BACKGROUND: Patients with multiple skeletal injuries are susceptible to acute respiratory distress syndrome and multiple organ failure, which result from hyperactivation of the immune system. This study was designed to evaluate in vitro the proinflammatory properties of fracture hematoma (FH). METHODS: FH was isolated from patients undergoing emergent open reduction and internal fixation for isolated closed fractures. Neutrophils (PMNs), isolated from healthy volunteers, were exposed to the FH supernatant and activation was examined (CD11b and CD18 adhesion receptor expression and respiratory burst). PMN phagocytosis, apoptosis, and transmigration across an endothelial barrier were also assessed. RESULTS: FH increased PMN respiratory burst (control, 100; FH-treated, 186) and phagocytosis (control, 100; FH-treated, 172) but had no effect on adhesion receptor expression. Transendothelial migration of PMNs was unaffected, although FH was toxic to endothelial cells. In contrast, apoptosis of FH-treated PMNs was delayed (control, 46; FH-treated, 8). CONCLUSION: These effects, although beneficial at the site of injury in the context of antibactericidal function, may cause PMN-mediated tissue injury systemically.
BACKGROUND:Patients with multiple skeletal injuries are susceptible to acute respiratory distress syndrome and multiple organ failure, which result from hyperactivation of the immune system. This study was designed to evaluate in vitro the proinflammatory properties of fracture hematoma (FH). METHODS: FH was isolated from patients undergoing emergent open reduction and internal fixation for isolated closed fractures. Neutrophils (PMNs), isolated from healthy volunteers, were exposed to the FH supernatant and activation was examined (CD11b and CD18 adhesion receptor expression and respiratory burst). PMN phagocytosis, apoptosis, and transmigration across an endothelial barrier were also assessed. RESULTS: FH increased PMN respiratory burst (control, 100; FH-treated, 186) and phagocytosis (control, 100; FH-treated, 172) but had no effect on adhesion receptor expression. Transendothelial migration of PMNs was unaffected, although FH was toxic to endothelial cells. In contrast, apoptosis of FH-treated PMNs was delayed (control, 46; FH-treated, 8). CONCLUSION: These effects, although beneficial at the site of injury in the context of antibactericidal function, may cause PMN-mediated tissue injury systemically.
Authors: Michael J Hausmann; Leonid Kachko; Anna Basok; Alla Shnaider; Gal Yom-Tov; Alexander Shefer Journal: Int Urol Nephrol Date: 2008-10-25 Impact factor: 2.370
Authors: Diane Hu; Chuanyong Lu; Anna Sapozhnikova; Michael Barnett; Carolyn Sparrey; Theodore Miclau; Ralph S Marcucio Journal: J Orthop Res Date: 2010-01 Impact factor: 3.494
Authors: K Horst; D Eschbach; R Pfeifer; S Hübenthal; M Sassen; T Steinfeldt; H Wulf; S Ruchholtz; H C Pape; F Hildebrand Journal: Mediators Inflamm Date: 2015-01-28 Impact factor: 4.711