Figure 3. Vitamin A deficiency results in impaired immunity to bacterial infections.

WT (A–D) and Rag1^−/− (E–K) mice treated with Veh or RAi were infected with C. rodentium. A) Percentile change of original body weight and frequency of surviving animals and B) colon length of WT mice treated with RAi or Veh. C) Large intestine lamina propria (LiLP) cells isolated from Veh or RAI treated WT mice 10 days after infection with C. rodentium, gated on CD4⁺ and TCRb⁺ cells and analyzed for RORγt (upper panel) and IL-22 expression (lower panel). D) Total numbers of RORγt⁺ and IL-22⁺ CD4⁺ T cells. E) Percentile change of original body weight and frequency of surviving Rag1^−/− mice treated with Veh or RAi and infected with C. rodentium. F) Colon length and G) representative H&E histological sections of colonic tissue analyzed 10 days post-infection. H) LILP ILC2 and ILC3 from Veh or RAI treated Rag1^−/− mice 10 days after infection with C. rodentium (upper panel) and intracellular IL-17A and IL-22 expression in ILC following stimulation with PMA and ionomycin (lower panel). I) Total numbers of RORγt expressing ILC and total numbers of IL-22 producing ILC per colon. J) Weight loss of Ctrl, VAI or VAI Rag1^−/− mice treated with IL-22 (VAI+IL-22) and infected with C. rodentium. K) Colon length analyzed 13 days post-infection. Data represent at least two independent experiments with 3–5 mice in each experimental group. All graphs display means ±SEM.