In a second version of this model, which employs S. Typhimurium mutants lacking a functional TTSS-1 (e.g. SL1344 ΔinvG, S. TminvG), the pathogen relies on CD11c+CX3CR1+ monocytic phagocytes to traverse the epithelial barrier, grows within CD11c−CX3CR1− monocytes of the LP and causes overt mucosal inflammation 3 days post infection (p.i.)[20], [21]. This evidence concerns the gene CX3CR1 and infection.