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Chapter 13 : Enteric Pathogens Exploit the Microbiota-generated Nutritional Environment of the Gut

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Abstract:

The mammalian gastrointestinal (GI) tract harbors a diverse collection of indigenous bacteria known as the microbiota. The number of bacterial cells within our bodies exceeds the number of our cells by one order of magnitude ( ). Homeostasis of the microbiota is maintained by differential nutrient utilization and physical separation from the gut mucosa ( ). However, environmental perturbations such as antibiotic treatment, changes in diet, and infection lead to substantial alterations in composition and structure of the microbiota, referred to as ( ).

Citation: Pacheco A, Sperandio V. 2015. Enteric Pathogens Exploit the Microbiota-generated Nutritional Environment of the Gut, p 279-296. In Conway T, Cohen P (ed), Metabolism and Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MBP-0001-2014
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Nutritional cues regulate the locus of enterocyte effacement (LEE) gene expression in enterohemorrhagic (EHEC). Glycophagic members of the microbiota such as make fucose from mucin accessible to EHEC, and EHEC interprets this information to recognize that it is in the lumen, where expression of its LEE-encoded type III secretion system (TTSS) is onerous and not advantageous. Using yet another nutrient-based environmental cue, EHEC also times LEE expression through recognition of glycolytic and gluconeogenic environments. The lumen is more glycolytic due to predominant glycophagic members of the microbiota degrading complex polysaccharides into monosaccharides that can be readily utilized by nonglycophagic bacterial species such as and . In contrast, the tight mucus layer between the lumen and the epithelial interface in the gastrointestinal (GI) tract is devoid of microbiota; it is known as a “zone of clearance.” At the epithelial interface, the environment is regarded as gluconeogenic. Hence, the coupling of LEE regulation to optimal expression under gluconeogenic and low-fucose conditions mirrors the interface with the epithelial layer environment in the GI tract, ensuring that EHEC will express only LEE at optimal levels to promote attaching and effacing lesion formation at the epithelial interface. doi:10.1128/microbiolspec.MBP-0001-2014.f1

Citation: Pacheco A, Sperandio V. 2015. Enteric Pathogens Exploit the Microbiota-generated Nutritional Environment of the Gut, p 279-296. In Conway T, Cohen P (ed), Metabolism and Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MBP-0001-2014
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