期刊
MOLECULAR AND CELLULAR BIOCHEMISTRY
卷 464, 期 1-2, 页码 83-91出版社
SPRINGER
DOI: 10.1007/s11010-019-03651-3
关键词
Kawasaki disease; Intestinal microbiota; Intestinal immune system; BIF; Autophagy
类别
Kawasaki disease is an immune-mediated acute, systemic vasculitis and is the leading cause of acquired heart disease in children in the developed world. Bifidobacterium (BIF) is one of the dominant bacteria in the intestines of humans and many mammals and is able to adjust the intestinal flora disorder. The Caco-2 cell monolayers were treated with tumor necrosis factor-alpha (TNF-alpha) at 10 ng/ml for 24 h to induce the destruction of intestinal mucosal barrier system. Cells viability was detected through Cell Counting Kit-8 assay. Cell apoptosis was measured by flow cytometry and the expression of apoptosis related proteins was also detected through Western blot. The level of pro-inflammatory cytokines interleukin-6 (IL-6) and IL-8 was detected through ELISA, Western blot and qRT-PCR, respectively. Transepithelial electrical resistance (TEER) assay was conducted to value the barrier function of intestinal mucosa. Cell autophagy and NF-kappa B and p38MAPK pathways associated proteins were examined through Western blot. In the absence of TNF-alpha treatment, cell viability and apoptosis showed no significant change. TNF-alpha decreased cell viability and increased cell apoptosis and BIF treatment mitigated the TNF-alpha-induced change. Then, we found that BIF treatment effectively suppressed TNF-alpha-induced overexpression of IL-6 and IL-8. Besides, the results of TEER assay showed that barrier function of intestinal mucosa which was destroyed by TNF-alpha was effectively recovered by BIF treatment. In addition, TNF-alpha induced autophagy was also suppressed by BIF. Moreover, TNF-alpha activated NF-kappa B and p38MAPK signal pathways were also blocked by BIF, SN50 and SB203580. Our present study reveals that BIF plays a protective role in TNF-alpha-induced inflammatory response in Caco-2 cells through NF-kappa B and p38MAPK pathways.
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