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小鼠对补充硫酸盐的饮用水的胃肠道和微生物反应。

Gastrointestinal and microbial responses to sulfate-supplemented drinking water in mice.

作者信息

Deplancke Bart, Finster Kai, Graham W Vallen, Collier Chad T, Thurmond Joel E, Gaskins H Rex

机构信息

Division of Nutritional Sciences, and Department of Animal Sciences, University of Illinois, Urbana, Illinois 61801, USA.

出版信息

Exp Biol Med (Maywood). 2003 Apr;228(4):424-33. doi: 10.1177/153537020322800413.

Abstract

There is increasing evidence that hydrogen sulfide (H2S), produced by intestinal sulfate-reducing bacteria (SRB), may be involved in the etiopathogenesis of chronic diseases such as ulcerative colitis and colorectal cancer. The activity of SRB, and thus H2S production, is likely determined by the availability of sulfur-containing compounds in the intestine. However, little is known about the impact of dietary or inorganic sulfate on intestinal sulfate and SRB-derived H2S concentrations. In this study, the effects of short-term (7 day) and long-term (1 year) inorganic sulfate supplementation of the drinking water on gastrointestinal (GI) sulfate and H2S concentrations (and thus activity of resident SRBs), and the density of large intestinal sulfomucin-containing goblet cells, were examined in C3H/HeJBir mice. Additionally, a PCR-denaturing gradient gel electrophoresis (DGGE)-based molecular ecology technique was used to examine the impact of sulfate-amended drinking water on microbial community structure throughout the GI tract. Average H2S concentrations ranged from 0.1 mM (stomach) to 1 mM (cecum). A sulfate reduction assay demonstrated in situ production of H2S throughout the GI tract, confirming the presence of SRB. However, H2S generation and concentrations were greatest in the cecum and colon. Sulfate supplementation of drinking water did not significantly increase intestinal sulfate or H2S concentrations, suggesting that inorganic sulfate is not an important modulator of intestinal H2S concentrations, although it altered the bacterial profiles of the stomach and distal colon of 1-year-old mice. This change in colonic bacterial profiles may reflect a corresponding increase in the density of sulfomucin-containing goblet cells in sulfate-supplemented compared with control mice.

摘要

越来越多的证据表明,肠道硫酸盐还原菌(SRB)产生的硫化氢(H2S)可能参与了溃疡性结肠炎和结直肠癌等慢性疾病的发病机制。SRB的活性以及H2S的产生可能取决于肠道中含硫化合物的可用性。然而,关于饮食或无机硫酸盐对肠道硫酸盐和SRB衍生的H2S浓度的影响知之甚少。在本研究中,研究了给C3H/HeJBir小鼠短期(7天)和长期(1年)补充饮用水中的无机硫酸盐对胃肠道(GI)硫酸盐和H2S浓度(以及常驻SRB的活性)以及大肠含硫粘蛋白杯状细胞密度的影响。此外,基于PCR-变性梯度凝胶电泳(DGGE)的分子生态学技术被用于研究添加硫酸盐的饮用水对整个胃肠道微生物群落结构的影响。H2S的平均浓度范围为0.1 mM(胃)至1 mM(盲肠)。硫酸盐还原试验证明了整个胃肠道中H2S的原位产生,证实了SRB的存在。然而,H2S的产生和浓度在盲肠和结肠中最高。饮用水中添加硫酸盐并没有显著增加肠道硫酸盐或H2S的浓度,这表明无机硫酸盐不是肠道H2S浓度的重要调节剂,尽管它改变了1岁小鼠胃和远端结肠的细菌谱。与对照小鼠相比,补充硫酸盐的小鼠结肠细菌谱的这种变化可能反映了含硫粘蛋白杯状细胞密度的相应增加。

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