E. coli O157:H7 catabolism of intestinal mucin-derived carbohydrates and colonization

Snider, Timothy A.; Fabich, Andrew J.; Conway, Tyrrell; Clinkenbeard, Kenneth D.

doi:10.1016/j.vetmic.2008.10.033

Cited by 35 publications

(42 citation statements)

References 21 publications

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“…Whole mucus may represent a combination of substrates that more closely meet requirements of the pathogen or, alternatively, a component of mucus not tested in this experiment may be a key ingredient for optimal growth of Nal R E. coli O157:H7. For example, an E. coli mutant deficient in the catabolic pathway for L-fucose demonstrated a marked decrease in colonization of the rectal mucus (Snider et al, 2009). Similar results were observed in mice and in vitro with E. coli MG1655 Fabich et al, 2008).…”

Section: Discussionsupporting

confidence: 67%

“…Bovine mucus is believed to display a certain level of heterogeneity between the different sections of the intestine, and this diversity is considered partly responsible for the bacterial tropism (Robbe et al, 2004;Snider et al, 2009). Our analysis of the ileum and colon mucus composition revealed no major differences in nitrogen or OM content.…”

Section: Discussionmentioning

confidence: 62%

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Capacity of the bovine intestinal mucus and its components to support growth of Escherichia coli O157:H7

Aperce

Heidenreich

Drouillard

2014

Animal

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Colonization of the gastrointestinal tract of cattle by Shiga toxin-producing Escherichia coli increases the risk of contamination of food products at slaughter. Our study aimed to shed more light on the mechanisms used by E. coli O157:H7 to thrive and compete with other bacteria in the gastrointestinal tract of cattle. We evaluated, in vitro, bovine intestinal mucus and its constituents in terms of their capacity to support growth of E. coli O157:H7 in presence or absence of fecal inoculum, with and without various enzymes. Growth of E. coli O157:H7 and total anaerobic bacteria were proportionate to the amount of mucus added as substrate. Growth of E. coli O157:H7 was similar for small and large intestinal mucus as substrate, and was partially inhibited with addition of fecal inoculum to cultures, presumably due to competition from other organisms. Whole mucus stimulated growth to the greatest degree compared with other compounds evaluated, but the pathogen was capable of utilizing all substrates to some extent. Addition of enzymes to cultures failed to impact growth of E. coli O157:H7 except for neuraminidase, which resulted in greater growth of E. coli O157 when combined with sialic acid as substrate. In conclusion, E. coli O157 has capacity to utilize small or large intestinal mucus, and growth is greatest with whole mucus compared with individual mucus components. There are two possible explanations for these findings (i) multiple substrates are needed to optimize growth, or alternatively, (ii) a component of mucus not evaluated in this experiment is a key ingredient for optimal growth of E. coli O157:H7.

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Section: Discussionsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 62%

Capacity of the bovine intestinal mucus and its components to support growth of Escherichia coli O157:H7

Aperce

Heidenreich

Drouillard

2014

Animal

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“…In the gut, EHEC also perceives and responds to the sugar fucose, which enhances EHEC colonization (34). In the mammalian intestine, fucose is abundant, reaching concentrations of ∼100 μM (35), because it is cleaved from host mucin glycoproteins by fucosidases produced by the commensal bacterium Bacterioides thetaiotamicron.…”

Section: Continuing the Intestinal Journeymentioning

confidence: 99%

“…Carbohydrate metabolism and signaling are clearly linked to virulence, and several studies have indicated that fucose is important for EHEC colonization (34,140). Resident Bacterioides spp.…”

