L-Fucose utilization provides Campylobacter jejuni with a competitive advantage

Campylobacter jejuni is a prevalent gastrointestinal pathogen in humans and a common commensal of poultry. When colonizing its hosts, C. jejuni comes into contact with intestinal carbohydrates, including L-fucose, released from mucin glycoproteins. Several strains of jejuni possess a genomic island...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2011-04, Vol.108 (17), p.7194-7199
Main Authors: Stahl, Martin, Friis, Lorna M., Nothaft, Harald, Liu, Xin, Li, Jianjun, Szymanski, Christine M., Stintzi, Alain, Cossart, Pascale
Format: Article
Language:English
Subjects:
Animal models
Animals
Bacteria
Biochemical pathways
Biological Sciences
Campylobacter
Campylobacter Infections - genetics
Campylobacter Infections - metabolism
Campylobacter Infections - microbiology
Campylobacter jejuni
Campylobacter jejuni - genetics
Campylobacter jejuni - growth & development
Campylobacter jejuni - metabolism
Carbohydrates
Cell growth
Colonization
Commensals
fucose
Fucose - metabolism
Fucose - pharmacology
Genomic Islands
Genomics
Glycoproteins
Gram-negative bacteria
Humans
Intestine
Islands
L-fucose
Membrane transport proteins
Metabolic pathways
Microbial colonization
mucin
Mucins
Mutation
Pathogens
permease
Polysaccharides
Poultry
Poultry - microbiology
Poultry Diseases - genetics
Poultry Diseases - metabolism
Poultry Diseases - microbiology
Statistical significance
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Summary:Campylobacter jejuni is a prevalent gastrointestinal pathogen in humans and a common commensal of poultry. When colonizing its hosts, C. jejuni comes into contact with intestinal carbohydrates, including L-fucose, released from mucin glycoproteins. Several strains of jejuni possess a genomic island (cj0480c-cj0490) that is up-regulated in the presence of both L-fucose and mucin and allows for the utilization of L-fucose as a substrate for growth. Strains possessing this genomic island show increased growth in the presence of L-fucose and mutation of cj0481, cj0486, and cj0487 results in the loss of the ability to grow on this substrate. Furthermore, mutants in the putative fucose permease (cj0486) are deficient in fucose uptake and demonstrate a competitive disadvantage when colonizing the piglet model of human disease, which is not paralleled in the colonization of poultry. This identifies a previously unrecorded metabolic pathway in select strains of C. jejuni associated with a virulent lifestyle.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.1014125108