News Use of Del-1 Protein Reduces Multiple Sclerosis Severity in Mouse Study Use of Del-1 Protein Reduces Multiple Sclerosis Severity in Mouse Study by Patricia Inacio, PhD | November 12, 2014 Share this article: Share article via email Copy article link In a study entitled āDevelopmental endothelial locus-1 is a homeostatic factor in the central nervous system limiting neuroinflammation and demyelinationā the authors report to have found a new protein, Del-1, that reduces the severity of multiple sclerosis disease in a mouse model of the disease. The study was published in the Molecular Psychiatry journal. Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system. Currently without any cure, MS affects more than 2.3 million people across the globe. The disease is characterized by destruction of the myelin layer within nerve cells leading to a wide range of neurological symptoms affecting visual, motor, and sensory capabilities. In this study, a team of researchers from the University of Pennsylvania and colleagues discovered that the protein Del-1 (developmental endothelial locus-1), previously identified by the team as an endogenous anti-inflammatory factor, is also highly expressed in the brain. In light of their previous results when studying Del-1 function in periodontitis, the authors hypothesized Del-1 could prevent inflammation in the central nervous tissue. When they analyzed brain tissue from deceased MS patients, they found Del-1 expression was reduced when compared to healthy brain tissue. In mice models for human MS, termed experimental autoimmune encephalomyelitis (EAE), the authors found decreased expression of Del-1 in n the spinal cords of these mice. The researchers performed further studies and found that mice lacking Del-1 exhibited more severe attacks of the EAE accompanied by more damage to myelin when compared to healthy mice. Moreover, these mice had increased penetration of inflammatory cells in their spinal cords due to higher levels of IL-17, a pro inflammatory cytokine predominantly produced by activated T cells. When these mice were treated with Del-1, the authors observed no more EAE attacks. [adrotate group=”4″] George Hajishengallis, a professor of microbiology in Pennās School of Dental Medicine and study author, commented, āWe see that two completely different disease entities share a common pathogenic mechanism. And in this case that means that they can even share therapeutic targets, namely Del-1.ā Senior author Triantafyllos Chavakis of Germanyās Technical University Dresden, added, āThis treatment prevented further disease relapse. Thus, administration of soluble Del-1 may provide the platform for developing novel therapeutic approaches for neuro inflammatory and demyelinating diseases, especially multiple sclerosis.ā Hajishengallis concluded, āItās amazing that our work in periodontitis has found application in a central nervous system disease. This shows that periodontitis can be a paradigm for other medically important inflammatory diseases.ā Print This Page About the Author Patricia Inacio, PhD Patricia holds her PhD in cell biology from the University Nova de Lisboa, Portugal, and has served as an author on several research projects and fellowships, as well as major grant applications for European agencies. She also served as a PhD student research assistant in the Department of Microbiology & Immunology, Columbia University, New York, for which she was awarded a Luso-American Development Foundation (FLAD) fellowship.
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