The cross talk between ECs and DCs helps maintain gut immune homeostasis. In the initial phases of infection, Salmonella typhimurium induces ECs to release proinflammatory chemokines like IL-8 (CXCL8) and PARC (CCL18), which attract neutrophils, granulocytes, and B and T cells that generate an inflamed site. Salmonella also induces the release of MIP-3α (CCL20), which recruits CCR6-expressing immature DCs. Newly recruited DCs creep between activated ECs, directly contact the bacteria, and release both IL-10 and IL-12, thus promoting Th1 and Th2 responses. This allows the establishment of protective anti-Salmonella responses. EC-derived factors can also activate “bystander” DCs that have not been in direct contact with the bacteria. DCs activated in this way are noninflammatory as they release IL-10 but not IL-12, and drive only Th2 T cells. Moreover, noninflammatory DCs release MCP-1 (CCL2), PARC (CCL18), and MDC (CCL22), thus recruiting monocytes, Th2, and T regulatory cells.