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. Author manuscript; available in PMC: 2014 Jul 17.
Published in final edited form as: Cell Host Microbe. 2013 Jul 17;14(1):26–37. doi: 10.1016/j.chom.2013.06.007

Figure 2. Intestinal host response in mice with persistent S. Typhimurium infection.

Figure 2

129X1/SvJ mice were infected with S. Typhimurium and were either left untreated or were treated with one dose of E. coli Nissle wild-type or tonB mutant three days after infection. Cecal samples were collected at 6 or 22 days after infection. (A) Blinded histopathology scores of cecal samples at 22 days after infection. The score of individual mice (circles) and the geometric mean for each group (bars) are indicated. (B) A detailed scoring for the animals shown in (A) is provided. Each stacked column represents an individual mouse. (C) H&E stained sections from representative animals for each group. Although E. coli Nissle wild-type had no effect on inflammatory cell infiltration, mucosal integrity (assessed by cryptitis and surface erosions) was modestly improved. (D) Transcript levels of Lcn2, Tnf-α and Inf-γ were determined in the ceca of 129X1/SvJ mice infected with S. Typhimurium (white bars), infected with S. Typhimurium and treated with either one dose of E. coli Nissle wild-type (black bars) or tonB mutant (gray bars) 3 days after infection. Samples were collected 6 days after infection. Data are expressed as fold-increase over mock-infected mice. Bars represent the geometric means ± standard deviation. STM=S. Typhimurium; EcN=E. coli Nissle; L; lumen, M, mucosa, SM; submucosa. Significant difference is indicated by * (P value ≤ 0.05) or ** (P value ≤ 0.01).