Toxin-Antitoxin Systems in Pathogenic Bacteria

Dear Colleagues,

Bacterial toxin–antitoxin (TA) systems, which are ubiquitously present in bacterial genomes, are not essential for normal cell proliferation. The TAs regulate fundamental cellular processes, facilitate survival under stress conditions, have essential roles in persistence and virulence, and represent potential therapeutic targets. These genetic TA loci are also shown to be involved in the maintenance of successful multidrug-resistant mobile genetic elements. TA systems encode a labile antitoxin and its stable toxin; degradation of the antitoxin renders a free toxin, which is bacteriostatic by nature. A free toxin generates a reversible state with low metabolic activity (quiescence) by affecting important functions of bacterial cells such as transcription, translation, DNA replication, replication and cell–wall synthesis, biofilm formation, phage predation, the regulation of nucleotide pool, etc., whereas antitoxins are toxin inhibitors. Under stress conditions, the TA systems might form networks. Understanding the basis of the unique response of TAs to stress, the prime causes for the emergence of drug-resistant strains, and their contribution to therapy failure and development of chronic and recurrent infections are necessary to grasp how TAs contribute to the mechanisms of phenotypic heterogeneity and pathogenesis that will enable the development of rational development of new treatment for infections caused by pathogens.

Prof. Dr. Juan Carlos Alonso
Guest Editor

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