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维生素A缺乏的宿主成为大肠杆菌样肠道感染的无症状储存宿主。

Vitamin A-Deficient Hosts Become Nonsymptomatic Reservoirs of Escherichia coli-Like Enteric Infections.

作者信息

McDaniel Kaitlin L, Restori Katherine H, Dodds Jeffery W, Kennett Mary J, Ross A Catharine, Cantorna Margherita T

机构信息

Department of Veterinary and Biomedical Science, The Pennsylvania State University, University Park, Pennsylvania, USA Pathobiology Graduate Program, The Pennsylvania State University, University Park, Pennsylvania, USA.

McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada.

出版信息

Infect Immun. 2015 Jul;83(7):2984-91. doi: 10.1128/IAI.00201-15. Epub 2015 May 11.

DOI:10.1128/IAI.00201-15
PMID:25964475
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4468526/
Abstract

Vitamin A deficiency (A(-)) remains a public health concern in developing countries and is associated with increased susceptibility to infection. Citrobacter rodentium was used to model human Escherichia coli infections. A(-) mice developed a severe and lethal (40%) infection. Vitamin A-sufficient (A(+)) mice survived and cleared the infection by day 25. Retinoic acid treatment of A(-) mice at the peak of the infection eliminated C. rodentium within 16 days. Inflammation levels were not different between A(+) and A(-) mouse colons, although the A(-) mice were still infected at day 37. Increased mortality of A(-) mice was not due to systemic cytokine production, an inability to clear systemic C. rodentium, or increased pathogenicity. Instead, A(-) mice developed a severe gut infection with most of the A(-) mice surviving and resolving inflammation but not eliminating the infection. Improvements in vitamin A status might decrease susceptibility to enteric pathogens and prevent potential carriers from spreading infection to susceptible populations.

摘要

维生素A缺乏症(A(-))在发展中国家仍然是一个公共卫生问题,并且与感染易感性增加有关。鼠柠檬酸杆菌被用于模拟人类大肠杆菌感染。A(-)小鼠发生了严重的致死性(40%)感染。维生素A充足(A(+))的小鼠存活下来,并在第25天时清除了感染。在感染高峰期用视黄酸治疗A(-)小鼠,可在16天内清除鼠柠檬酸杆菌。A(+)和A(-)小鼠结肠的炎症水平没有差异,尽管A(-)小鼠在第37天时仍被感染。A(-)小鼠死亡率增加并非由于全身性细胞因子产生、无法清除全身性鼠柠檬酸杆菌或致病性增加。相反,A(-)小鼠发生了严重的肠道感染,大多数A(-)小鼠存活并解决了炎症,但并未消除感染。改善维生素A状况可能会降低对肠道病原体的易感性,并防止潜在携带者将感染传播给易感人群。

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本文引用的文献

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Citrobacter rodentium: infection, inflammation and the microbiota.柠檬酸杆菌感染:感染、炎症与微生物组。
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Th22 cells are an important source of IL-22 for host protection against enteropathogenic bacteria.辅助性 T 细胞 22(Th22)是宿主抵抗肠道致病菌的重要 IL-22 来源。
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Colonic microbiota alters host susceptibility to infectious colitis by modulating inflammation, redox status, and ion transporter gene expression.肠道微生物群通过调节炎症、氧化还原状态和离子转运体基因表达改变宿主对感染性结肠炎的易感性。
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