Figure 2.

The dysbiosis of intestinal microbiota (bacteria and fungi) results in the occurrence of UC. Under the influence of risk factors, intestinal microbial homeostasis is disrupted. The dysbiosis of microbiota leads to changes in the tight junctions between intestinal epithelial cells, damage of intestinal epithelial barrier, disruption of the mucus layer, and an increase of intestinal permeability. Symbiotic microorganisms and pathogens cause direct damage to the intestinal wall. Furthermore, the main components of the bacterial cell wall (lipopolysaccharide, peptidoglycan, and lipoprotein) are recognized by TLRs, and C-type lectin receptors recognize the components of the fungal cell wall (β-glucan, α-mannan, and α-mannose). After recognition of the antigen, these receptors induce downstream signaling and activate the NF-κB signaling pathways, further induce abnormal immune responses in the host and ultimately leading to the occurrence of UC.TLR, Toll-like receptor; MyD88, Myeloid differentiation factor 88; IRAK, interleukin-1 receptor-associated kinase; NF-κB, nuclear factor κB; Mincle, Macrophage-inducible C-type lectin; SYK, spleen tyrosine kinase; CARD9, caspase recruitment domain family member nine.