The host immune signaling proteins RIPK1, RIPK3, TRIF and DAI, all contain receptor-interacting protein (RIP) homotypic interaction motifs (RHIM), and play a key role in cell death and inflammatory signaling. RHIM-dependent interactions help drive a caspase-independent form of cell death termed necroptosis. We have previously shown that some pathogenic E. coli encode a virulence protein (EspL) that directly cleaves all host RHIM proteins, suggesting a role for necroptosis in protecting against bacterial gut infection. While many studies have focused on the role off necroptosis in viral clearance, few studies have analysed the role of this recently discovered cell death pathway in bacterial infections in vivo. Furthermore, the main executioner of necroptosis, MLKL, is currently under scrutiny as the ‘only’ protein mediating cell lysis during necroptosis. Here we show that Ripk3-/- but not Mlkl -/- mice exhibited increased pathology and bacterial dissemination upon infection with the model mouse gut pathogen Citrobacter rodentium compared to wild type C57BL/6 mice. This suggests a role for RIPK3 in controlling bacterial gut infection, possibly independent of necroptosis and has opened several avenues for studying the role of RIPK3 in mediating inflammation, particularly regulation of T helper cell responses in this disease setting. Overall, this work will better define the role of RIPK3 in bacterial infections and help identify novel mechanisms of this key innate mediator in innate and adaptive host responses.