Chapter 27 : Regulation in Response to Host-Derived Signaling Molecules

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To survive in their environment, bacteria must sense the conditions in which they live and adapt accordingly. The best way to acquire this information is to sense various molecules produced by the host. This interaction, along with the host sensing bacterium-derived molecules, has been termed interkingdom signaling. Hormones, the principal signaling molecules in multicellular organisms, are present in every environment where bacteria interact with the host. Catecholamines are a family of three neuroendocrine hormones that are produced from the amino acid tyrosine. Opioids are neurotransmitters that play multiple roles in host responses such as stress, tissue damage, and regulation of the immune system. Natriuretic peptides are a class of peptide hormones involved in the osmoregulation of blood. The major signaling molecules used by the immune system are cytokines, which makes them a prime target for being eavesdropped on by bacteria. The immune system produces many other molecules aside from cytokines. Among these are cationic antimicrobial peptides (CAMPs). These peptides have a wide array of diversity but share a positive charge and amphipathic regions that allow them to interact with and disrupt the negatively charged bacterial membrane. Gram-positive bacteria also must face the wide array of antimicrobial peptides produced by the host. The ability to sense and respond to host signals has been identified in most major pathogens. The prevalence of this ability suggests that interkingdom signaling may be extremely common and that many more systems will be uncovered in the future.

Citation: Gruber C, Sperandio V. 2013. Regulation in Response to Host-Derived Signaling Molecules, p 545-565. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch27
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Figure 1

Model of interkingdom regulation in EHEC. QseC senses AI-3/epinephrine and NE to increase its autophosphorylation. It then transfers this phosphate to three response regulators: QseB (controls flagellar expression), KdpE (controls LEE gene expression), and QseF (controls pedestal formation). QseBC activate the expression of , where QseE senses Epi, sulfate, and phosphate and transfers its phosphate to QseF. doi:10.1128/9781555818524.ch27f1

Citation: Gruber C, Sperandio V. 2013. Regulation in Response to Host-Derived Signaling Molecules, p 545-565. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch27
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Figure 2

Model of interkingdom signaling in . NE influences the expression of GacA, which in turn influences the expression of , encoding the receptor for the 3-oxo-C12-AHL quorum-sensing signal. LasR controls the expression of that encodes the synthase of the 3-oxo-C12-AHL, forming a positive auto-regulatory loop. LasR also activates expression of the RlhRI quorum-sensing system, which represses expression of the PQS signal. Expression of PQS is positively activated by the presence of PMNs, and through MvfR by dynorphin. IFN-γ through OprF activates the expression of . doi:10.1128/9781555818524.ch27f2

Citation: Gruber C, Sperandio V. 2013. Regulation in Response to Host-Derived Signaling Molecules, p 545-565. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch27
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Figure 3

Model of activation of the serovar Typhimurium PhoQ sensor by CAMPs. doi:10.1128/9781555818524.ch27f3

Citation: Gruber C, Sperandio V. 2013. Regulation in Response to Host-Derived Signaling Molecules, p 545-565. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch27
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Figure 4

Activation of VirA through interaction with the periplasmic protein ChvE bound to plant-derived monosaccharides. doi:10.1128/9781555818524.ch27f4

Citation: Gruber C, Sperandio V. 2013. Regulation in Response to Host-Derived Signaling Molecules, p 545-565. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch27
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Table 1

Summary of interkingdom signaling systems

Citation: Gruber C, Sperandio V. 2013. Regulation in Response to Host-Derived Signaling Molecules, p 545-565. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch27

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