Chapter 20 : The Interplay between the Microbiota and Enterohemorrhagic

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The human gastrointestinal (GI) tract harbors trillions of bacterial cells belonging to more than 1,000 species ( ), and the number of bacterial cells within the GI tract is 10 times higher than the number of human cells within our bodies ( ). The GI microbiota plays essential roles in human nutrition, physiology, development, immunity, and behavior, with disruption of the structure and balance of this community leading to dysbiosis and disease ( ). This fundamental association between host and bacteria relies on chemical signaling and nutrient availability and exchange. It is also clear that this important balance between host and microbiota can be severely disrupted by environmental stimuli. Two of the most common insults on the microbiota that induce dysbiosis are antibiotic treatment and infectious diseases. Both insults can lead to several disease states ranging from autism, to inflammatory bowel disease, to inflammatory bowel syndrome (IBS). It is also noteworthy that stress exacerbates these syndromes ( ).

Citation: Pifer R, Sperandio V. 2015. The Interplay between the Microbiota and Enterohemorrhagic , p 421-436. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0015-2013
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Figure 1

Structure of known quorum-sensing ligands. -hexanoyl-l-homoserine lactone (C6-HSL) (A) and -(3-Oxo-octanoyl)-l-homoserine lactone (3-oxo-C8-HSL) (B) stabilize SdiA, which can suppress T3S. (2,4)-2-methyl-2,3,3,4-tetrahydroxytetrahydrofuran (AI-2) (C) appears to have a surprisingly modest effect on virulence. QseC responds to host-derived epinephrine (D) and is antagonized by synthetic LED209 (E), perhaps yielding clues to the identity of AI-3. Indole (F) is a tryptophan-derived metabolite that influences motility and type III secretion. Mucin degradation releases fucose (G), which activates the FusKR two-component system to downregulate T3S. SCFAs, including acetate (H) and butyrate (I), induce motility of EHEC, while only butyrate induces T3S via Lrp activity.

Citation: Pifer R, Sperandio V. 2015. The Interplay between the Microbiota and Enterohemorrhagic , p 421-436. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0015-2013
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Figure 2

The QseC signaling cascade. QseC senses AI-3 epinephrine and norepinephrine and phosphorylates QseB, QseF, and KdpE. QseE senses epinephrine and phosphorylates QseF. QseB activates flagella expression. QseF indirectly promotes Shiga toxin and EspFu expression. KdpE together with Cra activate LEE gene expression. Both QseBC and QseEF repress expression. FusK senses fucose and phosphorylates FusR that represses the LEE.

Citation: Pifer R, Sperandio V. 2015. The Interplay between the Microbiota and Enterohemorrhagic , p 421-436. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0015-2013
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Figure 3

EHEC gastrointestinal colonization.

Citation: Pifer R, Sperandio V. 2015. The Interplay between the Microbiota and Enterohemorrhagic , p 421-436. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0015-2013
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Figure 4

EHEC cattle colonization. Within the rumen EHEC senses AHLs through SdiA to decrease LEE expression and increase expression. Within the RAJ, in the absence of AHLs, LEE expression is promoted.

Citation: Pifer R, Sperandio V. 2015. The Interplay between the Microbiota and Enterohemorrhagic , p 421-436. In Sperandio V, Hovde C (ed), Enterohemorrhagic and Other Shiga Toxin-Producing . ASM Press, Washington, DC. doi: 10.1128/microbiolspec.EHEC-0015-2013
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