Effect of fatty acids on injury and repair of intestinal mucosal barrier

1. 脂肪酸对肠上皮细胞趋化因子产生的影响，短链脂肪酸Caco-2细胞丁酸降低肠上皮细胞白细胞介素(IL)-8的产生，ω-3脂肪酸如二十二碳六烯酸（DMA）和二十碳五烯酸（ERA）对IL-8的产生无影响。油酸（OA）和癸酸（CA）增加了IL-8的产量。蛋白激酶C和磷脂酶A2参与了oa诱导的IL-8产生的信号转导途径，但不参与ca诱导的IL-8产生的信号转导途径。全肠灌洗液（WGLF）和粪便中蛋白质的测定WGLF或粪便均可作为研究炎症性肠病（IBD）患者病理生理和疾病活动性的样本。在活动性IBD中，颗粒蛋白（乳铁蛋白、髓过氧化物酶、pmn弹性酶、溶菌酶）的浓度在上清和颗粒中均增加。这些发现表明，尽管中性粒细胞在活动性IBD中迁移到管腔的数量急剧增加，但许多迁移到管腔的中性粒细胞并没有释放颗粒蛋白。乳铁蛋白是这些蛋白中最适合作为肠道炎症的中性粒细胞源性WGLF标记物。氧化剂对人结肠T84细胞阴离子分泌的影响及细胞作用。氧化剂通过直接影响钙激活的基底侧K^+通道电导，降低其Ca^<2+>激活阈值，从而增强Ca^<2+>和camp刺激的Cl^-分泌。这种作用可能在放大和延长炎症肠黏膜的分泌反应，提高腹泻的严重程度方面发挥重要作用。

1. Effect of fatty acids on chemokine production in intestinal epithelial cells, Caco-2 cellsButyrate, a short-chain fatty acid, decreased interleukin(IL)-8 production in intestinal epithelial cells, ω-3 fatty acids such as docosahexaenoic acid (DMA) and eicosapentaenoic acid (ERA) showed no effect on IL-8 production. Oleic acid (OA) and capric acid (CA) increased IL-8 production. Protein kinase C and phospholipase A2 were involved in signal transduction pathways for OA-induced IL-8 production but not for CA-induced IL-8 production.2. Measurement of proteins in whole gut lavage fluid (WGLF) and fecesEither WGLF or feces can be used as a sample to investigate pathophysiology and disease activity in patients with inflammatory bowel disease (IBD). In active IBD, the concentrations of granular proteins (lactoferrin, myeloperoxidase, PMN-elastase, lysozyme) were increased both in the supernatant and pellet. These findings suggested that although the migration of neutrophils into the lumen is extremely increased in active IBD, a number of neutrophils that migrated into the lumen did not release granular proteins. And lactoferrin is the most suitable of these proteins for use as a neutrophilderived WGLF marker of intestinal inflammation.3. Effects and cellular actions of oxidants on anion secretion in human colonic T84 cells.Oxidants potentiate both Ca^<2+>- and CAMP-stimulated Cl^- secretion by a direct effect on calcium-activated basolateral K^+ channel conductance, lowering its Ca^<2+> activation threshold. This effect may play an important role in amplifying and prolonging the secretory response of inflamed intestinal mucosa and enhancing the severity of diarrhea.