Mouse models

Effects of ablation of specific innate immune components on C. rodentium infection


Mice lacking Toll-like receptor 2 (TLR2)

An augmented pathology due to an impaired epithelial barrier


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.


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


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


Mice lacking the p50 subunit of NF-κB

Reduced ability to clear C. rodentium infection.


Mice deficient in p38α

A continued bacterial load with no apparent histological lesions, however, fails to recruit CD4+ T cells and impaired chemokines expression.


Ablation of specific macrophage/monocyte compartment

Neither cell type is essential to trigger immunity


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


Mice lacking β7 integrin

Efficiently control infection and clear bacteria 5-6 week after inoculation


Mice deficient Muc2

Susceptible to the C. rodentium-induced colitis and display quick weight loss and exhibit 90% mortality

[87] [88]