Статті в журналах: "Escherichia coli infections Pathogenesis"

1

Hacker, Jörg. "Role of fimbrial adhesins in the pathogenesis of Escherichia coli infections." Canadian Journal of Microbiology 38, no. 7 (July 1, 1992): 720–27. http://dx.doi.org/10.1139/m92-118.

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Escherichia coli strains are able to cause intestinal (enteritis, diarrhoeal diseases) and extraintestinal (urinary tract infections, sepsis, meningitis) infections. Most pathogenic E. coli strains produce specific fimbrial adhesins, which represent essential colonization factors: intestinal E. coli strains very often carry transferable plasmids with gene clusters specific for fimbrial adhesins, like K88 and K99, or colonization factor antigens (CFA) I and II. In contrast, the fimbrial gene clusters of extraintestinal E. coli strains, such as P, S, or F1C fimbriae, are located on the chromosomes. The fimbrial adhesin complexes consist of major and minor subunit proteins. Their binding specificity can generally be assayed in hemagglutination tests. In the case of fimbrial adhesins of intestinal E. coli strains, the major subunit proteins preferentially represent the hemagglutinating adhesins, whereas minor subunit proteins are the hemagglutinins of extraintestinal E. coli strains. Recently "alternative" adhesin proteins were identified, which have the capacity to bind to eukaryotic structures different from the receptors of the erythrocytes. Fimbrial adhesins are not constitutively expressed but are stringently regulated on the molecular level. Extraintestinal E. coli wild-type strains normally carry three or more fimbrial adhesin determinants, which have the capacity to influence the expression of one another (cross talk). Furthermore the fimbrial gene clusters undergo phase variation, which seems to be important for their contribution to pathogenesis of E. coli. Key words: fimbriae, adhesins, Escherichia coli, pathogenicity.

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2

Paton, James C., and Adrienne W. Paton. "Pathogenesis and Diagnosis of Shiga Toxin-Producing Escherichia coli Infections." Clinical Microbiology Reviews 11, no. 3 (July 1, 1998): 450–79. http://dx.doi.org/10.1128/cmr.11.3.450.

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SUMMARY Since their initial recognition 20 years ago, Shiga toxin-producing Escherichia coli (STEC) strains have emerged as an important cause of serious human gastrointestinal disease, which may result in life-threatening complications such as hemolytic-uremic syndrome. Food-borne outbreaks of STEC disease appear to be increasing and, when mass-produced and mass-distributed foods are concerned, can involve large numbers of people. Development of therapeutic and preventative strategies to combat STEC disease requires a thorough understanding of the mechanisms by which STEC organisms colonize the human intestinal tract and cause local and systemic pathological changes. While our knowledge remains incomplete, recent studies have improved our understanding of these processes, particularly the complex interaction between Shiga toxins and host cells, which is central to the pathogenesis of STEC disease. In addition, several putative accessory virulence factors have been identified and partly characterized. The capacity to limit the scale and severity of STEC disease is also dependent upon rapid and sensitive diagnostic procedures for analysis of human samples and suspect vehicles. The increased application of advanced molecular technologies in clinical laboratories has significantly improved our capacity to diagnose STEC infection early in the course of disease and to detect low levels of environmental contamination. This, in turn, has created a potential window of opportunity for future therapeutic intervention.

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3

Serna, Antonio, and Edgar C. Boedeker. "Pathogenesis and treatment of Shiga toxin-producing Escherichia coli infections." Current Opinion in Gastroenterology 24, no. 1 (January 2008): 38–47. http://dx.doi.org/10.1097/mog.0b013e3282f2dfb8.

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4

Vel, W. A. C., A. M. J. J. Verweij-Van Vught, F. Namavar, and D. M. MacLaren. "Pathogenesis of mixed infections by Escherichia coli and Bacteroides species." Antonie van Leeuwenhoek 51, no. 5-6 (1985): 598. http://dx.doi.org/10.1007/bf00404584.

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5

Servin, Alain L. "Pathogenesis of Afa/Dr Diffusely Adhering Escherichia coli." Clinical Microbiology Reviews 18, no. 2 (April 2005): 264–92. http://dx.doi.org/10.1128/cmr.18.2.264-292.2005.

