Figure 1.

Alternative responses are activated in monocytes from septic patients. (a) to (f) Monocytes from septic patients (age 51 ± 12 years, mean ± standard deviation), who met the diagnostic criteria for sepsis, were isolated (n = 17). Blood samples were taken when they met the sepsis criteria for the first time. The following exclusion criteria were imposed: malignancy and chronic inflammatory diseases, treatments with steroids or immunosuppressive drugs during the past month, hepatic failure (serum aspartate aminotransferase and/or alanine aminotransferase level >100 IU/l; prothrombin time <60%, total bilirubin level >60 μmol/l), renal insufficiency (plasma creatinine level >200 μmol/l), AIDS, virus B orvirus C hepatitis, gestation, and age >70 years. Total RNA was then isolated and the levels of (a) TNFα, (b) NF-κB2/p100, (c) NF-κB-inducing kinase (NIK), (d) lymphotoxin β-receptor (LTBR), (e) v-rel reticuloendotheliosis viral oncogene homologue A (p65) (RelA) and (f) serine/threonine proteinkinase (AKT) were determined by real-time quantitative PCR. (a) In the case of TNFα, induction levels were also analysed when monocytes were challenged with lipopolysaccharide (LPS) (10 ng/ml) for 3 hours, ex vivo. (g) to (i) Lymphocytes from septic patients were isolated (n = 17). Total RNA was then isolated and the levels of (g) T-cell antigen receptor (TCR), (h) linked for activation of T cells (LAT) and (i) ΔCD3-TCR complex (CD3D) were determined by real-time quantitative PCR. The fold induction with respect to the basal is depicted. *P < 0.01 septic phase versus recovery phase (1 month afterwards).