The innate immune cells called macrophages are known to be important coordinators of regeneration, in addition to their role in protecting tissues from invading pathogens. In recent years, researchers have investigated the altered behavior of macrophages with aging, and linked this to a range of age-related conditions. In older individuals, macrophages are more likely to be inflammatory and aggressive rather than acting to assist tissue regeneration, and the consequence is a much reduced capacity for tissue maintenance.
If the methods by which macrophages act to induce greater regenerative activity on the part of other cell populations can be deciphered, boiled down to a set of signal molecules, then this may open the door to the development of comparatively straightforward therapies that incrementally enhance healing and tissue maintenance in older people. This doesn't address the underlying problems, the damage of aging that causes macrophages to behave badly, but the size of the effect may nonetheless be worth the cost of development.
For a child, recovering from a broken bone is typically a short-lived, albeit painful, convalescence. But for older adults, it can be a protracted and potentially life-threatening process. Researchers have previously shown that introducing bone marrow stem cells to a bone injury can expedite healing, but the exact process was unclear. Now, the same team believes it has pinpointed the "youth factor" introduced alongside bone marrow stem cells - it's the macrophage, a type of white blood cell, and the proteins it secretes that can have a rejuvenating effect on tissue.
After tissue injury, the body dispatches macrophages to areas of trauma, where they undergo functional changes to coordinate tissue repair. During fracture healing, macrophages are found at the fracture site. But when they're depleted, fractures will not heal effectively. Macrophage populations and characteristics can change with aging.
"We show that young macrophage cells produce factors that lead to bone formation, and when introduced in older mice, improves fracture healing. While macrophages are known to play a role in repair and regeneration, prior studies do not identify secreted factors responsible for the effect. Here we show that young macrophage cells play a role in the rejuvenation process, and injection of one of the factors produced by the young cells into a fracture in old mice rejuvenates the pace of repair. This suggests a new therapeutic approach to fracture rejuvenation."