LOS ANGELES—A new UCLA study sheds light on the link between high cholesterol and osteoporosis and identifies a new way that the body's immune cells play a role in bone loss, which affects 10 million Americans. The research, published in Clinical Immunology, could lead to new immune-based approaches for treating osteoporosis.
Researchers examined how high levels of oxidized LDL affect bone and whether a type of immune cell called a T cell plays a role in the process. Using blood samples from healthy human volunteers, the team isolated the participants' T cells and cultured them in a dish. Half of the T cells were combined with normal LDL; the rest were combined with oxidized LDL. The scientists stimulated half of the T cells to mimic an immune response and left the other half alone. The T cells exposed to oxidized LDL displayed a striking response.
"Both the resting and the activated T cells started churning out a chemical that stimulates cells whose sole purpose is to destroy bone," said Rita Effros, professor of pathology at the David Geffen School of Medicine at UCLA. Called RANKL, the chemical is involved in immune response and bone physiology.
The scientists repeated the experiment in a mouse model. Half the animals were fed a high-fat diet starting at one month of age, while the control group ate a normal diet. At 11 months, the mice on the high-fat diet showed elevated cholesterol and thinner bones. When researchers tested the T cells of the mice on the high-fat diet, they discovered that the cells acted differently than those of the mice on the normal diet. The T cells switched on the gene that produces RANKL. The chemical also appeared in the animals' bloodstream, suggesting that the cellular activity contributed to their bone loss.
