclerosis treatment that alleviates the chronic inflammation caused by the disease in mice models.

The study revealed that a type of lipid that mediates inflammation called Maresin-1, which is essential for resolving the inflammatory process when it is no longer beneficial, is present in low levels in multiple sclerosis patients and rodent models of the disease. The researchers believe that targeting these mediators may be a promising strategy for future multiple sclerosis treatment.

Experts from the Institut de Neurociències at the Universitat Autònoma de Barcelona (INc-UAB), the University of Montreal, and the Universidad de La República collaborated on the project, which is published in the journal Neuroinflammation.

Chronic inflammation

Acute inflammation is the body’s protective response to infection, driving tissue regeneration after an injury. However, once its function is completed, this inflammation is reduced by various mechanisms moderated by lipids that act as mediators.

Uncontrolled inflammation can occur when there is an error in this resolution process, which can have adverse outcomes for the tissues. Furthermore, in multiple sclerosis, an autoimmune disease where the body’s defence cells attack the lining of the tail of neurons, this inflammation is relentless, which crucially increases the development of the disease.

Designing a new multiple sclerosis treatment

In the study, the researchers examined samples from patients and mice models with multiple sclerosis, discovering they were deficient in producing Maresin-1 and several other lipid mediators that end inflammation. The levels of these immunosuppressive substances were so low that they prevented the inflammatory process from stopping.

The research team was able to mitigate this chronic inflammation associated with multiple sclerosis in mice models by administering Maresin-1. The lipid elicited a therapeutic effect on the mice, significantly reducing the number of inflammation-promoting proteins – cytokines – and the amount of the cells in the immune system in the spinal cord and blood. Additionally, prolonged implementation of the multiple sclerosis treatment safeguarded neurons from demyelination and improved the effects of neurological deterioration caused by the disease.

Dr Rubén López-Vales, Professor of Physiology at the UAB and researcher at the Neuroplasticity and Regeneration Group, INC-UAB, who led the research, said: “Our results 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 research findings suggest that future multiple sclerosis treatment strategies should focus on inflammatory-resolving mediators, and the researchers are now looking to perform a series of tests and experiments to verify the safety of administering Maresin-1, enabling them to address potential efficacy studies in humans.


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