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SUMMARY Over the last few years, dramatic increases in our knowledge about diffusely adhering Escherichia coli (DAEC) pathogenesis have taken place. The typical class of DAEC includes E. coli strains harboring AfaE-I, AfaE-II, AfaE-III, AfaE-V, Dr, Dr-II, F1845, and NFA-I adhesins (Afa/Dr DAEC); these strains (i) have an identical genetic organization and (ii) allow binding to human decay-accelerating factor (DAF) (Afa/DrDAF subclass) or carcinoembryonic antigen (CEA) (Afa/DrCEA subclass). The atypical class of DAEC includes two subclasses of strains; the atypical subclass 1 includes E. coli strains that express AfaE-VII, AfaE-VIII, AAF-I, AAF-II, and AAF-III adhesins, which (i) have an identical genetic organization and (ii) do not bind to human DAF, and the atypical subclass 2 includes E. coli strains that harbor Afa/Dr adhesins or others adhesins promoting diffuse adhesion, together with pathogenicity islands such as the LEE pathogenicity island (DA-EPEC). In this review, the focus is on Afa/Dr DAEC strains that have been found to be associated with urinary tract infections and with enteric infection. The review aims to provide a broad overview and update of the virulence aspects of these intriguing pathogens. Epidemiological studies, diagnostic techniques, characteristic molecular features of Afa/Dr operons, and the respective role of Afa/Dr adhesins and invasins in pathogenesis are described. Following the recognition of membrane-bound receptors, including type IV collagen, DAF, CEACAM1, CEA, and CEACAM6, by Afa/Dr adhesins, activation of signal transduction pathways leads to structural and functional injuries at brush border and junctional domains and to proinflammatory responses in polarized intestinal cells. In addition, uropathogenic Afa/Dr DAEC strains, following recognition of β1 integrin as a receptor, enter epithelial cells by a zipper-like, raft- and microtubule-dependent mechanism. Finally, the presence of other, unknown virulence factors and the way that an Afa/Dr DAEC strain emerges from the human intestinal microbiota as a “silent pathogen” are discussed.

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6

Tang, Fengyi, and Milton H. Saier. "Transport proteins promoting Escherichia coli pathogenesis." Microbial Pathogenesis 71-72 (June 2014): 41–55. http://dx.doi.org/10.1016/j.micpath.2014.03.008.

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7

Neill, Marguerite A. "Pathogenesis of Escherichia coli O157:H7 infection." Current Opinion in Infectious Diseases 7, no. 3 (June 1994): 295–303. http://dx.doi.org/10.1097/00001432-199406000-00003.

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8

Nicholson, Tracy F., Kristin M. Watts, and David A. Hunstad. "OmpA of Uropathogenic Escherichia coli Promotes Postinvasion Pathogenesis of Cystitis." Infection and Immunity 77, no. 12 (September 21, 2009): 5245–51. http://dx.doi.org/10.1128/iai.00670-09.

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ABSTRACT Type 1 pilus directs bladder epithelial binding and invasion by uropathogenic Escherichia coli (UPEC) in the initial stage of cystitis, but the bacterial determinants of postinvasion events in the pathogenesis of cystitis are largely undetermined. We show here that the UPEC outer membrane protein A (OmpA), a monomeric, major, integral protein component of the bacterial outer membrane, functions as a critical determinant of intracellular virulence for UPEC, promoting persistent infection within bladder epithelium. Using a murine urinary tract infection (UTI) model, we demonstrate that whereas deletion of the UPEC ompA gene did not disrupt initial epithelial binding and invasion by UPEC, it did preclude completion of the intracellular bacterial community (IBC) pathway, accompanied by diminishing bacterial loads in the bladder. This defect in epithelial persistence of the ompA mutant was enhanced in competitive infections with wild-type UPEC. Microscopic examinations revealed that the ompA mutant formed significantly fewer IBCs, and those that were initiated were unable to progress past the early stages of maturation. These defects could be corrected by complementation of ompA. In addition, expression of ompA during wild-type UTI was sharply increased at time points correlated with IBC development and the arrival of host immune effector cells. Our findings establish OmpA as a key UPEC virulence factor that functions after epithelial invasion to facilitate IBC maturation and chronic bacterial persistence.

