Open AccessPromoting mechanism of serum amyloid a family expression in mouse intestinal epithelial cells
Author(s) -
Masaki Wakai,
Ryohei Hayashi,
Yoshitaka Ueno,
Kana Onishi,
Takeshi Takasago,
Takuro Uchida,
Hidehiko Takigawa,
Ryo Yuge,
Yuji Urabe,
Shiro Oka,
Yasuhiko Kitadai,
Shinji Tanaka
Publication year - 2022
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0264836
Subject(s) - serum amyloid a , flagellin , inflammation , acute phase protein , tumor necrosis factor alpha , lipopolysaccharide , tlr5 , biomarker , immunology , ulcerative colitis , toll like receptor , proinflammatory cytokine , medicine , cancer research , receptor , chemistry , tlr4 , innate immune system , immune system , tlr2 , biochemistry , disease
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-α 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-κB) 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-κB/SAA1 axis may represent one of the mechanisms by which 5-ASA suppresses intestinal inflammation.