Fig. 1

The mechanisms of gut inflammation caused by colonization of IBD-associated pathobionts. AIEC can adhere to and invade the epithelial cells, impairing the epithelial barrier. After invasion to the host, AIEC triggers IL-1β secretion from mononuclear phagocytes, such as macrophages, promoting the differentiation to Th17 cells. Oral pathobionts, including K. pneumoniae and K. aerogenes, can ectopically colonize the gut during gut inflammation. Ectopic colonization of oral pathobionts promotes the production of proinflammatory cytokines from DCs and macrophages, which facilitate the differentiation into Th1 and Th17 cells. Mucolytic bacteria, such as R. gnavus, may promote the encroachment of other bacteria to the epithelial niche. R. gnavus also produces the polysaccharide that promotes tumor necrosis factor (TNF) secretion from DCs