CadA Negatively Regulates
            <i>Escherichia coli</i>
            O157:H7 Adherence and Intestinal Colonization

Vázquez-Juárez, Ricardo; Kuriakose, Jeeba A.; Rasko, David A.; Ritchie, Jennifer M.; Kendall, Melissa M.; Slater, Terry M.; Sinha, Mala; Luxon, Bruce A.; Popov, Vsevolod L.; Waldor, Matthew K.; Sperandio, Vanessa; Torres, Alfredo G.

doi:10.1128/iai.00677-08

Cited by 29 publications

(33 citation statements)

References 39 publications

(48 reference statements)

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“…Pathoadaptive events of EIEC and Shigella are discussed in more detail below. Pathoadaptation is not limited to Shigella, as loss of lysine decarboxylase activity has been shown in EPEC, ETEC, STEC, and EAEC (39,40), and these pathoadaptive lesions may contribute to enhanced virulence in STEC O157:H7 and outbreak strains of EAEC (39,41). The description of pathotypes has usually relied on a signature set of genotypic and phenotypic traits.…”

Section: Evolution Of Pathogenic E Colimentioning

confidence: 99%

Recent Advances in Understanding Enteric Pathogenic Escherichia coli

et al. 2013

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SUMMARY Although Escherichia coli can be an innocuous resident of the gastrointestinal tract, it also has the pathogenic capacity to cause significant diarrheal and extraintestinal diseases. Pathogenic variants of E. coli (pathovars or pathotypes) cause much morbidity and mortality worldwide. Consequently, pathogenic E. coli is widely studied in humans, animals, food, and the environment. While there are many common features that these pathotypes employ to colonize the intestinal mucosa and cause disease, the course, onset, and complications vary significantly. Outbreaks are common in developed and developing countries, and they sometimes have fatal consequences. Many of these pathotypes are a major public health concern as they have low infectious doses and are transmitted through ubiquitous mediums, including food and water. The seriousness of pathogenic E. coli is exemplified by dedicated national and international surveillance programs that monitor and track outbreaks; unfortunately, this surveillance is often lacking in developing countries. While not all pathotypes carry the same public health profile, they all carry an enormous potential to cause disease and continue to present challenges to human health. This comprehensive review highlights recent advances in our understanding of the intestinal pathotypes of E. coli .

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Section: Evolution Of Pathogenic E Colimentioning

confidence: 99%

Recent Advances in Understanding Enteric Pathogenic Escherichia coli

et al. 2013

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“…EHEC strain 86-24 was isolated in 1986 from a patient in Seattle, WA, experiencing hemorrhagic colitis (30). Moreover, strain 86-24 has been used extensively to study EHEC infection and disease in all EHEC animal models (15,19,54,57,58,63,94,98). Transcriptome analyses were undertaken using Affymetrix gene arrays.…”

Section: Hfq Is a Global Regulator In Ehecmentioning

confidence: 99%

Hfq Virulence Regulation in Enterohemorrhagic Escherichia coli O157:H7 Strain 86-24

et al. 2011

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Enterohemorrhagic Escherichia coli O157:H7 (EHEC) causes bloody diarrhea and hemolytic-uremic syndrome. EHEC encodes the sRNA chaperone Hfq, which is important in posttranscriptional regulation. In EHEC strain EDL933, Hfq acts as a negative regulator of the locus of enterocyte effacement (LEE), which encodes most of the proteins involved in type III secretion and attaching and effacing (AE) lesions. Here, we deleted hfq in the EHEC strain 86-24 and compared global transcription profiles of the hfq mutant and wild-type (WT) strains in exponential growth phase. Deletion of hfq affected transcription of genes common to nonpathogenic and pathogenic strains of E. coli as well as pathogen-specific genes. Downregulated genes in the hfq mutant included ler, the transcriptional activator of all the LEE genes, as well as genes encoded in the LEE2 to -5 operons. Decreased expression of the LEE genes in the hfq mutant occurred at middle, late, and stationary growth phases. We also confirmed decreased regulation of the LEE genes by examining the proteins secreted and AE lesion formation by the hfq mutant and WT strains. Deletion of hfq also caused decreased expression of the two-component system qseBC, which is involved in interkingdom signaling and virulence gene regulation in EHEC, as well as an increase in expression of stx 2AB , which encodes the deadly Shiga toxin. Altogether, these data indicate that Hfq plays a regulatory role in EHEC 86-24 that is different from what has been reported for EHEC strain EDL933 and that the role of Hfq in EHEC virulence regulation extends beyond the LEE.Enterohemorrhagic Escherichia coli O157:H7 (EHEC) is a food-borne pathogen that causes severe bloody diarrhea and is often associated with complications, including hemolytic-uremic syndrome (HUS), seizures, cerebral edema, and/or coma (42). EHEC attaches intimately to intestinal epithelial cells and triggers extensive cytoskeletal rearrangements, resulting in attaching and effacing (AE) lesions and formation of a characteristic pedestal structure (40,41,46). Most of the genes involved in AE lesion formation are carried within a chromosomal pathogenicity island called the locus of enterocyte effacement (LEE) (53). The LEE contains five major operons (LEE1 to -5) that encode a type III secretion (TTS) system and effector proteins. EHEC's arsenal of virulence factors also includes non-LEE-encoded effector proteins that increase adherence or mediate colonization of host epithelial cells (8,16,26,27,32,84,87,88).The mortality associated with EHEC infections is due to the production and release of a Shiga toxin (Stx) by these bacteria. EHEC expresses Stx, and this potent inhibitor of protein synthesis can be absorbed systemically, where it binds to receptors found in the kidneys and the central nervous system, thus causing the complications associated with EHEC disease (42).Regulation of EHEC virulence genes is extremely complex and involves interkingdom signaling (12). EHEC senses the host-derived signals epinephrine and norepinephrine as well...

