An antibody against human IAP succeeded in keeping the affected red blood cells from sticking to thrombospondin in the blood flow system, she said. From that they concluded that IAP may cause part of the impaired blood flow.
Thrombospondin also is elevated in blood plasma of sickle cell disease patients, Parise said. That might be important in causing the crises if the circulating thromobospondin acts like a glue. Blood vessel walls damaged by the illness might boost clogging as the two proteins interact more readily because of the damage.
"The next step will be to test our results in a mouse model of sickle cell disease and evaluate potential blockers there," Brittain said. "We are still years away from taking this into the clinic, but we are one step closer than we were a year ago."
About 150 in every 100,000 U.S. black children suffer from sickle cell disease, also known as sickle cell anemia, according to the American Medical Association. About one in 12 blacks has sickle cell trait, which means they carry a gene that produces a defective kind of hemoglobin, the complex protein that carries oxygen to tissues throughout the body.
If a person inherits the gene from a parent, he or she is a carrier like the parent but usually is symptom free. When two carriers have a child, there's a 25 percent chance the child will have sickle cell disease, 50 percent chance the child will be a carrier and a 25 percent chance he or she will have neither.
Until about 1960, most infants born with the illness died in childhood, but today with improved treatments many survive into adulthood. A relatively simple blood test can show who carries the sickle cell gene, and doctors advise that couples who both carry it should undergo genetic counseling before starting a family.