Figure 3.

The ΔoatA mutant has a strongly attenuated virulence in mice and triggers an increased cytokine response early after infection. A, BALB/c mice were challenged by intravenous injection of 10⁶ EGDe (black circles) or ΔoatA (white squares). Survival of infected mice was determined over time (n = 5). B, BALB/c mice were challenged by intravenous injection of a sublethal dose (10⁴ bacteria per mouse) of EGDe (black bars) or ΔoatA (white bars). Colonization of liver, spleen, and blood was followed 6, 24, and 48 hours postinfection. Data are means ± SD (n = 4). C, Transgenic human E-cadherin mice were used as a permissive model for the oral route of infection. These mice were infected with 10¹⁰ EGDe (black bars) or ΔoatA (white bars). After 3 hours and 24 hours, mice were euthanized and the number of bacteria in the intestinal lumen and intestinal tissue was determined. Data are means ± SD (n = 3–5). D, BALB/c mice were inoculated intravenously with 5 × 10³ bacteria. The liver was dissected and homogenized. Homogenates were assayed using a multiplex immunoassay to determine cytokine level in response to infection with EGDe (black bars) or ΔoatA (white bars). Data are means ± SD (n = 4). Student t test was performed to determine statistical significance: *, **, and *** indicate P < .05, P < .01, and P < .001, respectively.