The two major forms of inflammatory bowel disease (IBD) are Crohn's disease and ulcerative colitis, which are characterized by Th1/Th17- or Th2-cell-mediated inflammation, respectively. The mechanisms underlying these diseases remain unclear, however, studies from germ-free animals reveal an important role of the intestinal microflora within these diseases. Since pathogen recognition receptors (PRR), like Toll like receptors (TLRs) and nucleotide-binding oligomerization domains (NOD)-like receptors (NLRs), can induce immune responses against intestinal microflora, PRRs may contribute to the development of IBD. Colitis was induced by adding 1.25% dextran sodium sulfate (DSS) into the drinking water of mice. On day 7, mice were sacrificed; the colons were isolated and divided into four equal sections. The mRNA expression level of PRRs, cytokines, and T cell subset-associated master transcription factors has been determined by using quantitative PCR. Both NLRs and TLRs were up-regulated in colonic regions with intense inflammation, except TLR1 and TLR5. Furthermore, the Th1/Th17 associated transcription factors for cytokines were up-regulated in inflamed colons. Th1-associated master transcription factor was also increased. The Th2 associated transcription factor did show an increased mRNA expression, but the expression level of associated cytokines did not change. In adition, the regulatory T cell- and Th17 associated transcription factors did not show an up-regulated mRNA expression in inflamed colons, however, their associated cytokines were up-regulated. This study provides an overview of mRNA expression of PRRs along the colon in both healthy mice and mice suffering from DSS-induced colitis. An analysis of T cell subset-associated transcription factors and their associated cytokines suggests Th1/Th17 polarization within the DSS-induced colitis. These data will help us to further understand the role of PRRs during the intestinal inflammation and the involvement of TLRs in the mechanism of action of probiotics in IBD.