Abstract
Aim: The aim of this study was to investigate whether cholesterol plays a pivotal role in cytolethal distending toxin (CDT) mediated pathogenic effects in hosts. Materials & methods: The molecular mechanisms underlying cholesterol sequestering conferred resistance to CDT-induced DNA double-strand breaks (DSBs) and cell cycle arrest were investigated. Histopathological analysis was conducted for evaluating CDT-induced intestinal inflammation in mouse. Results: CDT actions were attenuated by treatment of cells with methyl-β-cyclodextrin (MβCD). Severe intestinal inflammation induced by CDT treatment was observed in high-cholesterol diet-fed mice, but not in normal diet-fed mice, indicating that cholesterol is essential for CDT intoxication. Conclusion: Our findings demonstrate a molecular link between Campylobacter jejuni CDT and cholesterol, which is crucial to facilitate CDT-induced pathogenesis in hosts.
Original language | English |
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Pages (from-to) | 489-501 |
Number of pages | 13 |
Journal | Future Microbiology |
Volume | 10 |
Issue number | 4 |
DOIs | |
State | Published - 01 04 2015 |
Bibliographical note
Publisher Copyright:© 2015 Future Medicine Ltd.
Keywords
- Campylobacter jejuni
- DNA double-strand breaks
- cell cycle
- cholesterol
- cytolethal distending toxin