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“…It is induced by low pH under anaerobic conditions, and it requires arginine decarboxylase (AdiA) and arginine/agmatine antiporter (AdiC) (6, 10). AR4 is a lysine-dependent system that requires lysine decarboxylase (CadA) and a lysine/cadaverin antiporter (CadB) (22,40).In addition to these enzymes, multiple global regulators, such as H-NS, CysB, SspA, and HU (1,7,19,34,35), small RNAs (DsrA and GadY) (17, 25), topoisomerase I (37), and Asr (33) have been reported to have some roles in AR, either directly or indirectly. Furthermore, some small molecules, such as indole (9) and CO 2 (38), induced AR.…”

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ATP Requirement for Acidic Resistance in Escherichia coli

et al. 2011

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ATP participates in many cellular metabolic processes as a major substrate to supply energy. Many systems for acidic resistance (AR) under extremely acidic conditions have been reported, but the role of ATP has not been examined. To clarify whether or not ATP is necessary for the AR in Escherichia coli, the AR of mutants deficient in genes for ATP biosynthesis was investigated in this study. The deletion of purA or purB, each of which encodes enzymes to produce AMP from inosinate (IMP), markedly decreased the AR. The content of ATP in these mutants decreased rapidly at pH 2.5 compared to that of the wild type. The AR was again decreased significantly by the mutation of adk, which encoded an enzyme to produce ADP from AMP. The DNA damage in the purA and purB mutants was higher than that in the wild type. These results demonstrated that metabolic processes that require ATP participate in survival under extremely acidic conditions, and that one such system is the ATP-dependent DNA repair system.Since the normal human stomach averages pH 2 for approximately 2 h after it becomes empty, to survive in the mammalian host both commensal and pathogenic enteric bacteria have resistance systems to protect themselves against acidic stress (5,32,36).Four acidic resistance (AR) systems that are induced under different conditions have been proposed for Escherichia coli (5). Acidic resistance system 1 (AR1), which is induced in cells grown to stationary phase in a moderately acidic medium, requires the sigma factor RpoS (3, 27) and the cyclic AMP receptor protein CRP (2). The underlying mechanism remains unclear. The other three systems depend on the presence of specific amino acids. The second AR system (AR2) is a glutamate-dependent system that requires two glutamate decarboxylases (GadA and GadB) and a putative glutamate/␥-aminobutyric acid (GABA) antiporter, GadC (3,8,31). AR3 is an arginine-dependent system. It is induced by low pH under anaerobic conditions, and it requires arginine decarboxylase (AdiA) and arginine/agmatine antiporter (AdiC) (6, 10). AR4 is a lysine-dependent system that requires lysine decarboxylase (CadA) and a lysine/cadaverin antiporter (CadB) (22,40).In addition to these enzymes, multiple global regulators, such as H-NS, CysB, SspA, and HU (1,7,19,34,35), small RNAs (DsrA and GadY) (17, 25), topoisomerase I (37), and Asr (33) have been reported to have some roles in AR, either directly or indirectly. Furthermore, some small molecules, such as indole (9) and CO 2 (38), induced AR. These reports have suggested that multiple metabolic processes besides amino acid decarboxylation are required for survival under acidic conditions.The maintenance of energy is required for many metabolic processes, including the biosynthesis of cellular materials, the membrane transport of ions and organic compounds, DNA repair, cell division and cell motility, and the degradation of macromolecules. E. coli has two major energy sources, ATP and the proton-motive force. The latter is generated via the respiratory chain and i...

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CadA Negatively Regulates Escherichia coli O157:H7 Adherence and Intestinal Colonization

Cited by 29 publications

References 39 publications

Recent Advances in Understanding Enteric Pathogenic Escherichia coli

Recent Advances in Understanding Enteric Pathogenic Escherichia coli

Hfq Virulence Regulation in Enterohemorrhagic Escherichia coli O157:H7 Strain 86-24

ATP Requirement for Acidic Resistance in Escherichia coli

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