碳酸钙-2
粪便
发病机制
代谢物
炎症性肠病
肠易激综合征
刺激
溃疡性结肠炎
内科学
串扰
结直肠癌
医学
体外
生物
化学
内分泌学
疾病
微生物学
生物化学
癌症
物理
光学
作者
Luiza Holst,Cristina Iribarren,Maria Sapnara,Otto Savolainen,Hans Törnblom,Yvonne Wettergren,Hans Strid,Magnus Simrén,Maria K. Magnusson,Lena Öhman
标识
DOI:10.3390/ijms232415505
摘要
Previous in vitro studies have shown that the intestinal luminal content, including metabolites, possibly regulates epithelial layer responses to harmful stimuli and promotes disease. Therefore, we aimed to test the hypothesis that fecal supernatants from patients with colon cancer (CC), ulcerative colitis (UC) and irritable bowel syndrome (IBS) contain distinct metabolite profiles and establish their effects on Caco-2 cells and human-derived colon organoids (colonoids). The metabolite profiles of fecal supernatants were analyzed by liquid chromatography-mass spectrometry and distinguished patients with CC (n = 6), UC (n = 6), IBS (n = 6) and healthy subjects (n = 6). Caco-2 monolayers and human apical-out colonoids underwent stimulation with fecal supernatants from different patient groups and healthy subjects. Their addition did not impair monolayer integrity, as measured by transepithelial electrical resistance; however, fecal supernatants from different patient groups and healthy subjects altered the gene expression of Caco-2 monolayers, as well as colonoid cultures. In conclusion, the stimulation of Caco-2 cells and colonoids with fecal supernatants derived from CC, UC and IBS patients altered gene expression profiles, potentially reflecting the luminal microenvironment of the fecal sample donor. This experimental approach allows for investigating the crosstalk at the gut barrier and the effects of the gut microenvironment in the pathogenesis of intestinal diseases.
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