Department of Gastroenterology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310016, Zhejiang Province, China.
Division of Gastroenterology, Loma Linda University Medical Center, Loma Linda, CA 92354, United States.
World J Gastroenterol. 2017 Dec 21;23(47):8321-8333. doi: 10.3748/wjg.v23.i47.8321.
To determine whether fructo-oligosaccharide (FOS) affects visceral sensitivity, inflammation, and production of intestinal short-chain fatty acids (SCFA) in an irritable bowel syndrome (IBS) mouse model.
Mice were randomly assigned to daily oral gavage of saline solution with or without FOS (8 g/kg body weight) for 14 d. Mice were further assigned to receive either daily one-hour water avoidance stress (WAS) or sham-WAS for the first 10 d. After 2 wk, visceral sensitivity was measured by abdominal withdrawal reflex in response to colorectal distension and mucosal inflammation was evaluated. Gas chromatography, real-time reverse transcription PCR, and immunohistochemistry assays were used to quantify cecal concentrations of SCFA, intestinal cytokine expression, and number of intestinal mast cells per high-power field (HPF), respectively.
Mice subjected to WAS exhibited visceral hypersensitivity and low-grade inflammation. Among mice subjected to WAS, FOS increased visceral hypersensitivity and led to higher cecal concentrations of acetic acid (2.49 ± 0.63 mmol/L 1.49 ± 0.72 mmol/L, < 0.05), propionic acid (0.48 ± 0.09 mmol/L 0.36 ± 0.05 mmol/L, < 0.01), butyric acid (0.28 ± 0.09 mmol/L 0.19 ± 0.003 mmol/L, < 0.05), as well as total SCFA (3.62 ± 0.87 mmol/L 2.27 ± 0.75 mmol/L, < 0.01) compared to saline administration. FOS also increased ileal interleukin (IL)-23 mRNA (4.71 ± 4.16 1.00 ± 0.99, < 0.05) and colonic IL-1β mRNA (2.15 ± 1.68 0.88 ± 0.53, < 0.05) expressions as well as increased mean mast cell counts in the ileum (12.3 ± 2.6 per HPF 8.3 ± 3.6 per HPF, < 0.05) and colon (6.3 ± 3.2 per HPF 3.4 ± 1.2 per HPF, < 0.05) compared to saline administration in mice subjected to WAS. No difference in visceral sensitivity, intestinal inflammation, or cecal SCFA levels was detected with or without FOS administration in mice subjected to sham-WAS.
FOS administration intensifies visceral hypersensitivity and gut inflammation in stress-induced IBS mice, but not in the control mice, and is also associated with increased intestinal SCFA production.
确定果寡糖(FOS)是否会影响肠易激综合征(IBS)小鼠模型中的内脏敏感性、炎症和肠道短链脂肪酸(SCFA)的产生。
将小鼠随机分为每日口服生理盐水组和 FOS 组(8g/kg 体重),共 14d。小鼠进一步分为每日接受 1 小时水回避应激(WAS)或假-WAS 处理 10d。2 周后,通过结肠扩张反应测量内脏敏感性,并评估黏膜炎症。使用气相色谱、实时逆转录 PCR 和免疫组织化学检测分别定量回肠 SCFA 浓度、肠道细胞因子表达和每个高倍视野(HPF)的肠道肥大细胞数量。
接受 WAS 的小鼠表现出内脏高敏性和低度炎症。在接受 WAS 的小鼠中,FOS 增加了内脏高敏性,并导致回肠中乙酸(2.49±0.63mmol/L 比 1.49±0.72mmol/L,<0.05)、丙酸(0.48±0.09mmol/L 比 0.36±0.05mmol/L,<0.01)、丁酸(0.28±0.09mmol/L 比 0.19±0.003mmol/L,<0.05)和总 SCFA(3.62±0.87mmol/L 比 2.27±0.75mmol/L,<0.01)的浓度增加。FOS 还增加了回肠白细胞介素(IL)-23 mRNA(4.71±4.16 比 1.00±0.99,<0.05)和结肠 IL-1β mRNA(2.15±1.68 比 0.88±0.53,<0.05)的表达,并增加了回肠(12.3±2.6/HPF 比 8.3±3.6/HPF,<0.05)和结肠(6.3±3.2/HPF 比 3.4±1.2/HPF,<0.05)中肥大细胞的平均数量,与接受 WAS 的小鼠给予生理盐水相比。在接受假-WAS 的小鼠中,无论是否给予 FOS,内脏敏感性、肠道炎症或回肠 SCFA 水平均无差异。
在应激诱导的 IBS 小鼠中,FOS 给药会加剧内脏高敏性和肠道炎症,而在对照小鼠中则不会,并且还与肠道 SCFA 产生增加有关。