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

Gastrointestinal and microbial responses to sulfate-supplemented drinking water in mice
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DOI:
10.1177/153537020322800413
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发表时间:
2003-04-01
影响因子:
3.2
通讯作者:
Gaskins, HR
Gaskins, HR
中科院分区:
医学4区
文献类型:
--
作者:
DePlancke, B;Finster, K;Gaskins, HR

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越来越多的证据表明,由肠道硫酸盐还原细菌(SRB)产生的硫化氢(H2S)可能参与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,以及由此产生的硫化氢,很可能取决于肠道中含硫化合物的可用性。然而,关于饲料或无机硫酸盐对肠道硫酸盐和SRB来源的H_2S浓度的影响,人们知之甚少。本研究观察了短期(7天)和长期(11年)补充无机硫酸盐对C3H/HeJBir小鼠胃肠(GI)硫酸盐和H_2S浓度(以及驻留SRB活性)和大肠含硫粘蛋白杯状细胞密度的影响。此外,基于聚合酶链式反应-变性梯度凝胶电泳(DGGE)的分子生态学技术被用来检测硫酸盐修饰的饮用水对整个胃肠道微生物群落结构的影响。H_2S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在整个胃肠道内原位产生了硫化氢,证实了SRB的存在。然而,盲肠和结肠中硫化氢的生成量和浓度最大。补充饮用水中的硫酸盐没有显著增加肠道硫酸盐或硫化氢的浓度,这表明无机硫酸盐并不是肠道硫化氢浓度的重要调节剂,尽管它改变了1岁小鼠胃和远端结肠的细菌分布。结肠细菌图谱的这种变化可能反映了与对照组相比,添加硫酸盐的小鼠含硫粘蛋白的杯状细胞密度相应增加。
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 (11 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.