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Published on: October 22, 2013
Campylobacter jejuni cocultured with epithelial cells reduces surface capsular polysaccharide expression
N Corcionivoschi1, M Clyne, A Lyons
1The Children's Research Centre, Our Lady's Children's Hospital, Crumlin, Dublin 12, Ireland.
Campylobacter jejuni reduces its surface polysaccharides when interacting with human epithelial cells. This bacterial adaptation impacts pathogenicity, suggesting a communication mechanism during infection.
Area of Science:
- Microbiology
- Cell Biology
- Infectious Diseases
Background:
- The host cell environment significantly influences bacterial pathogenicity.
- Understanding host-pathogen interactions is crucial for controlling infections.
Purpose of the Study:
- To investigate the impact of epithelial cell coculture on Campylobacter jejuni polysaccharide expression.
- To elucidate the mechanisms underlying changes in bacterial surface polysaccharides.
Main Methods:
- Coculture of Campylobacter jejuni with HCT-8 epithelial cells.
- Analysis of polysaccharide expression using cellular and molecular techniques, including microarray profiling.
- Experiments with conditioned media and various treatments (Proteinase K, heat, formaldehyde, cycloheximide, chloramphenicol).
Main Results:
- Coculture led to a significant reduction in membrane-bound high-molecular-weight polysaccharide and downregulation of capsular polysaccharide (CPS) locus genes.
- Sugar depletion was dependent on direct bacterial-epithelial cell coculture and specific to C. jejuni-derived conditioned media.
- The effect was abrogated by treatments targeting proteins or host cell viability, but not by mutations in fliQ or luxS genes.
- Passaged C. jejuni exhibited reduced invasiveness and increased serum sensitivity.
Conclusions:
- Campylobacter jejuni actively alters its surface polysaccharides in response to epithelial cell contact.
- A cross-talk mechanism between bacteria and host cells modulates CPS expression.
- These alterations in polysaccharide expression likely contribute to changes in bacterial pathogenicity during infection.
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