Monocyte response to bacterial toxins, expression of cell surface receptors, and release of anti-inflammatory cytokines during sepsis

摘要: Exposure to endotoxin produces a state of macrophage hyporesponsiveness on subsequent stimulation. Monocytes in patients with septic shock demonstrate similar endotoxin. The purpose this study was examine whether extends other inflammatory stimuli and the relationship cell surface receptor expression release anti-inflammatory cytokines. Twelve normal volunteers, 10 severe sepsis, 9 were included study. from each subject isolated stimulated lipopolysaccharide (LPS), staphylococcal enterotoxin B (SEB), phorbol myristate acetate (PMA). Tumor necrosis factor-alpha (TNF-alpha) interleukin-1beta (IL-1beta) measured supernatants by enzyme-linked immunosorbent assay (ELISA). Serum levels transforming growth factor-beta1 (TGF-beta1), prostaglandin E2 (PGE2), interleukin-10 (IL-10) also ELISA. monocyte CD14 HLA-DR whole blood flow cytometry. Patients demonstrated significantly decreased TNF-alpha IL-1beta as compared subjects response LPS. In SEB, sepsis patient IL-1beta. Significant decreases found after PMA There no significant differences different between gram-positive gram-negative sepsis. (58 +/- fluorescence units (flU)) (102 14 flU) (p < 0.05). No observed. IL-10 increased (16 4 pg/ml) (42 15 detectable 1 subject. TGF-beta1 (25 6 those (37 2 pg/ml)(p PGE2 These data are consistent more generalized bacterial toxins that may be related altered