Inflammatory priming of immune cells in early life may optimize the response to a subsequent inflammatory challenge later in life. To prime the immune cells in the gut in vivo through a short inflammatory insult, we administered a low dose of dextran sulfate sodium (DSS) to 5-weeks-old BALB/c mice in the drinking water. We hypothesized that DSS-primed mice would show decreased inflammation and difference in immunological profiling, when subjected to presensitizing and oxazolone-induced colitis by rectal instillation at 9 weeks compared to non-DSS-primed control mice. In fact, this low-dose DSS priming apparently decreased the acute inflammation, as colitis scores along with IFNγ, IL-1ß, and IL-4 were significantly decreased with the same tendency for IL-5, TNFα, and IL-2 on day 3 post-induction compared to control mice. On day 7, both DSS-primed and control mice had significantly higher numbers of FoxP3+CD8+ regulatory T cells, while they did not differ in any inflammation parameters. No significant differences were found for intraepithelial lymphocytes or mesenteric lymphocytes at any time point after colitis induction. In conclusion, the priming did decrease local acute tissue inflammation of the colon in this commonly applied mouse model of T helper cell type 2-dominated model of inflammatory bowel disease.
Keywords:acute inflammation; colitis; dextran sulfate sodium; oxazolone; priming.