In people suffering from hypertension, atherosclerosis, as well as during the post-infarction period, the production of immune cells is activated in the bone marrow.
Immunocytes owe their formation to stem blood cells that live in the bone marrow . The structures of the bone marrow respond to absolutely all impulses supplied to the immune system from various tissues and organs. At the same time, hematopoietic cells occupy special places (cells) that have their own microenvironment. The structures that support it also influence the processes of stem cell division, but the activity of these structures themselves is regulated by molecular impulses entering the bone marrow. The nervous system, the state of the intestinal flora, and the functionality of the pancreas also play their role - in particular, in diabetes mellitus, normal immunocytes change the rate of exit from their bone marrow cells and the intensity of entry into the circulatory system.
Scientists representing the Massachusetts General Hospital found that in patients with hypertension, atherosclerosis , as well as in patients who survived a heart attack , hematopoiesis is accelerated - the formation of new blood cells, and especially myeloid immunocytes. The highest level is noted among leukocytes and neutrophils: it is they who first of all encounter an infectious pathogen and start the development of an inflammatory reaction.
Scientists conducted experiments with rodents prone to voiced pathologies: the bone marrow of these animals really began to produce more myeloid immunocytes. In addition, changes were noted in the blood vessels supplying the bone marrow. The number of vessels increased, the vascular walls thickened, their permeability increased. Due to the increase in permeability, more immune cells, previously located in the cells of the bone marrow, began to enter the blood. As a result, the division of stem cells was activated, new mature immunocytes appeared.
Experts traced the whole mechanism of the process. In the post-infarction state, the blood is saturated with vascular endothelial growth factor A, a protein substance that stimulates vascular growth and has a specific receptor that acts on cells. Blocking this receptor leads to inhibition of blood vessels in the bone marrow after a heart attack. In addition, against the background of atherosclerotic and post-infarction changes in the bloodstream, the content of the signal immune protein interleukin-6 and versican, a proteoglycan that stimulates hematopoiesis, increases. To date, scientists are investigating the origin of these molecular factors that affect bone marrow structures in pathologies of the cardiovascular system.
How useful these observations and discoveries will be, time will tell. It is possible that drugs will be created that block the link between cardiovascular disease and bone marrow function.
Information is presented on the pages of the NCR publication