Innate immunity restricts Citrobacter rodentium A/E pathogenesis initiation to an early window of opportunity
Fig 6
Ongoing A/E lesion induction in mice deficient for innate signaling through MyD88 and Trif.
(A) Colonic colonization dynamics in MyD88-/-Triflps/lps germ-free mice consecutively infected, first with mCherry+ KanR TetS C. rodentium wild type (WT) or an isogenic Δler mutant (1010 CFU, red squares and triangles), and 18 hours later superinfected with mCherry- KanS TetR C. rodentium wild type (104 CFU, blue circles). Total C. rodentium counts are depicted as black symbols. Connecting lines connect means; error bars indicate standard deviation; horizontal dotted lines indicate detection limit. (B and C) Representative fluorescent microscopy images of distal colon of MyD88-/-Triflps/lps mice shown in panel A pre-infected with wild type (B) and Δler (C) C. rodentium, respectively. Grey, F-actin/phalloidin; green, anti-Citrobacter O-antigen antibody (pre-infection strain and superinfecting strain); red, mCherry-expressing C. rodentium (pre-infection strain only; none detectable). Scale bars: 50 μm.