Figure 3.

Potential implications of NETs in the pathogenesis of UC. Inflammatory factors such as IL-6 and TNF-α are potent inducers of NETosis in UC models. In addition, high levels of antineutrophil cytoplasm autoantibodies (ANCA) in serum induce neutrophil infiltration and foster NET generation. Several researches have identified DAMPs capable of inducing NET formation in UC, including cfDNA and HMGB1. Increasing evidence indicates that excess NETs exacerbate the inflammatory response in UC, disrupting the structure and function of the intestinal mucosal barrier and increasing the risk of thrombosis. IL-6, interleukin 6; TNF-α, tumour necrosis factor α; cfDNA, cell-free DNA; HMGB1, high-mobility group box 1; DAMP, damage-associated molecular pattern; ROS, reactive oxygen species; PS, phosphatidylserine.