Fig. 1. Survival of mice with gut-derived sepsis caused by P. aeruginosa. IL-1-deficient mice (n = 14) and wild-type mice (n = 10) were treated with cyclophosphamide intraperitoneally on the indicated days (arrow). There was a significant difference between the groups (P < 0.01). Closed circles, IL-1-deficient mice; open triangles, wild-type mice. SM, streptomycin; CY, cyclophosphamide treatment.

Fig. 2. Viable numbers of P. aeruginosa strain D4 in blood, liver and mesenteric lymph node (MLN). There was a significant difference between IL-1-deficient mice (closed columns) and wild-type mice (open columns). Data are mean ± SEM values of eight mice. Symbols: *P < 0.05; **P < 0.01.

Fig. 3. Production of TNF-α, IL-6 and IL-10 in the liver. Livers were removed 2 days after the second cyclophosphamide administration. There were significant differences between IL-1-deficient mice (closed columns) and control mice (open columns) in TNF-α and IL-6. Data are mean ± SEM values of eight mice. Symbols: **P < 0.01.

Fig. 4. Effects of anti-TNF-α MAb on gut-derived sepsis caused by P. aeruginosa in IL-1-deficient mice. Anti-TNF-α MAb-treated mice (n = 10) and control mice (n = 13) were administered cyclophosphamide (75 mg/kg, arrowhead) and anti-TNF-α MAb or bovine serum albumin (200 μg/mouse, arrow) intraperitoneally on the indicated days. Mice treated with TNF-α MAb were significantly more susceptible than control mice (P < 0.01). Closed circles; control IL-1-deficient mice, open circles; anti-TNF MAb-treated IL-1-deficient mice. SM, streptomycin; CY, cyclophosphamide treatment; MAb, anti-TNF MAb, or bovine serum albumin.

Fig. 5. (A) Number of P. aeruginosa D4 phagocytosed by peritoneal macrophages. Phagocytic index represents the number of bacteria per 100 macrophages. There was a significant difference between IL-1-deficient mice (closed columns) and wild-type mice (open columns). Data are mean ± SEM values of four wells. Symbols: *P < 0.05. (B) Viable bacteria counts in the cell culture supernatant 3 h after bacterial inoculation. There was a significant difference between IL-1-deficient mice (closed columns) and wild-type mice (open columns). Data are mean ± SEM values of four wells. Symbols: **P < 0.01.

Fig. 6. Cytokines production by peritoneal macrophage 24 h after bacterial stimulation. The concentrations of TNF-α, IL-6 and IL-10 produced by peritoneal macrophages of IL-1-deficient mice (closed columns) were significantly lower than those of wild-type mice (open columns). Data are mean ± SEM values of four wells. **P < 0.01.