Section: A Regulated Infection Continuummentioning

confidence: 99%

Enterohemorrhagic Escherichia coli Virulence Gene Regulation

Mellies

Lorenzen

2014

Microbiol Spectr

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Coordinated expression of enterohemorrhagic Escherichia coli virulence genes enables the bacterium to cause hemorrhagic colitis and the complication known as hemolytic-uremic syndrome. Horizontally acquired genes and those common to E. coli contribute to the disease process, and increased virulence gene expression is correlated with more severe disease in humans. Researchers have gained considerable knowledge about how the type III secretion system, secreted effectors, adhesin molecules, and the Shiga toxins are regulated by environmental signals and multiple genetic pathways. Also emergent from the data is an understanding of how enterohemorrhagic E. coli regulates response to acid stress, the role of flagellar motility, and how passage through the human host and bovine intestinal tract causes disease and supports carriage in the cattle reservoir, respectively. Particularly exciting areas of discovery include data suggesting how expression of the myriad effectors is coordinately regulated with their cognate type III secretion system and how virulence is correlated with bacterial metabolism and gut physiology.As a species, Escherichia coli is highly successful, adapting to inhabit the lower intestine of warm-blooded animals. Commensal E. coli, part of the normal biota, resides harmlessly in the gut, producing vitamin K. However, E. coli also causes three types of disease in humans: urinary tract infections, sepsis in newborns, and diarrheal disease. Enterohemorrhagic E. coli (EHEC) plays a prominent role in the third type of illness. It has been estimated that, for the pan genome of E. coli, the nonpathogenic and pathogenic strains only contain a core set of genes comprising approximately 20% of any one genome (1, 2). Much of the horizontally acquired genetic information is clustered within genomic islands in pathogens. As for EHEC, this has allowed the organism to not only attach and colonize the large intestine of humans and other animals, to outcompete commensal E. coli and other bacteria at the site of infection, but also to cause serious disease.Horizontally acquired genetic information in EHEC results in evolution into a specific pathotype-genotype dictates phenotype. How this genetic information is controlled is of equal importance for the success and virulence of the organism. Indeed, investigated differences in virulence gene regulation in two distinct EHEC isolate lineages, clade 8 and clade 2. A clade is a group of EHEC isolates with one ancestor and all its descendants. Eight clades of E. coli O157 isolates were defined by single nucleotide polymorphism (SNP) analyses, where clade 8 was a group of hypervirulent bacteria compared to the other seven clades (4). By examining multiple strains per lineage, the investigators found increased expression of horizontally acquired virulence genes in clade 8 versus clade 2. Genes expressed to higher levels in clade 8, which is associated with a greater number of cases of E. coli hemorrhagic

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“…Because the sialic acids are synthesized almost exclusively by deuterostomes, it is unsurprising that a nanAT deletion might be deficient for colonization in a rodent model (36,37), though this phenotype might only be true for commensals and extraintestinal E. coli, while a transient such as E. coli O157 seems to be less dependent on sialometabolism (38,39). In addition to nutritional aspects of sialometabolism during colonization, intracellular accumulation of Neu5Ac inhibits cell growth (4).…”

Section: Figurementioning

confidence: 99%

Control of the Escherichia coli Sialoregulon by Transcriptional Repressor NanR

2013

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NanR, one of >8,500 GntR superfamily helix-turn-helix transcriptional regulators, controls expression of the genes required for catabolism of sialic acids in Escherichia coli. It is predicted to do the same in related bacteria harboring orthologs of nanR. The sialic acids are a family of over 40 naturally occurring nine-carbon keto-sugar acids found mainly in the animal lineage, which includes starfish to humans in the deuterostome lineage. Sialic acids function in development, immunity, protein localization and stability, and homeostasis. They also serve as microbial carbon and nitrogen sources and ligands for cell recognition during host colonization. The importance of microbial sialic acid metabolism for host-microbe interactions has made it a target for therapeutic development. Exploiting this target depends on understanding sialometabolic pathways in a wide range of evolutionarily distinct bacteria. Here, we show by transcriptome, genetic, and biochemical analyses that the most common sialic acid, N-acetylneuraminate, induces the nanATEK-yhcH, yjhATS (nanCMS), and yjhBC operons by directly inactivating NanR, converting the predominantly dimeric form of the repressor to an inactive monomer of approximately 30-kDa. Additionally, other results identify critical amino acid residues and nucleotides in the regulator and operator, respectively. The combined results better define how sialic acids, acting through NanR, affect the metabolic flux of an important group of host-derived metabolites. Thus, E. coli serves as a valuable model for understanding sialocatabolic pathways in bacteria.

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E. coli O157:H7 catabolism of intestinal mucin-derived carbohydrates and colonization

Cited by 35 publications

References 21 publications

Capacity of the bovine intestinal mucus and its components to support growth of Escherichia coli O157:H7

Capacity of the bovine intestinal mucus and its components to support growth of Escherichia coli O157:H7

Enterohemorrhagic Escherichia coli Virulence Gene Regulation

Control of the Escherichia coli Sialoregulon by Transcriptional Repressor NanR

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