TLR9 and colitis: O’Hara et al., in 2012, revealed that infection by Campylobacter jejuni reduces the expression of apical TLR9 in intestinal epithelial cells, thereby disrupting TLR9-induced reinforcement of the intestinal epithelial barrier, and that mice previously exposed to Campylobacter jejuni develop a more severe colitis after low doses of DSS administration, with a significant reduction in levels of the anti-inflammatory cytokine IL-25 and an increase in IL-17, which has an ambiguous role in the pathogenesis of IBD [135].