Promoting mechanism of serum amyloid a family expression in mouse intestinal epithelial cells

Serum amyloid A (SAA) is an acute phase inflammatory protein that we previously described as a robust biomarker of colorectal inflammation in patients with ulcerative colitis (UC) in clinical remission. However, what induces SAA expression in UC remains unclear. This study demonstrates that SAA is significantly expressed in the intestinal tract of UC mouse models when compared with C-reactive protein, another inflammatory biomarker. Moreover, interleukin-6 and tumor necrosis factor-alpha were found to promote SAA1 expression, as were Toll-like receptor ligands flagellin and lipopolysaccharide. Furthermore, results suggested that the nuclear factor-kappa B (NF-kappa B) pathway may be involved in the promotion of SAA1 expression by flagellin, which was inhibited by treatment with 5-aminosalicylic acid (5-ASA). Therefore, the flagellin/NF-kappa B/SAA1 axis may represent one of the mechanisms by which 5-ASA suppresses intestinal inflammation.

Automated summary

This study found higher expression of serum amyloid A (SAA) in the intestinal tract of ulcerative colitis (UC) mouse models compared to C-reactive protein. The expression of SAA1 was promoted by interleukin-6, tumor necrosis factor-alpha, flagellin, and lipopolysaccharide. The nuclear factor-kappa B (NF-kappa B) pathway may be involved in flagellin-induced SAA1 expression, which was inhibited by 5-aminosalicylic acid (5-ASA).