Heart and immunity

Cardiovascular diseases affect the bone marrow

Kirill Stasevich, Science and Life (nkj.ru )

Immune cells are formed from blood stem cells that live in the bone marrow. Since the immune system cares about everything, the bone marrow reacts to a variety of signals that come to it from all tissues and organs. Blood stem cells (or hematopoietic cells) sit in special places (or niches) with its own microenvironment. The service cells that provide this microenvironment affect how intensively stem cells will divide, how quickly they will specialize into specific cells of the immune system, and which cells will be obtained from them. The molecular signals that come to the bone marrow act just on the service cells. It is known that the work of hematopoietic niches is influenced by the nervous system, that signals from the intestinal microflora come to them, that the service cells of the bone marrow are sensitive to the condition of the pancreas — that is, for example, diabetes greatly affects the intensity with which ready-made immune cells leave their bone marrow niches and enter the bloodstream.

The staff of the Massachusetts General Hospital studied how the bone marrow is affected by cardiovascular diseases. In an article published in Nature Cardiovascular Research (Rohde et al., Bone marrow endothelial dysfunction promotes myeloid cell expansion in cardiovascular disease), researchers write that people with high blood pressure, atherosclerosis and those who have recently had a heart attack, hematopoiesis increases — that is, there are especially many new ones in the bone marrow blood cells. And to a greater extent, this applies to myeloid immune cells. The most numerous of them are neutrophil leukocytes, which are the first to encounter a variety of infections and trigger inflammation.

Experiments with mice predisposed to high blood pressure, atherosclerosis and heart attack showed the same thing: the bone marrow of such mice produced especially many myeloid immune cells. Moreover, their blood vessels that supplied the bone marrow with blood changed — the vessels themselves became larger, the vascular walls became thicker and at the same time more permeable. As the walls of the vessels became more permeable, more immune cells formed in the bone marrow niches went through them into the bloodstream. This, in turn, spurred the division of stem cells and the emergence of new mature immune cells.

The researchers were able to partially decipher the molecular mechanism that causes the vessels to grow and become more permeable. After a myocardial infarction, a lot of VEGF-A protein appears in the blood — vascular endothelial growth factor A, or vascular endothelial growth factor A. As you can guess from the name, it stimulates vascular growth, and it has a special receptor through which it acts on cells. If this receptor is blocked, then the vessels in the bone marrow after a heart attack will not grow, and there will be no jump in myeloid immune cells. In addition, with a heart attack and atherosclerosis, the level of the signaling immune protein interleukin-6 and a complex proteoglycan called versican increases in the blood — both of them act on the bone marrow, stimulating hematopoiesis. However, it is still unclear exactly where all these molecular factors that affect the bone marrow in cardiovascular diseases come from.

The fact that cardiovascular diseases are associated with immunity has been known for a long time, but until now it was believed that the connection here is one-sided, that some immune abnormalities occurring in the bone marrow only add to the likelihood of increased pressure, atherosclerosis, etc. However, as we can see, cardiovascular disorders affect in response to what is happening in the bone marrow. Although it would be strange if it were otherwise — after all, as we said at the beginning, immunity cares about everything, and it catches a variety of molecular signals, no matter where they come from. It is still unclear how much the new data will help in the treatment of atherosclerosis, high blood pressure and the consequences of a heart attack. On the one hand, it is already possible to think about some medications that would prevent cardiovascular drugs from interfering with the life of the bone marrow, on the other hand, the study was conducted here mostly on mice, so, as usual, we need to wait for human confirmation of mouse results.

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