Open AccessCampylobacter jejuniCytolethal Distending Toxin Promotes DNA Repair Responses in Normal Human Cells
Author(s) -
Duane C. Hassane,
Robert B. Lee,
Carol L. Pickett
Publication year - 2003
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.71.1.541-545.2003
Subject(s) - cytolethal distending toxin , biology , campylobacter jejuni , rad50 , dna damage , dna repair , microbiology and biotechnology , cell cycle , toxin , dna , cell , programmed cell death , campylobacter , apoptosis , bacteria , microbial toxins , genetics , gene , dna binding protein , transcription factor
Cytolethal distending toxin (CDT) is a multisubunit protein found in various gram-negative bacterial pathogens of humans which is thought to cause cell death by direct DNA damage of host cells. We sought to determine if a cellular response to DNA damage could be detected by exogenous addition of the holotoxin. Exogenous addition of the Campylobacter jejuni 81-176 CDT to primary human fibroblasts resulted in formation of Rad50 foci, which are formed around double-stranded-DNA breaks. Moreover, such foci are formed in both proliferating and nonproliferating cells that are treated with C. jejuni CDT. Fibroblasts that were intoxicated and later stimulated to proliferate failed to divide and remained arrested in the G(1) phase of the cell cycle.