Fig 1. Propofol inhibits immune clearance of Lm from infected tissues.

(a). Mice were intravenously infected with a sublethal dose of 2 x 10⁴ CFU Lm in the presence and absence of propofol exposure. Graph shows bacterial burdens present in target organs at the indicated time points post-infection. ‘X’ indicates animals with bacterial burdens that were below detection limits. Double dagger indicates animals that succumbed to infection prior to experimental endpoints. Data shown is from two independent experiments. (b). Propofol does not increase host susceptibility to Lm strains attenuated for virulence. Mice were intravenously infected with 2 x 10⁴ CFU Lm ΔactA (deficient for bacterial cell-to-cell spread) in the presence and absence of propofol exposure. Graph depicts bacterial burdens present in target organs at the indicated time points post-infection. ‘X’ indicates animals with bacterial burdens that were below detection limits. Data shown is from two independent experiments. (c). Propofol enhances Lm translocation across the blood-brain barrier. Mice were intravenously infected with 2 x 10⁴ CFU Lm in the presence and absence of propofol exposure. Graph depicts bacterial burdens present in the brain at the indicated time points. ‘X’ indicates animals with bacterial burdens that were below detection limits. Data shown is from two independent experiments. (d). The immunosuppressive effects of propofol are evident for up to four days post-sedation. Mice were intravenously infected with a low dose of 2 x 10³ CFU of Lm at 24 or 96 hours following brief propofol sedation. Bacterial burdens in the livers and spleens were determined at 96 hours post-infection. ‘X’ indicates animals with bacterial burdens that were below detection limits. Double dagger indicates animals that succumbed to infection prior to experimental endpoints. Data shown is representative of two independent experiments, error bars indicate data ± SEM. * p<0.05, ** p<0.005, *** p<0.001.