Abstract
Bacterial genotoxins are unique among bacterial toxins as their molecular target is DNA. The consequence of intoxication or infection is induction of DNA breaks that, if not properly repaired, results in irreversible cell cycle arrest (senescence) or death of the target cells. At present, only three bacterial genotoxins have been identified. Two are protein toxins: the cytolethal distending toxin (CDT) family produced by a number of Gram-negative bacteria and the typhoid toxin produced by Salmonella enterica serovar Typhi. The third member, colibactin, is a peptide-polyketide genotoxin, produced by strains belonging to the phylogenetic group B2 of Escherichia coli. This review will present the cellular effects of acute and chronic intoxication or infection with the genotoxins-producing bacteria. The carcinogenic properties and the role of these effectors in the context of the host-microbe interaction will be discussed. We will further highlight the open questions that remain to be solved regarding the biology of this unusual family of bacterial toxins.
Highlights
Cells of our body are exposed to several physical (UV, X-rays) and numerous chemical agents that promote DNA damage
The first bacterial toxin shown to induce DNA single strand (SSBs) and double strand (DSBs) breaks is the family of the cytolethal distending toxins (CDTs) [2,3], which are produced by several Gram negative bacteria, such as Escherichia coli, Aggregatibacter actinomycetemcomitans, Haemophilus ducreyi, Shigella dysenteriae, Campylobacter sp., and Helicobacter sp
Regarding the type of DNA damage induced by CDTs, a detailed kinetic analysis has been performed by Fedor and colleagues who demonstrated that low doses of the E. coli CDT-I (50 pg/mL) induce SSBs from 3 h–6 h post-intoxication
Summary
Cells of our body are exposed to several physical (UV, X-rays) and numerous chemical agents that promote DNA damage. The latter includes reactive oxygen species (ROS) produced by our own cellular. Biomolecules 2015, 5 metabolism or as a consequence of acute and chronic infections [1] To this long list, we need to add a new category of effectors, namely bacterial genotoxins. Helicobacter pylori [10] promote DNA damage in a ROS-independent manner. The role of these effectors in the context of bacterial-associated carcinogenesis and infection/colonization will be discussed
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