Vitamin A-Deficient Hosts Become Nonsymptomatic Reservoirs of Escherichia coli-Like Enteric Infections
Vitamin A-Deficient Hosts Become Nonsymptomatic Reservoirs of Escherichia coli-Like Enteric Infections
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DOI：
10.1128/iai.00201-15
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发表时间：
2015-07-01
影响因子：
3.1
通讯作者：
Cantorna, Margherita T.
中科院分区：
文献类型：
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作者：
McDaniel, Kaitlin L.;Restori, Katherine H.;Cantorna, Margherita T.
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，并与感染易感性增加有关。用轮状柠檬酸杆菌模拟人的大肠杆菌感染。A(-)小鼠发生了严重和致命的感染(40%)。维生素A充足(A(+))的小鼠存活下来，并在第25天清除了感染。在感染高峰期用维甲酸治疗A(-)小鼠，在16天内消除了轮状芽胞杆菌。尽管A(-)小鼠在第37天仍被感染，但A(+)和A(-)小鼠之间的炎症水平没有差异。A(-)小鼠死亡率的增加不是由于全身性细胞因子的产生，不能清除全身性轮状芽胞杆菌，也不是由于致病性增加。相反，A(-)小鼠出现了严重的肠道感染，大多数A(-)小鼠存活并消退了炎症，但没有消除感染。维生素A状况的改善可能会降低对肠道病原体的易感性，并防止潜在的携带者将感染传播到易感人群。
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.