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空肠弯曲菌可结合肠道H(O)抗原(岩藻糖α1,2-半乳糖β1,4-N-乙酰葡糖胺),而人乳中的岩藻糖基低聚糖可抑制其结合及感染。

Campylobacter jejuni binds intestinal H(O) antigen (Fuc alpha 1, 2Gal beta 1, 4GlcNAc), and fucosyloligosaccharides of human milk inhibit its binding and infection.

作者信息

Ruiz-Palacios Guillermo M, Cervantes Luz Elena, Ramos Pilar, Chavez-Munguia Bibiana, Newburg David S

机构信息

Department of Infectious Diseases, National Institute of Medical Sciences and Nutrition, Vasco de Quiroga 15, Mexico D. F. 14000, Mexico.

出版信息

J Biol Chem. 2003 Apr 18;278(16):14112-20. doi: 10.1074/jbc.M207744200. Epub 2003 Jan 31.

Abstract

The most common cause of infant mortality is diarrhea; the most common cause of bacterial diarrhea is Campylobacter jejuni, which is also the primary cause of motor neuron paralysis. The first step in campylobacter pathogenesis is adherence to intestinal mucosa. We found that such binding was inhibited in vitro by human milk and, with high avidity, by alpha1,2-fucosylated carbohydrate moieties containing the H(O) blood group epitope (Fuc alpha 1,2Gal beta 1,4GlcNAc em leader ). In studies on the mechanism of adherence, campylobacter, which normally does not bind to Chinese hamster ovary cells, bound avidly when the cells were transfected with a human alpha1,2-fucosyltransferase gene that caused overexpression of H-2 antigen; binding was specifically inhibited by H-2 ligands (lectins Ulex europaeus and Lotus tetragonolobus and H-2 monoclonal antibody), H-2 mimetics, and human milk oligosaccharides. Human milk oligosaccharides inhibited campylobacter colonization of mice in vivo and human intestinal mucosa ex vivo. Campylobacter colonization of nursing mouse pups was inhibited if their dams had been transfected with a human alpha1,2-fucosyltransferase gene that caused expression of H(O) antigen in milk. We conclude that campylobacter binding to intestinal H-2 antigen is essential for infection. Milk fucosyloligosaccharides and specific fucosyl alpha1,2-linked molecules inhibit this binding and may represent a novel class of antimicrobial agents.

摘要

婴儿死亡的最常见原因是腹泻;细菌性腹泻的最常见病因是空肠弯曲菌,它也是运动神经元麻痹的主要病因。弯曲菌致病的第一步是黏附于肠黏膜。我们发现,人乳在体外可抑制这种黏附,而含有H(O)血型抗原表位的α1,2-岩藻糖基化碳水化合物部分(Fucα1,2Galβ1,4GlcNAc前导序列)则能高效抑制。在关于黏附机制的研究中,正常情况下不与中国仓鼠卵巢细胞结合的弯曲菌,当细胞转染了人α1,2-岩藻糖基转移酶基因并导致H-2抗原过表达时,会强烈结合;H-2配体(lectins Ulex europaeus和Lotus tetragonolobus以及H-2单克隆抗体)、H-2模拟物和人乳寡糖可特异性抑制这种结合。人乳寡糖在体内可抑制弯曲菌在小鼠体内的定植,在体外可抑制其在人肠黏膜上的定植。如果给哺乳的小鼠幼崽的母鼠转染人α1,2-岩藻糖基转移酶基因,使其乳汁中表达H(O)抗原,则可抑制弯曲菌在小鼠幼崽体内的定植。我们得出结论,弯曲菌与肠道H-2抗原的结合对于感染至关重要。乳岩藻糖基寡糖和特定的α1,2-连接的岩藻糖基分子可抑制这种结合,可能代表一类新型抗菌剂。

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