Multiple sclerosis (MS) is a chronic inflammatory disorder that causes degeneration of the nerves in the brain and spinal cord, leading to various symptoms including muscle// weakness and pain.

Most individuals with MS go through cycles of disease and remission, leading to the suggestion that there are regulatory mechanisms that counter the disease-causing inflammation. Using a mouse model of MS (known as EAE), researchers from the Gulbenkian Institute in Portugal show that increased expression of a protein known as HO-1, as well as administration of carbon monoxide, protect mice from disease.

In the study Miguel Soares and colleagues show that mice lacking HO-1 develop more severe EAE than wild-type mice. Conversely, in mice already suffering the symptoms of EAE, disease is reversed if HO-1 expression is induced. The function of HO-1 is to degrade excess heme (a component of many important cellular proteins) and one of the by-products of heme degradation is carbon monoxoide. Surprisingly, like the induction of HO-1 expression, administration of carbon monoxide to mice already suffering the symptoms of EAE decreased disease. The authors therefore suggest that modulating HO-1 expression or administering carbon monoxide might be useful therapeutic strategies to treat patients with MS.

Source-Eurekalert
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