TY - JOUR T1 - PReferential loss of cxcr-2 receptor expression and function in patients who have undergone trauma AU - Quaid GA, Cave C, Robinson C, Williams MA, Solomkin JS Y1 - 1999/12/01 N1 - 10.1001/archsurg.134.12.1367 JO - Archives of Surgery SP - 1367 EP - 1372 VL - 134 IS - 12 N2 - Background  In response to traumatic injury or infection, human neutrophils are directed to the site of injury or infection by CXC chemokines that signal via 2 receptors, CXCR-1 and CXCR-2. In vitro studies have shown preferential loss of CXCR-2 expression and function after exposure to interleukin 8, N-formyl-methionyl-leucyl-phenylalanine (fMLP), C5a, and tumor necrosis factor α.Hypothesis  CXCR-2 expression and function are preferentially down-regulated in severely injured patients.Methods  We studied 20 patients within 24 hours of admission to the hospital. Patients with head injuries were excluded. Injury Severity Scores (range, 1-50; mean, 35) were calculated for each patient. To determine expression of CXCR-1 and CXCR-2, flow cytometry was used. Intracellular calcium mobilization and neutrophil migration to 10 nmol of interleukin 8, growth-related oncogene α, and fMLP was measured to determine receptor function.Results  Compared with CXCR-1, there is a greater loss of CXCR-2 receptor expression in the severely injured group (P = .01). Neutrophils from patients with Injury Severity Scores greater than 16 did not mobilize calcium in response to growth-related oncogene α. However, there was no loss of calcium mobilization to interleukin 8 or fMLP. Chemotaxis to various stimulants is decreased in all injury groups.Conclusions  CXCR-2 expression and function are preferentially down-regulated in severely injured patients. Our data suggest that there are multiple mechanisms, in addition to receptor down-regulation, that play a role in the loss of migration and calcium flux in human neutrophils after injury. SN - 0004-0010 M3 - doi: 10.1001/archsurg.134.12.1367 UR - http://dx.doi.org/10.1001/archsurg.134.12.1367 ER -