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. 2014 Sep;82(9):3753–3763. doi: 10.1128/IAI.02045-14

FIG 2.

FIG 2

IEC-MyD88−/− mice suffer accelerated tissue damage during S. Typhimurium infection. (A) Representative H&E staining of cecal tissues from WT and IEC-MyD88−/− mice taken under uninfected conditions or at D1 and D3 pi. IEC-MyD88−/− mice exhibited increased edema, inflammatory cell infiltrate (*, mucosal infiltration; #, submucosal infiltration), and damage to IEC integrity (arrows) at D1 and D3 pi. (B) Comparative histological damage scores of uninfected and infected (D1 and D3 pi) IEC-MyD88−/− and WT mice. Cecal tissues of IEC-MyD88−/− mice displayed significantly higher histological damage scores at both D1 and D3 pi. Bars represent the damage scores from at least 3 experiments, each with 3 to 5 mice. Error bars indicate SEM. **, P < 0.005; ***, P < 0.0005. (C) Infected WT and IEC-MyD88−/− mice show similar increases in gene transcript levels for the chemokines MCP-1 and MIP2-α, as well as for IFN-γ, IL-1β, and IL-17A. In contrast, compared to WT mice, the IEC-MyD88−/− mice showed significantly decreased transcript levels for TNF-α after infection with the S. Typhimurium ΔaroA mutant. Results are representative of 3 independent infections. Original magnification, ×200.