Adherence of platelets to human endothelial cells infected by Rickettsia rickettsii

Abstract

Rickettsia rickettsii, the etiologic agent of Rocky Mountain spotted fever, causes widespread vasculitis due to extensive injury of endothelial cells lining small blood vessels. Injury to these cells can lead to denudation of the endothelial lining and exposure of the thrombogenic subendothelium. Modification of the cell surface, either through minor trauma or as a result of altered cell surface biochemistry, could induce changes reflected in increased platelet reactivity. Because membrane modification is likely when R. rickettsii enters endothelial cells, the possibility that infection by this organism caused increased reactivity of platelets with the endothelial cell surface was examined. A fourfold increase in adherence of platelets to cultured endothelial cells from the human umbilical vein infected by R. rickettsii compared with uninfected cells was found. These studies suggest that the adherence of platelets to the surface of Rickettsia-infected endothelial cells can contribute to reduction in the number of circulating platelets in blood during human infection.