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J. Biol. Chem., Vol. 278, Issue 16, 14112-14120, April 18, 2003
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From the 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
Campylobacter jejuni Binds Intestinal H(O) Antigen
(Fuc
1, 2Gal
1, 4GlcNAc), and Fucosyloligosaccharides of Human Milk
Inhibit Its Binding and Infection*
§,,,
Department of Infectious Diseases, National
Institute of Medical Sciences and Nutrition, Vasco de Quiroga 15, Mexico D. F. 14000, Mexico, the ¶ Department of Experimental
Pathology, Centro de Investigacion y Estudios Avanzados, I. P. N.,
Av. Instituto Politecnico Nacional 2508, Mexico D. F. 07360, Mexico,
and the Program in Glycobiology, Shriver Center, University
of Massachusetts Medical School, Waltham, Massachusetts 02452
1,2-fucosylated carbohydrate moieties containing the H(O) blood
group epitope (Fuc1,2Gal
1,4GlcNAc ... ). 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 1,2-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 1,2-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 1,2-linked molecules
inhibit this binding and may represent a novel class of antimicrobial agents.
*
This work was supported by National Institutes of Health
Grant HD13021, by National Council for Science and Technology (Conacyt) (Mexico) Grant 1428, and a fellowship from Conacyt (to
L. E. C.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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