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 s...

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Bibliographic Details
Published in:PloS one 2022-03, Vol.17 (3), p.e0264836-e0264836
Main Authors: Wakai, Masaki, Hayashi, Ryohei, Ueno, Yoshitaka, Onishi, Kana, Takasago, Takeshi, Uchida, Takuro, Takigawa, Hidehiko, Yuge, Ryo, Urabe, Yuji, Oka, Shiro, Kitadai, Yasuhiko, Tanaka, Shinji
Format: Article
Language:English
Subjects:
Amyloid
Analysis
Animal models
Animals
Antibodies
Biology and Life Sciences
Biomarkers
C-reactive protein
Colitis, Ulcerative - drug therapy
Colorectal cancer
Endoscopy
Epithelial cells
Epithelial Cells - metabolism
Epithelium
Flagellin
Flagellin - therapeutic use
Gastroenterology
Gene expression
Genetic aspects
Hospitals
Humans
Inflammation
Inflammation - pathology
Inflammatory bowel disease
Inflammatory bowel diseases
Interleukin 6
Intestine
Laboratory animals
Lipopolysaccharides
Medicine and Health Sciences
Mesalamine - therapeutic use
Metabolism
Mice
NF-kappa B - metabolism
NF-κB protein
Pathogens
Proteins
Remission
Research and Analysis Methods
Serum Amyloid A Protein - metabolism
Small intestine
Toll-like receptors
Tumor necrosis factor-TNF
Tumor necrosis factor-α
Ulcerative colitis
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Summary: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.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0264836