Washington, Jan. 26: Conducting a study on mice, researchers from the Gulbenkian Institute in Portugal have shown that an increased expression of a protein called HO-1, and administration of carbon monoxide, protect the animal from Multiple sclerosis (MS).

Multiple sclerosis 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, suggesting that there are regulatory mechanisms that counter the disease-causing inflammation.

During the study, published in the Journal of Clinical Investigation, Miguel Soares and colleagues observed that mice lacking HO-1 developed more severe EAE than wild-type mice.

Conversely, in mice already suffering the symptoms of EAE, the 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 monoxide.

The researchers also observed that just like the induction of HO-1 expression, administration of carbon monoxide to mice already suffering the symptoms of EAE decreased the disease.

The authors suggested that modulating HO-1 expression or administering carbon monoxide might be useful therapeutic strategies to treat patients with MS. (ANI)