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標題: Cholesterol Depletion Reduces Entry of Campylobacter jejuni Cytolethal Distending Toxin and Attenuates Intoxication of Host Cells
作者: 蘇鴻麟
Lin, C.D.
Lai, C.K.
Lin, Y.H.
Hsieh, J.T.
Sing, Y.T.
Chang, Y.C.
Chen, K.C.
Wang, W.C.
Su, H.L.
Lai, C.H.
關鍵字: helicobacter-pylori vaca;intestinal epithelial-cells;actinobacillus-actinomycetemcomitans;lipid rafts;escherichia-coli;cycle arrest;signal-transduction;tumor-suppressor;membrane domains;cholera-toxin
Project: Infection and Immunity
期刊/報告no:: Infection and Immunity, Volume 79, Issue 9, Page(s) 3563-3575.
Campylobacter jejuni is a common cause of pediatric diarrhea worldwide. Cytolethal distending toxin, produced by Campylobacter jejuni, is a putative virulence factor that induces cell cycle arrest and apoptosis in eukaryotic cells. Cellular cholesterol, a major component of lipid rafts, has a pivotal role in regulating signaling transduction and protein trafficking as well as pathogen internalization. In this study, we demonstrated that cell intoxication by Campylobacter jejuni cytolethal distending toxin is through the association of cytolethal distending toxin subunits and membrane cholesterol-rich microdomains. Cytolethal distending toxin subunits cofractionated with detergent-resistant membranes, while the distribution reduced upon the depletion of cholesterol, suggesting that cytolethal distending toxin subunits are associated with lipid rafts. The disruption of cholesterol using methyl-beta-cyclodextrin not only reduced the binding activity of cytolethal distending toxin subunits on the cell membrane but also impaired their delivery and attenuated toxin-induced cell cycle arrest. Accordingly, cell intoxication by cytolethal distending toxin was restored by cholesterol replenishment. These findings suggest that membrane cholesterol plays a critical role in the Campylobacter jejuni cytolethal distending toxin-induced pathogenesis of host cells.
ISSN: 0019-9567
DOI: 10.1128/iai.05175-11
Appears in Collections:生命科學系所

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