**4.** *E. coli* **virulence**

The species *E. coli* encompasses commensals of the gut, pathogens and probiotics. Conditions conducive to SOS induction are encountered by *E. coli* at various host anatomical sites. Recently, the SOS response has been shown to play a vital role in maintaining colonization of the murine gut by commensal *E. coli.* Competing commensal organisms could be a source of genotoxic stress [12].

Pathogenic *E. coli* strains producing virulence factors such as adhesins, iron uptake systems, capsules, toxins and invasins, can provoke infections [36]. Pathogenic strains are broadly classified into two major groups, with regard to their virulence factors and diseases they provoke, the nondiarrheagenic and diarrheagenic. The nondiarrheagenic are designated extraintestinal pathogenic *E. coli* (ExPEC) while diarrheagenic provoke diarrhea and include the Shiga toxin (Stx) producing *E. coli* (STEC) as well as enterohemorrhagic *E. coli* (EHEC) [37].

Among ExPEC infections, the most common are urinary tract infections (UTI) followed by septicaemia and meningitis [36, 38].

UTIs represent a serious worldwide health problem [39] with uropathogenic *E. coli* strains (UPEC) responsible for 75–95% of community-acquired UTIs [40].

To provoke UTI, UPEC undergo a complex intracellular cycle [41] and the SOS response plays an important role in bacterial dissemination and persistence within the urinary tract. UPEC enter the urinary tract through an ascending route and travel up the urethra to colonize the bladder via internalization by the umbrella cells. Infected cells produce nitric oxide that attacks bacterial DNA, inducing the SOS response with inhibition of cell division and UPEC filamentation. Filamentous UPEC successfully resist phagocyte killing, allowing dissemination and persistence

#### *The* Escherichia coli *SOS Response: Much More than DNA Damage Repair DOI: http://dx.doi.org/10.5772/intechopen.100353*

within the urinary tract. UTI frequently lead to chronic infection and a persister subpopulation could be responsible for generating relapsing infections [42].

In the intestinal tract, DNA damage and subsequent SOS induction, can be provoked by host factors, e.g. bile salts, and by competing microbes. Intestinal inflammation triggered by infection or the gut immune system involving ROS, also induces the SOS response.

All EHEC strains, including the notorius serotype O157;H7, produce Stx the main virulence factor associated with hemorrhagic colitis [37].

Production of Stx, by O157:H7 is mediated by quorum sensing [43] however, it is also well documented that the SOS response amplifies Shiga toxin production in enterohemorrhagic *E. coli* (EHEC). Stx is encoded on a lambdoid prophage. Induction of the prophage, via repressor autocleavage, and the subsequent upregulation of *stx* expression are controlled by the SOS response [25]. Therefore, DNA-damaging agents, including certain antibiotics, increase Stx synthesis and are counterindicated during treatment of infection [44]. In addition to SOS inducing antibiotics, bacteriocins and microcins secreted by members of the gut microbiota have been shown to amplify Stx synthesis. In the complex intestinal environment, survival involves competition for space and nutrients [45, 46]. Bacteria have therefore evolved mechanisms to counteract competitors [47] such as, production of bacteriocins, proteinaceous toxins, that inhibit growth and survival of usually closely related bacteria competing for similar resources [48]. A subtype of bacteriocins, known as colicins, are produced by *Enterobacteriaceae* while microcins are bacteriocins that are generally smaller than 10 kDa [49].

Thus, a strain producing the nuclease colicin E9 (ColE9) as well as extracted DNase colicins were shown to induce Stx [50]. Recently, microcin B17 (MccB17), a DNA gyrase inhibitor, as well as a putative microcin, were also shown to amplify Stx2a production [51, 52]. Thus in the gut, nonpathogenic *E. coli* strains could, via secretion of DNA damaging colicins and microcins, increase Stx production by O157:H7.

In addition to DNA damage induced by host factors, e.g. bile salts, and by competing microbes, intestinal inflammation triggered by infection or the gut immune system involving ROS, also provokes the SOS response and dysbiosis, suppressing anaerobes and inciting *Enterobacteriaceae* overgrowth with competition for nutrients [53].
