Cj1136 is required for lipooligosaccharide biosynthesis, hyperinvasion, and chick colonization by Campylobacter jejuni

  1. Get@NRC: Cj1136 is required for lipooligosaccharide biosynthesis, hyperinvasion, and chick colonization by Campylobacter jejuni (Opens in a new window)
DOIResolve DOI: http://doi.org/10.1128/IAI.00151-12
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Journal titleInfection and Immunity
Pages23612370; # of pages: 10
Subjectbile salt; deoxycholate sodium; lipooligosaccharide; polymyxin B; taurocholic acid; animal experiment; animal model; antibiotic resistance; antibiotic sensitivity; article; bacterial colonization; bacterial gene; bacterial mutation; bacterial virulence; bacterium adherence; Campylobacter jejuni; carbohydrate synthesis; cell invasion; chick; controlled study; enteritis; environmental stress; food poisoning; gene disruption; gene inactivation; host pathogen interaction; in vitro study; in vivo study; intestine epithelium cell; mutagenesis; nonhuman; priority journal; Animals; Campylobacter jejuni; Cell Line; Chickens; Disease Models, Animal; DNA Transposable Elements; Epithelial Cells; Galactosyltransferases; Gene Deletion; Genetic Complementation Test; Humans; Lipopolysaccharides; Mutagenesis, Insertional; Virulence Factors
AbstractCampylobacter jejuni is a major cause of bacterial food-borne enteritis worldwide, and invasion into intestinal epithelial cells is an important virulence mechanism. Recently we reported the identification of hyperinvasive C. jejuni strains and created a number of transposon mutants of one of these strains, some of which exhibited reduced invasion into INT-407 and Caco-2 cells. In one such mutant the transposon had inserted into a homologue of cj1136, which encodes a putative galactosyltransferase according to the annotation of the C. jejuni NCTC11168 genome. In the current study, we investigated the role of cj1136 in C. jejuni virulence, lipooligosaccharide (LOS) biosynthesis, and host colonization by targeted mutagenesis and complementation of the mutation. The cj1136 mutant showed a significant reduction in invasion into human intestinal epithelial cells compared to the wild-type strain 01/51. Invasion levels were partially restored on complementing the mutation. The inactivation of cj1136 resulted in the production of truncated LOS, while biosynthesis of a full-length LOS molecule was restored in the complemented strain. The cj1136 mutant showed an increase in sensitivity to the bile salts sodium taurocholate and sodium deoxycholate and significantly increased sensitivity to polymyxin B compared to the parental strain. Importantly, the ability of the mutant to colonize 1-day-old chicks was also significantly impaired. This study confirms that a putative galactosyltransferase encoded by cj1136 is involved in LOS biosynthesis and is important for C. jejuni virulence, as disruption of this gene and the resultant truncation of LOS affect both colonization in vivo and invasiveness in vitro. © 2012, American Society for Microbiology.
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AffiliationNational Research Council Canada (NRC-CNRC); NRC Institute for Biological Sciences (IBS-ISB)
Peer reviewedYes
NPARC number21269312
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Record identifierc16fe2a0-2c97-4571-89f5-474224ae1f91
Record created2013-12-12
Record modified2016-05-09
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