Heart attack: Reboot
Myocardial infarction triggers an acute inflammatory reaction, after which the inflammation resolves and the damage heals. However, severe myocardial infarction can cause the development of chronic persistent inflammation, which leads to heart failure and death of the patient.
In experiments on mice, researchers at the University of Alabama at Birmingham, working under the guidance of Dr. Sumanth Prabhu, have developed a method of "rebooting the immune system", interrupting the vicious circle of chronic inflammation.
In an earlier work, the authors found that in a mouse model of myocardial infarction, global proliferation and activation of CD4+ T-lymphocytes, including the so-called regulatory T-lymphocytes, or T-regulators, occurs. This is accompanied by the development of persistent inflammation and activation of effector T cells, despite the increase in the number of T regulators, whose function is to suppress inflammation. This observation formed the basis of the hypothesis tested in the latest study. According to this hypothesis, under conditions of inflammation, T-regulators lose their functionality and begin to have a destructive pro-inflammatory effect on the tissue. This contributes to the development of persistent inflammation and pathological enlargement of the left ventricle, which is the main pumping department of the heart, which worsens its function.
This hypothesis was also supported by data obtained by researchers studying another disease – autoimmune arthritis. They demonstrated that the inflammatory microenvironment changes the phenotype of T-regulators, transferring them to a pro-inflammatory status, which exacerbates damage to the arthritic joint. However, until now, the possibility of the appearance of dysfunctional T-regulators in chronic heart failure has not been studied.
In their latest work, the authors showed that in myocardial infarction, T-regulators really lose their immunomodulatory properties and begin to behave inappropriately. Instead of performing their normal function of suppressing inflammation, they begin to secrete pro-inflammatory cytokines, prevent the growth of new capillaries and contribute to the pathological proliferation of fibrous scar tissue.
Experimental removal of such abnormal T-lymphocytes from the bloodstream of mice 4 weeks after induced myocardial infarction ensured the elimination of symptoms of heart failure, including remodeling (enlargement) of the left ventricle. According to Dr. Prabhu, all this demonstrates an important pathological role belonging to dysfunctional regulatory T-lymphocytes in the development of chronic ischemic heart failure.
It is very important that the newly formed T-regulators in the body of mice no longer had pro-inflammatory properties. They had normal immunosuppressive activity and contributed to the suppression of inflammation, as well as the restoration of damaged tissue. Thus, the removal of abnormal T-regulators acted as a kind of "reset" for the immune system. The authors hope that in the future this approach may form the basis of a new method of rehabilitation of patients with myocardial infarction.
Article by Shyam S Bansal et al. Dysfunctional and pro-inflammatory regulatory T-lymphocytes are essential for adverse cardiac remodeling in ischemic cardiomyopathy published in the journal Circulation.
Evgenia Ryabtseva, portal "Eternal Youth" http://vechnayamolodost.ru