These are on the whole very good things for platelets to do, Morrell says, but in the context of organ transplants, their pro-inflammatory function gets out of control, and they do more bad than good after contributing to initial wound healing.
Strategies using drugs or other means to keep platelets quiet and non-inflammatory might benefit transplant patients in the long run because chronic rejection as contrasted with acute or immediate organ rejection is a major complication for which there is little current treatment, according to Hamid Rabb, M.D., medical director of kidney transplantation and a professor of medicine at the Johns Hopkins University School of Medicine.
In prior research using mice with skin transplants, Morrell and his team noted that increased platelet interactions led to increased and prolonged white cell interactions with the inner lining of the blood vessels and worsened transplant vessel damage.
"We watched platelets flowing through the blood vessels of transplanted skin in mice with and without platelets and determined tissue-platelet interactions by comparing the speeds of those flows," says Morrell, whose team ultimately demonstrated that antibodies made in reaction to the transplanted tissue sparked platelet activation and white cell recruitment.
Studies on tissue from platelet-depleted mice helped confirm the importance of platelets in white cell activation and recruitment, strongly suggesting that limiting the inflammatory response might improve transplanted tissue survival.
Mounting evidence suggesting that platelets are activated not only post-transplant, but also during organ harvest, presents new opportunities for attacking organ injury and rejection head-on, says Rabb. The traditional target of current anti-rejection medicine is the so-called T lymphocyte a white blood cell believed to
|Contact: Maryalice Yakutchik|
Johns Hopkins Medical Institutions