Proinflammatory cytokines increase in sepsis after anti-adhesion molecule therapy.

摘要: Cytokine mediators and leukocyte-endothelial cell adhesion molecules are critical interdependent components of the acute inflammatory response in sepsis. We hypothesized that administration monoclonal antibodies to intercellular molecule-1 (CD54) or E- L-selectin (CD62E/L) would decrease serum levels proinflammatory cytokines interleukin-1beta (IL-1), IL-6, IL-8 tumor necrosis factor receptor (TNFR-1) baboons during Adult male received infusions 1 x 10(9) colony forming units (CFU)/kg heat-killed Escherichia coli (E. coli) followed 12 h later by live E. (1 10(10) CFU/kg). At time bacterial infusion, six septic animals were treated with a antibody CD54 an CD62E L mg/kg). Eight untreated served as controls. Sequentially drawn samples assayed for IL-1, IL-8, TNFR-1 using enzyme-linked immunoassay (ELISA). Data compared Mann-Whitney U tests Chi-square analyses. Median survival was decreased both treatment groups controls (P < 0.05). Peak IL-1 level higher than anti-CD54 but not anti-CD62E/L 0.05, P = NS, respectively). Elevations increased prolonged These results provide first vivo evidence CD62E/L regulate cytokine production