Table 2.

Bacteria and DNA damage.

Bacteria	Effects on Host’s DNA Repair
Helicobacter pylori	The infection causes a systematic reduction in DNA repair capacities by downregulating 58 genes more than two-fold (such as NBS1, ATR, MLH1, and TP53) [161]; The infection results in ROS and RNS production leading to a number of gastric diseases [162,163]; The infection is associated with increased γH2AX expression, and γH2AX was found to correlate with a number of clinicopathological characteristics in GC tissues infected by H. pylori [164]; Type IV secretion system protein complex interacts with host cell integrin β1, eventually resulting in NF-κB activation and subsequent recruitment of XPG and XPF [165,166]; Cag mediates NF-κB activation leading to aberrant expression of activation-induced cytidine deaminase AID [167,168].
Listeria monocytogenes	It causes nucleotide pool depletion to support its own replication and growth, leading to replication fork stalling and, consequently, DNA breaks [169].
Escherichia coli, Gram-negative bacteria, Shigella dysenteriae and Neisseria gonorrhoeae	They all produce toxins that cause DNA lesions [170], potentially resulting in genome instability, tumor initiation and progression: Colibactin (E. coli) [171], Cytolethal distending toxin (CDT) (Gram-negative bacteria) [172], Shiga toxin (S. dysenteriae) [173,174,175] Endonucleases (N. gonorrhoeae) [176,177,178].
Mycoplasma fermentans	DnaK hampered PARylation activity of PARP1 upon DNA damage [179,180]; DnaK co-immunoprecipitates with USP10, thus impairing p53-dependent anti-cancer functions, resulting in reduced efficacy of anti-cancer drugs that depend on p53 activation to exert their effect [180].