Escherichia coli: Physiological Clues Which Turn On the Synthesis of Antimicrobial Molecules

Abstract

Zoonotic pathogens, like Shiga toxin-producing Escherichia coli (STEC) are a food safety and health risk. To battle the increasing emergence of virulent microbes, novel mitigation strategies are needed. One strategy being considered to combat pathogens is antimicrobial compounds produced by microbes, coined microcins. However, effectors for microcin production are poorly understood, particularly in the context of complex physiological responses along the gastro-intestinal tract (GIT). Previously, we identified an E. coli competitor capable of producing a strong diffusible antimicrobial with microcin-associated characteristics. Our objective was to examine how molecule production of this competitor is affected by physiological properties associated with the GIT, namely the effects of carbon source, bile salt concentration and growth phase. Using previously described liquid- and agar-based assays determined that carbon sources do not affect antimicrobial production of E. coli O103F. However, bile salt concentrations affected production significantly, suggesting that E. coli O103F uses cues along the GIT to modulate the expression of antimicrobial production. Furthermore, E. coli O103F produces the molecule during the exponential phase, contrary to most microcins identified to date. The results underscored the importance of experimental design to identify producers of antimicrobials. To detect antimicrobials, conventional microbiological methods can be a starting point, but not the gold standard.

Bacterial and Viral Co-Infection in the Intestine: Competition Scenario and Their Effect on Host Immunity

“…On the one hand, enteric bacteria may also assist a wide range of enteroviruses in infections, e.g., many enteric bacteria improve PV miscibility efficiency and fitness by promoting viral DNA recombination [46]; certain polysaccharides and lipids on the surface of enteric bacteria can improve the thermal stability of some enteric viruses [10]. On the other hand, enteric bacteria can inhibit viral infection, e.g., Salmonella inhibits NoV replication in mouse macrophages [45]; the bacteriocin CRL35 (ECRL) secreted by E. faecalis inhibits the synthesis of viral glycoproteins necessary for viral infection and replication [47]; the presence of microbacteriocins with antiviral activity in bacterial supernatants significantly reduces viral titers in vitro [48].…”