Citrobacter rodentium induces an acute, self‐limited colitis in mice which is histologically associated with crypt hyperplasia. The infection serves as a model for human infectious colitis induced by enteropathogenic Escherichia coli. We investigated if Balb/c mice, which had spontaneously cleared C. rodentium infection, were protected against re‐infection and if resistance against intestinal infection can be systemically transferred using spleen cells. The course of infection was monitored by faecal excretion. Spleen cells, splenic CD3⁺ and CD4⁺ cells were transferred from resistant mice to non‐infected recipients prior to infection. Cytokine secretion, serum and faecal antibody titres and histological disease severity were assessed. Balb/c mice were resistant against re‐infection. The course of infection was shorter in mice receiving primed spleen cells, CD3⁺ and CD4⁺ cells. Transfer of CD4⁺ T cells from resistant mice induced γ‐interferon, interleukin (IL)‐2 and IL‐17 secretion and suppressed IL‐10 secretion. Anti‐Citrobacter serum IgG1 and IgG2a enzyme‐linked immunosorbent assay OD levels were increased. Faecal IgA secretion was increased while serum IgA was suppressed in recipients of CD4⁺ cells. Large bowel histology showed protection from colitis in recipients of primed cells as indicated by normal colonic epithelium. In Balb/c mice, C. rodentium infection is followed by resistance, which can be transferred by CD4⁺ cells. Transfer of protection is associated with IL‐17 secretion, enhanced serum IgG and faecal IgA secretion. This is the first study to demonstrate the mechanisms by which systemic resistance from previously C. rodentium‐infected mice can be transferred to non‐infected animals.