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饮食选择会影响产志贺毒素大肠杆菌(STEC)O157:H7 的定植和疾病。

Dietary choice affects Shiga toxin-producing Escherichia coli (STEC) O157:H7 colonization and disease.

机构信息

Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814-4799, USA.

出版信息

Proc Natl Acad Sci U S A. 2013 Jun 4;110(23):E2126-33. doi: 10.1073/pnas.1222014110. Epub 2013 May 20.

Abstract

The likelihood that a single individual infected with the Shiga toxin (Stx)-producing, food-borne pathogen Escherichia coli O157:H7 will develop a life-threatening sequela called the hemolytic uremic syndrome is unpredictable. We reasoned that conditions that enhance Stx binding and uptake within the gut after E. coli O157:H7 infection should result in greater disease severity. Because the receptor for Stx, globotriaosylceramide, is up-regulated in the presence of butyrate in vitro, we asked whether a high fiber diet (HFD) that reportedly enhances butyrate production by normal gut flora can influence the outcome of an E. coli O157 infection in mice. To address that question, groups of BALB/c mice were fed high (10%) or low (2%) fiber diets and infected with E. coli O157:H7 strain 86-24 (Stx2+). Mice fed an HFD exhibited a 10- to 100-fold increase in colonization, lost 15% more body weight, exhibited signs of morbidity, and had 25% greater mortality relative to the low fiber diet (LFD)-fed group. Additionally, sections of intestinal tissue from HFD-fed mice bound more Stx1 and expressed more globotriaosylceramide than did such sections from LFD-fed mice. Furthermore, the gut microbiota of HFD-fed mice compared with LFD-fed mice contained reduced levels of native Escherichia species, organisms that might protect the gut from colonization by incoming E. coli O157:H7. Taken together, these results suggest that susceptibility to infection and subsequent disease after ingestion of E. coli O157:H7 may depend, at least in part, on individual diet and/or the capacity of the commensal flora to produce butyrate.

摘要

单个感染产志贺毒素(Stx)的食源性病原体大肠杆菌 O157:H7 的个体是否会发展为危及生命的后遗症——溶血性尿毒症综合征是不可预测的。我们推断,在大肠杆菌 O157:H7 感染后,增强 Stx 在肠道内的结合和摄取的条件应该会导致更严重的疾病。因为 Stx 的受体——神经节苷脂,在体外存在丁酸盐的情况下会被上调,所以我们想知道,高纤维饮食(HFD)是否能通过增加正常肠道菌群的丁酸盐产生来影响小鼠的大肠杆菌 O157 感染结果。为了回答这个问题,我们将一组 BALB/c 小鼠分别用高(10%)或低(2%)纤维饮食喂养,并感染大肠杆菌 O157:H7 菌株 86-24(Stx2+)。用 HFD 喂养的小鼠定植增加了 10-100 倍,体重减轻了 15%,出现了病态迹象,死亡率比低纤维饮食(LFD)喂养组高 25%。此外,与 LFD 喂养组相比,HFD 喂养组的肠道组织切片结合了更多的 Stx1,表达了更多的神经节苷脂。此外,与 LFD 喂养组相比,HFD 喂养组的肠道微生物群中本土大肠杆菌属的水平降低,这些生物体可能会保护肠道免受进入的大肠杆菌 O157:H7 的定植。综上所述,这些结果表明,摄入大肠杆菌 O157:H7 后的感染易感性和随后的疾病可能至少部分取决于个体饮食和/或共生菌群产生丁酸盐的能力。

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