Endotoxin-induced adhesion of red blood cells to pulmonary artery endothelial cells. Tissot, Martha C., Van Patot, Scott Mackenzie, Alan Tucker, Norbert F. Voelkel. Department of Physiology, Colorado State University, Fort Collins, CO 80524
APStracts 2:0135L, 1995.
Cell-cell interactions are important in intravascular inflammation. Neutrophils and monocytes adhere to the vascular endothelium and release mediators, such as TNFa, IL-1b, and reactive oxygen species. Red blood cells (RBC) from patients with malaria, sickle cell anemia and diabetes also adhere to endothelial cells. The objectives of this investigation were to develop a bovine system of RBC adhesion to endothelial cells and to begin to investigate the mechanisms involved in the RBC adhesion. We show that 51Cr-RBC adhere to bovine pulmonary artery endothelial cells (BPAEC) following stimulation of both cell types with endotoxin (ETX: 50 [mu]g/ml). RBC adhesion to BPAEC depended on the ETX concentration and the presence of divalent cations. TNFa, IL-1b, and antioxidants; SOD, catalase and DMSO, all induced RBC adhesion to BPAEC. Phosphatidylserine, which has been implicated in adhesion of sickle cells and aged RBC to endothelium, reduced RBC adhesion to BPAEC whether endotoxin-treated or not. In conclusion: ETX, pro-inflammatory cytokines and surprisingly antioxidants increase RBC adherence to BPAEC monolayers. RBC adhesion to endothelium is decreased by phosphatidylserine. 

Received 4 August 1994; accepted in final form 19 July 1995.
APS Manuscript Number L220-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 14 August 1995.