Campylobacter jejuni cocultured with epithelial cells reduces surface capsular polysaccharide expression.
Authors
Corcionivoschi, NClyne, M
Lyons, A
Elmi, A
Gundogdu, O
Wren, B W
Dorrell, N
Karlyshev, A V
Bourke, B
Affiliation
The Children's Research Centre, Our Lady's Children's Hospital, Crumlin, Dublin, 12, Ireland.Issue Date
2012-02-01T10:24:21ZMeSH
Campylobacter jejuni/*physiologyCell Line
Coculture Techniques
Culture Media, Conditioned
Epithelial Cells/*microbiology
Gene Expression Profiling
Humans
Oligonucleotide Array Sequence Analysis
Polysaccharides, Bacterial/*biosynthesis
Metadata
Show full item recordCitation
Infect Immun. 2009 May;77(5):1959-67. Epub 2009 Mar 9.Journal
Infection and immunityDOI
10.1128/IAI.01239-08PubMed ID
19273563Abstract
The host cell environment can alter bacterial pathogenicity. We employed a combination of cellular and molecular techniques to study the expression of Campylobacter jejuni polysaccharides cocultured with HCT-8 epithelial cells. After two passages, the amount of membrane-bound high-molecular-weight polysaccharide was considerably reduced. Microarray profiling confirmed significant downregulation of capsular polysaccharide (CPS) locus genes. Experiments using conditioned media showed that sugar depletion occurred only when the bacterial and epithelial cells were cocultured. CPS depletion occurred when C. jejuni organisms were exposed to conditioned media from a different C. jejuni strain but not when exposed to conditioned media from other bacterial species. Proteinase K or heat treatment of conditioned media under coculture conditions abrogated the effect on the sugars, as did formaldehyde fixation and cycloheximide treatment of host cells or chloramphenicol treatment of the bacteria. However, sugar depletion was not affected in flagellar export (fliQ) and quorum-sensing (luxS) gene mutants. Passaged C. jejuni showed reduced invasiveness and increased serum sensitivity in vitro. C. jejuni alters its surface polysaccharides when cocultured with epithelial cells, suggesting the existence of a cross talk mechanism that modulates CPS expression during infection.Language
engISSN
1098-5522 (Electronic)0019-9567 (Linking)
ae974a485f413a2113503eed53cd6c53
10.1128/IAI.01239-08