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Bacterial toxin–antitoxin (TA) systems, which are ubiquitously present in bacterial genomes, are not essential for normal cell proliferation. The TA systems regulate fundamental cellular processes, facilitate survival under stress conditions, have essential roles in 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. The TA systems are classified as types I to VI, according to the nature of the antitoxin and to the mode of toxin inhibition. Type II 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. To understand the basis of the unique response of TA systems to stress, the prime causes of the emergence of drug-resistant strains, and their contribution to therapy failure and the development of chronic and recurrent infections, must be known in order to grasp how TA systems contribute to the mechanisms of phenotypic heterogeneity and pathogenesis that will enable the rational development of new treatments for infections caused by pathogens.

tuberculosis --- toxin-antitoxin systems --- bacterial cell death --- NAD+ --- stress-response --- toxin–antitoxin system --- mazF --- type II --- toxin --- mRNA interferase --- X-ray crystallography --- cognate interactions --- cross-interactions --- molecular insulation --- antitoxin --- TA systems --- addiction --- anti-addiction --- type I toxin–antitoxin system --- small protein toxin structure --- Fst/Ldr family --- toxin–antitoxin --- M. tuberculosis --- bacteria --- pathogenesis --- protein–protein interactions --- cross-talk --- protein interface --- tolerance --- persistence --- cross-resistance --- toxin-antitoxin system --- PemI/PemK --- Klebsiella pneumoniae --- toxin–antitoxin systems --- toxin activation --- antibacterial agents --- bacterial persistence --- Stenotrophomonas maltophilia --- opportunistic pathogen --- clinical origin --- environmental origin --- biofilm --- antibiotic resistance --- cell wall inhibition --- nucleotide hydrolysis --- uridine diphosphate-N-acetylglucosamine --- n/a --- type I toxin-antitoxin system --- toxin-antitoxin --- protein-protein interactions

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Staphylococcus aureus is a common inhabitant of the human body with which we co-exist. However, this species can also cause disease in humans when an appropriate opportunity arises, such as a cut or some other breakdown in our body’s defenses. S. aureus is able to initiate infections due, in part, to the diverse group of toxins that they secrete. The exotoxins produced by S. aureus can cause direct damage, thwart our own body’s defenses, or trigger massive amounts of cytokines that lead to indirect damage within the human body. In this book are 12 research articles that deal with different aspects of staphylococcal exotoxins. Some of the work gives an overview about how the toxins contribute to the disease process. Other articles discuss different aspects of several exotoxins, and two articles are centered on countermeasures against S. aureus infections. Overall, this book will give the reader a good overview of how staphylococcal exotoxins contribute to initiating and sustaining infections in humans.

n/a --- HigBA --- cell physiology --- airway epithelial cells --- PPIase --- atopic dermatitis --- adaptive immunity --- staphylococcal enterotoxin --- sortase A --- canned meat --- inhibitor --- innate immunity --- low cytotoxic strains --- Staphylococcus aureus --- in vivo models --- toxin neutralization --- enterotoxin --- LukGH --- PSMs --- microbiome --- eye --- molecular mechanism --- chronic infection --- gene regulation --- toxins --- alpha-toxin --- superantigen-like protein --- fermentation --- erianin --- PpiB --- HACCP --- infection --- enzymes --- methicillin-resistant Staphylococcus aureus --- virulence factor --- enterotoxins --- mouse abscess --- toxin-antitoxin systems --- S. aureus --- polyclonal antibody --- defined minimal medium --- mastitis --- butyric acid derivative --- LukAB --- toxoid vaccine --- superantigen --- pathogenicity islands --- PrsA --- sphingomyelin --- Leukocidin --- lux fusion