Inicio / UGRDivulga

Scientists show the anti-inflammatory and autoimmune action of a molecule produced by the nervous system in the myocardium

Spanish version: sl.ugr.es/09IY

French version: sl.ugr.es/09J0

Researchers at the Spanish National Research Council (Centro Superior de Investigaciones Científicas, CSIC) and the University of Granada confirmed that the human body generates a compound that stops inflammation and improves the immune response caused by viruses which provoke severe and irreversible heart disease

Researchers from the Institute of Parasitology and Biomedicine López-Neyra in Granada, in collaboration with the University of Granada (UGR) Department of Pathology and Harvard Medical School, proved, for the first time, the response capacity of damaged cells after myocardium inflammation by a substance with anti-inflammatory, analgesic and autoimmune qualities produced by the nervous system.

Over the course of their investigations, these scientists were able to prove that the myocardium, or the heart muscle, possesses its own receptors of this molecule, called cortistatin. Thus, the heart muscle can also produce cortistatin, activating the anti-inflammatory capacity of muscle cells in the heart against infections. Experts explained this in the article, ‘The neuropeptide cortistatin attenuates experimental autoimmune myocarditis via inhibition of cardiomyogenic T cell-driven inflammatory responses’, published in the British Journal of Pharmacology.

The study focused on myocarditis, an inflammation of the myocardium that affects the heart’s ability to pump efficiently. After a viral infection, the immune system responds sending antibodies to combat the infection. However, in myocarditis, the immune system not only fights against the virus, but the human organism understands that the very own myocardium cells are foreign and damages them. If too many cells become involved, the cardiac muscle can be weakened, causing heart failure or even sudden cardiac death. Even when the heart attempts to regenerate, the muscle cell remains damaged and can produce congestive heart failure or a cardiomyopathy, conditions that chronically impede a normal life. This substance also overrides the autoimmune response that is produced before the spread of a virus, significantly reducing the damage.

The investigation linked the organism’s immune response with the inflammation associated with the pathology. The authors of this investigation confirmed that this was the first study to show that cortistatin prevents the damage that would be produced from an inflammatory and immune response against a virus in the myocardium, even when a disease is in the advanced stage, which is key in conditions with serious diagnoses. The effect of this substance could result in an adequate treatment especially in cases that are complicated because of an autoimmune response against cardiac components, such as the production of autoantibodies. As the authors relayed to Fundación Descubre («the Discover Foundation»), a Spanish organization dedicated to the promotion of innovation and scientific knowledge, for this reason, they must continue with their clinical investigations.

Autoimmunity control

Cortistatin is considered a neuropeptide, a compound that is formed by the union of a reduced number of amino acids coming from a neural system. Amino acids are organic molecules that, when bonded together, form proteins if the number of peptides they contain is greater than 100.

Previous studies have directly linked cortistatin with its anti-inflammatory, analgesic and autoimmune capacity in processes like rheumatoid arthritis, Crohn’s disease or multiple sclerosis. As myocarditis is an inflammatory and autoimmune-based disease, experts suggested that this molecule could also be effective in its treatment.

In this manner, the scientists have been able to imitate what occurs in humans in an autoimmune myocarditis in mice, injecting in them a protein called myosin. They have proven how this neuropeptide reverses the immunological and inflammatory response, preventing damage to cells and peripheral muscle tissue. The tests were performed in different stages of the disease, from its appearance until 21 days into its development, confirming that the treatment of the different stages responded in an adequate way.

This way, with the investigations having been performed, the pre-study clinics, or laboratory studies prior to human tests, have been resolved. This opens the door for the development of new therapeutic products based on cortistatin.

This study was financed by the National Plan by the Spanish Ministry of Economics and Competitiveness and is included within the project, ‘Estudio del papel de la cortistatina en fibrosis: potencial aplicación terapéutica en enfermedades crónicas asociadas al daño tisular’ (‘Study of the role of cortistatin in fibrosis: potential therapeutical application in chronic diseases associated with tissue damage’).

References:

Delgado-Maroto V, Falo CP, Forte-Lago I, Adan N, Morell M, Maganto-Garcia E, Robledo G, O’Valle F, Lichtman AH, Gonzalez-Rey E, Delgado M: ‘The neuropeptide cortistatin attenuates experimental autoimmune myocarditis via inhibition of cardiomyogenic T cell-driven inflammatory responses’. British Journal of Pharmacology.

Images:

Inflammatory and Autoimmune Disease Neuroimmunology Group from the Institute of Parasitology and Biomedicine López-Neyra of the Spanish National Research Council (CSIC) Granada

https://www.flickr.com/photos/fundaciondescubre/34139036172/in/dateposted-public/

For more information:

FUNDACIÓN DESCUBRE

Department of Communication

Telephone: (+34) 954 239 422

E-mail: comunicacion@fundaciondescubre.es

Contact:

Francisco Javier O’Valle Ravassa                                                  

Department of Anatomical Pathology and History of Science

Universidad de Granada

Telephone: (+34) 958 246 180

E-mail: fovalle@ugr.es

Mario Delgado Mora

Institute of Parasitology and Biomedicine“López – Neyra” of the Spanish National Research Council (CSIC)

Telephone: (+34) 958 181 665

E-mail: mdelgado@ipb.csic.es