| Mouse models | Effects of ablation of specific innate immune components on C. rodentium infection | Refs |
| Mice lacking Toll-like receptor 2 (TLR2) | An augmented pathology due to an impaired epithelial barrier | [75] |
| Mice lacking MYD88 | Have greater bacterial loads in colon and peripheral tissues and suffer from severe colitis and death | [76] [77] |
| IL-1R deficient mice | Increased susceptibility to tissue damage but do not display amplified pathogen burdens in colon. | [78] |
| Deficiency of TLR4 | Decreased tissue pathology and inflammatory cell infiltration in gut. While the extent of infection is unaffected, dissemination of bacteria through colon is hindered | [79] |
| Mice deficient in Nlrp3, Nlrc4, and caspase-1 | Hyper susceptible to C. rodentium induced intestinal inflammation. However, exhibit only mild defects and do not die after infection | [80] [81] |
| IL-1β−/− and IL-18−/− mice | Increased bacterial burdens and severe histopathology. | [80] [81] |
| Nod2−/− mice | Diminished intestinal clearance to C. rodentium. due to impaired secretion of CCL2 from colonic cells | [82] |
| Mice lacking the p50 subunit of NF-κB | Reduced ability to clear C. rodentium infection. | [83] |
| Mice deficient in p38α | A continued bacterial load with no apparent histological lesions, however, fails to recruit CD4+ T cells and impaired chemokines expression. | [84] |
| Ablation of specific macrophage/monocyte compartment | Neither cell type is essential to trigger immunity | [85] |
| Mice lacking PSGL-1 and P, E and L-selectin | Mice defective in PSGL-1 and P-selectin suffer morbidity, extensive inflammatory responses and augmented bacterial burden, however, mice defective in either E or L-selectin do not exhibit severe infection | [86] |
| Mice lacking β7 integrin | Efficiently control infection and clear bacteria 5-6 week after inoculation | [59] |
| Mice deficient Muc2 | Susceptible to the C. rodentium-induced colitis and display quick weight loss and exhibit 90% mortality | [87] [88] |