Abstract

This chapter presents a general overview of type III secretion system (T3SS) regulation in the main pathogenic bacteria, and focuses on the different aspects of the regulation of T3SS gene expression in Pseudomonas aeruginosa. Pathogenic bacteria occupy very different infection foci; for instance, the animal pathogens Shigella spp. and Salmonella spp. live intracellularly after successful invasion, whereas Yersinia spp., P. aeruginosa, and enteropathogenic Escherichia coli (EPEC) predominantly remain extracellular. Therefore, different stimuli could be used to up or downregulate the expression of T3SS genes: temperature, divalent cations, host cell contact, serum, or other factors. Although the mechanism by which metabolic pathways influence virulence gene expression in bacteria is unclear, the example of P. aeruginosa detailed could facilitate progress in that field. It has been shown that T3SS expression is dependent on cell density and that exsCEBA operon expression decreases rapidly in the second part of stationary phase, and also that indole-3-acetic acid (IAA), naphthalenacetic, and 3-hydroxykynurenine inhibit exsCEBA operon expression at millimolar concentrations. In 2005, Wu and coworkers proposed that the opportunistic pathogen P. aeruginosa could adapt to the host by sensing alterations in the host immune function and respond by enhancing the virulence phenotype. Despite the large number of genes that influence the regulation of the expression of T3SS genes in P. aeruginosa, only a minority have been shown to have a precise role. Both fundamental and applied research can make the inhibition of T3SS expression as one of the first new antibacterial therapeutics.

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