作者: John D. Belcher , Paul H. Marker , Jill P. Weber , Robert P. Hebbel , Gregory M. Vercellotti
DOI: 10.1182/BLOOD.V96.7.2451.H8002451_2451_2459
关键词: E-selectin 、 Tumor necrosis factor alpha 、 Immunology 、 Endothelium 、 Internal medicine 、 Endocrinology 、 Cell adhesion molecule 、 Monocyte 、 Inflammation 、 Medicine 、 Peripheral blood mononuclear cell 、 Endothelial activation
摘要: Sickle cell anemia is characterized by painful vaso-occlusive crises. It hypothesized that monocytes are activated in sickle disease and can enhance vaso-occlusion activating endothelium. To test this hypothesis, human umbilical vein endothelial cells (HUVEC) microvascular (MVEC) with normal mononuclear leukocytes were incubated, activation was measured. Endothelial incubated more than those leukocytes, as judged the increased expression of adhesion molecules tissue factor polymorphonuclear (PMNL). Monocytes, not lymphocytes or platelets, responsible for cells. triggered nuclear factor-kappa B (NF-κB) translocation. Cell-to-cell contact endothelium enhanced, but required for, activation. Antibodies to tumor necrosis factor-alpha (TNF-α) interleukin-1-beta (IL-1β) blocked monocytes. Peripheral blood from patients had 34% IL-1β ( P = .002) 139% TNF-α per Sixty percent expressed molecule ligand CD11b on their surfaces compared only 20% = .002). Serum C-reactive protein, a marker systemic inflammation, 12-fold serum = .003). These results demonstrate can, turn, activate speculated vascular marked endothelium, plays significant role pathophysiology anemia.