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

FIG 3.

FIG 3

Disease severity of IEC-MyD88−/− mice is associated with altered S. Typhimurium localization within cecum. (A) No differences in S. Typhimurium ΔaroA mutant pathogen burdens (CFU/g) were identified among the ceca, luminal contents, spleens, or livers from IEC-MyD88−/− and WT mice at D1 or D3 pi. Error bars indicate SEM from at least 9 mice unless otherwise indicated. (B) Immunofluorescence staining for Salmonella LPS (red), β-actin (green), and DNA (blue) in cecal tissues at D1 pi. The presence of MyD88 in IECs (WT) prevents the S. Typhimurium ΔaroA mutant (location indicated by white arrow) from associating closely with the epithelium, sequestering them to the lumen, whereas S. Typhimurium in the IEC-MyD88−/− ceca was found in close proximity to the epithelial surface. Original magnification, ×200. (C) The commensal microbiota found in WT and IEC-MyD88−/− mice under uninfected conditions and after streptomycin treatment at D1 pi, as measured by qPCR. No significant differences were found between the intestinal bacterial populations (at phylum level) present in WT and IEC-MyD88−/− mice.