In an animal model, angiotensin influences the immune system / Heidelberg and Stanford neurologists publish in the Journal of Clinical Investigation
Researchers in Heidelberg and Stanford have discovered a new signalling pathway of brain cells that explains how widely used antihypertensive drugs could keep inflammation in multiple sclerosis (MS) in check. The peptide angiotensin not only raises blood pressure but also activates the immunological messenger substance TGF beta on a previously unknown communication pathway in the brain. The study was conducted by Professor Lawrence Steinman at Stanford University in California together with the group of Professor Platten and published in the "Journal of Clinical Investigation". The Heidelberg team of researchers consisted of Dr. Tobias Lanz, lead author of the study and Professor Dr. Michael Platten, lead author of the previous study on that topic. Professor Platten is the senior consultant at the Department of Neurooncology at Heidelberg University Hospital and the head of the Helmholtz University Young Investigators Group "Experimental Neuroimmunology" at the German Cancer Research Center (DKFZ) in Heidelberg.
Angiotensin II is known as a molecule that regulates blood pressure. Drugs that block the angiotensin receptors, (AT1R blockers), are prescribed to millions of people to lower high blood pressure. These receptors have now also been found on numerous organs and cells that have nothing to do with regulating blood pressure, for example on the T cells of the immune system. These are immune cells that are involved in autoimmune reactions and chronic-inflammatory diseases such as MS. MS is characterized by multifocal areas of inflammation in the brain and spinal cord that lead to paralysis and other neurological symptoms.
Paralysis resolved in an animal model
The scientists working with Professor Platten showed in a mouse model that angiotensin II promotes inflammation in the brain and spinal cord. When the angiotensin receptors, i.e. the sites where angiotensin docks onto cells and can develop its effect, were blocked by the orally administered blood pressure drug Candesartan, the inflammation decreased and the paralysis resolved.