Regular exercise is very beneficial for long-term health, generating sweeping changes in metabolism and improving tissue and organ function across the board. Research suggests that present recommendations for the optimal amount of exercise are probably half or less of what they should be. Given that most people do not reach those recommendations, and all too many are entirely sedentary, there is certainly room for improvement. Studies show that structured exercise programs reverse a surprisingly large degree of age-related loss of function and mortality, a fraction of the declines of old age that is entirely self-inflicted. An era of low-cost comfort, telecommunication, and omnipresent engines of transport has allowed us to self-sabotage ourselves into losing years of health and life span.
Researchers have discovered that forces created from walking or running are transmitted from bone surfaces along arteriolar blood vessels into the marrow inside bones. Bone-forming cells that line the outside of the arterioles sense these forces and are induced to proliferate. This not only allows the formation of new bone cells, which helps to thicken bones, but the bone-forming cells also secrete a growth factor that increases the frequency of cells that form lymphocytes around the arterioles. Lymphocytes are the B cells and T cells that allow the immune system to fight infections. When the ability of the bone-forming cells to sense pressure caused by movement was blocked, it reduced the formation of new bone cells and lymphocytes, causing bones to become thinner and reducing the ability of mice to clear a bacterial infection.
The skeletal stem cells that give rise to most of the new bone cells that form during adulthood in the bone marrow. They are Leptin Receptor+ (LepR+) cells. They line the outside of blood vessels in the bone marrow and form critical growth factors for the maintenance of blood-forming cells. Researchers also found that a subset of LepR+ cells synthesize a previously undiscovered bone-forming growth factor called Osteolectin. Osteolectin promotes the maintenance of the adult skeleton by causing LepR+ to form new bone cells.
In the current study, researchers looked more carefully at the subset of LepR+ cells that make Osteolectin. They discovered that these cells reside exclusively around arteriolar blood vessels in the bone marrow and that they maintain nearby lymphoid progenitors by synthesizing stem cell factor (SCF) - a growth factor on which those cells depend. Deleting SCF from Osteolectin-positive cells depleted lymphoid progenitors and undermined the ability of mice to mount an immune response to bacterial infection. "The findings in this study show Osteolectin-positive cells create a specialized niche for bone-forming and lymphoid progenitors around the arterioles. Therapeutic interventions that expand the number of Osteolectin-positive cells could increase bone formation and immune responses, particularly in the elderly."