Fig. 1
Goblet cell-associated antigen passage (GAP) formation is inhibited by Salmonella in a MyD88 and EGFR dependent manner. a Fluorescent images of SI villus cross section of C57BL/6 mice given luminal 10 kD dextran (red) and DAPI (blue), 1h after receiving luminal PBS (left), 5 × 108 CFU invasion-deficient Salmonella (ΔinvG Sal; center) or 5 × 108 CFU wildtype Salmonella (WT-Sal; right). b Density of GAPs in C57BL/6 mice, given 5 × 108 CFU or wildtype or ΔinvG Salmonella in the SI lumen 1 hour (hr) earlier (left side) or given 5 × 107 CFU wildtype or ΔinvG Salmonella orally 2 days earlier (right side). c MyD88fl/fl Math1Cre*PR and d EGFRf/f Math1Cre*PR mice and littermate controls were treated with RU486 to delete MyD88 or EGFR from GCs and were administered with 5 × 108 CFU of wildtype Salmonella or PBS for 1 h within the SI lumen (left side), or gavaged with 5 × 107 CFU wildtype Salmonella and SI tissue sections were evaluated 2 days later (right side). Graphs depict the density of GAPs in SI villus cross section of uninfected and infected mice. Data presented as the mean ± SEM. Scale bar in a = 50 μm; *p < 0.05, ns = not significant, n = 5 or more mice with 60 or more villus cross sections per mouse examined for each condition
