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促进鼠肠上皮细胞中血清淀粉样 A 家族表达的机制。

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

机构信息

Department of Gastroenterology and Metabolism, Hiroshima University Hospital, Hiroshima, Japan.

Department of Endoscopy, Hiroshima University Hospital, Hiroshima, Japan.

出版信息

PLoS One. 2022 Mar 18;17(3):e0264836. doi: 10.1371/journal.pone.0264836. eCollection 2022.

Abstract

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.

摘要

血清淀粉样蛋白 A(SAA)是一种急性期炎症蛋白,我们之前曾描述其为溃疡性结肠炎(UC)患者临床缓解期结直肠炎症的一种强有力的生物标志物。然而,诱导 UC 中 SAA 表达的原因尚不清楚。本研究表明,与另一种炎症生物标志物 C 反应蛋白(CRP)相比,SAA 在 UC 小鼠模型的肠道中表达显著。此外,白细胞介素 6 和肿瘤坏死因子-α 被发现可促进 SAA1 的表达,Toll 样受体配体鞭毛蛋白和脂多糖也是如此。此外,结果表明核因子-κB(NF-κB)通路可能参与了鞭毛蛋白促进 SAA1 表达的过程,而 5-氨基水杨酸(5-ASA)的治疗可抑制这一过程。因此,鞭毛蛋白/NF-κB/SAA1 轴可能是 5-ASA 抑制肠道炎症的机制之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72cb/8932556/56167757c1e9/pone.0264836.g001.jpg

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