Abstract
During infection, bacterial pathogens successfully sense, respond and adapt to a myriad of harsh environments presented by the mammalian host. This exquisite level of adaptation requires a robust modulation of their physiological and metabolic features. Additionally, virulence determinants, which include host invasion, colonization and survival despite the host's immune responses and antimicrobial therapy, must be optimally orchestrated by the pathogen at all times during infection. This can only be achieved by tight coordination of gene expression. A large body of evidence implicate the prolific roles played by bacterial regulatory RNAs in mediating gene expression both at the transcriptional and post-transcriptional levels. This review describes mechanistic and regulatory aspects of bacterial regulatory RNAs and highlights how these molecules increase virulence efficiency in human pathogens. As illustrative examples, Staphylococcus aureus, Listeria monocytogenes, the uropathogenic strain of Escherichia coli, Helicobacter pylori, and Pseudomonas aeruginosa have been selected.
Highlights
Numerous bacterial species are infamous for their role in causing human diseases (Kusters et al, 2006; Gellatly and Hancock, 2013; Dayan et al, 2016; Terlizzi et al, 2017; Radoshevich and Cossart, 2018)
One major function of bacterial toxicity is to kill surveilling immune cells such as neutrophils. While this is an immune-evading mechanism employed by pathogenic bacteria, the proteins constituting these toxins and their delivery conduits are highly immunostimulatory (Miao et al, 2010; Gall-Mas et al, 2018)
Pathogenic bacteria cannot afford to constitutively express toxin genes but must modulate their expression according to the site and stage of the infection
Summary
Numerous bacterial species are infamous for their role in causing human diseases (Kusters et al, 2006; Gellatly and Hancock, 2013; Dayan et al, 2016; Terlizzi et al, 2017; Radoshevich and Cossart, 2018) These bacterial pathogens possess certain key distinguishing features. One major function of bacterial toxicity is to kill surveilling immune cells such as neutrophils (do Vale et al, 2016) While this is an immune-evading mechanism employed by pathogenic bacteria, the proteins constituting these toxins and their delivery conduits are highly immunostimulatory (Miao et al, 2010; Gall-Mas et al, 2018). Pathogenic bacteria cannot afford to constitutively express toxin genes but must modulate their expression according to the site and stage of the infection
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