Figure 6

NOS inhibition and iNOS deficiency enhance in vivo IL-1β and IL-18 secretion, and increase susceptibility to LPS-induced death. (A) Production of IL-1β in peritoneal lavage fluid at 8 h after intraperitoneal injection of LPS (1.5 mg/kg of body weight) without (PBS, n = 17) or with (L-NAME, n = 17) NOS inhibitor L-NAME (100 mg/kg of body weight) into 7-week-old female C57BL/6 mice. (B) Survival of 7-week-old female C57BL/6 mice injected intraperitoneally with LPS (5 mg/kg of body weight) without (PBS, n = 14) or with (L-NAME, n = 14) NOS inhibitor L-NAME (100 mg/kg of body weight). Lethality was recorded for 96 h. (C) Production of IL-1β in peritoneal lavage fluid and IL-18 in serum 24 h after intraperitoneal injection of LPS (10 mg/kg of body weight) into female WT and iNOS^−/− mice. (D) Survival of female WT (n = 10) and iNOS^−/− (n = 9) mice injected intraperitoneally with LPS (10 mg/kg of body weight). Lethality was recorded for 96 h. (E) Production of serum IL-1β and IL-18 at 8 h after intraperitoneal injection of LPS (5 mg/kg of body weight) without (PBS) or with (L-NAME) NOS inhibitor L-NAME (100 mg/kg of body weight) into 7-week-old female WT and CMV-NLRP3 KO mice. n.s., not significant. (F) Survival of 7-week-old female C57BL/6 and CMV-NLRP3 KO mice (n = 9 per group) injected intraperitoneally with LPS (5 mg/kg of body weight) without (PBS) or with (L-NAME) NOS inhibitor L-NAME (100 mg/kg of body weight). Lethality was recorded for 96 h. The data are representative of two independent experiments.