News & Events
Created a medicine to suppress dangerous immune attacks
- October 24, 2019
- Posted by: Wiley M. Wagner
- Category: Science
Stopping and treating some injuries in some patients can be a really difficult and lengthy process, due to a medical condition such as a systematic inflammatory response syndrome. This syndrome is a reaction of the body’s immune system in which during injuries the volume of inflammation and infections increases gradationally, causing rupture of cellular mitochondria, from which many protein compounds enter the bloodstream, while they themselves are destroyed by an overexcited immune system. However, specialists from the College of Medicine at the University of Augusta in the United States have found a new way to prevent this.
At the heart of their new study is the use of the so-called peptide of the H-formyl family – judging by the results of tests previously performed on mice, this type of peptide actually significantly reduces the level of inflammation and the threat from various infections in injuries of all kinds. Thus, this peptide prevents systematic inflammation and does not allow the immune system to destroy healthy cells along with infected cells.
An article with this study has already appeared in the journal Nature Communications, and N-formyl peptide itself will be presented by one of the project team leaders, Professor Martinez Kenones, during the next annual medical conference in Scottsdale, Arizona. Scientists are sure that this particular peptide will soon form the basis of new anti-inflammatory drugs.
In addition, some assumptions made during the preliminary results hint that the family of these peptides can be changed in such a way as to further improve their functionality and properties, thereby increasing the coefficient of benefit of their use in the composition of drugs. It remains only to wait for additional tests by the research team and only then it will be possible to say for sure whether these peptides will actually be used as part of modern drugs or not.