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9

Herthelius, B. M., K. G. Hedström, R. Möllby, Lena Pettersson, J. Winberg, and C. E. Nord. "Pathogenesis of urinary tract infections — Amoxicillin induces genital escherichia coli colonization." Infection 16, no. 5 (September 1988): 263–66. http://dx.doi.org/10.1007/bf01645066.

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10

Bogdanos, Dimitrios P., Harold Baum, Diego Vergani, and Andrew K. Burroughs. "The Role ofE. coliInfection in the Pathogenesis of Primary Biliary Cirrhosis." Disease Markers 29, no. 6 (2010): 301–11. http://dx.doi.org/10.1155/2010/595078.

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Among various infectious agents possibly involved in the pathogenesis of primary biliary cirrhosis (PBC),Escherichia Coli (E. coli)has received special attention because of epidemiological and experimental evidence linking this bacterium with the disease's development. This review discusses early and more recent epidemiological studies associating recurrent urinary tract infections withE. coliand the development of PBC. We also critically review data provided over the years demonstrating disease-specific humoral and cellular immune responses againstE. coliantigens in patients with PBC. Finally, we assess the relevance of experimental findings reporting cross-reactive immunity between mimicking sequences ofE. coliand the major PBC mitochondrial antigens in the pathogenesis of the PBC. We also address the extent to which molecular mimicry and immunological cross-reactivity can be considered as a critical pathogenic process linking infection with self destruction.

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11

Wang, Caihong, Jane W. Symington, Emily Ma, Bin Cao, and Indira U. Mysorekar. "Estrogenic Modulation of Uropathogenic Escherichia coli Infection Pathogenesis in a Murine Menopause Model." Infection and Immunity 81, no. 3 (December 21, 2012): 733–39. http://dx.doi.org/10.1128/iai.01234-12.

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ABSTRACTRecurrent urinary tract infections (UTIs), primarily caused by uropathogenicEscherichia coli(UPEC), annually affect over 13 million patients in the United States. Menopausal women are disproportionally susceptible, suggesting estrogen deficiency is a significant risk factor for chronic and recurrent UTI. How estrogen status governs susceptibility to UTIs remains unknown, and whether hormone therapy protects against UTIs remains controversial. Here, we used a mouse model of surgical menopause by ovariectomy and demonstrate a protective role for estrogen in UTI pathogenesis. We found that ovariectomized mice had significantly higher bacteriuria, a more robust inflammatory response, and increased production of the proinflammatory cytokine interleukin-6 (IL-6) upon UPEC infection compared to sham-operated controls. We further show that response of the urothelial stem cell niche to infection, normally activated to restore homeostasis after infection, was aberrant in ovariectomized mice with defective superficial urothelial cell differentiation. Finally, UPEC-infected ovariectomized mice showed a significant increase in quiescent intracellular bacterial reservoirs, which reside in the urothelium and can seed recurrent infections. Importantly, this and other ovariectomy-induced outcomes of UTI were reversible upon estrogen supplementation. Together, our findings establish ovariectomized mice as a model for UTIs in menopausal women and pinpoint specific events during course of infection that are most susceptible to estrogen deficiency. These findings have profound implications for the understanding of the role of estrogen and estrogen therapy in bladder health and pathogen defense mechanisms and open the door for prophylaxis for menopausal women with recurrent UTIs.

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12

Vlisidou, Isabella, Mark Lyte, Pauline M. van Diemen, Pippa Hawes, Paul Monaghan, Timothy S. Wallis, and Mark P. Stevens. "The Neuroendocrine Stress Hormone Norepinephrine Augments Escherichia coli O157:H7-Induced Enteritis and Adherence in a Bovine Ligated Ileal Loop Model of Infection." Infection and Immunity 72, no. 9 (September 2004): 5446–51. http://dx.doi.org/10.1128/iai.72.9.5446-5451.2004.

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ABSTRACT The role of the neuroendocrine environment in the pathogenesis of enteric bacterial infections is increasingly being recognized. Here we report that norepinephrine augments Escherichia coli O157:H7-induced intestinal inflammatory and secretory responses as well as bacterial adherence to intestinal mucosa in a bovine ligated ileal loop model of infection. Norepinephrine modulation of enteritis and adherence was dependent on the ability of E. coli O157:H7 to form attaching and effacing lesions.

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13

Guiton, Pascale S., Corinne K. Cusumano, Kimberly A. Kline, Karen W. Dodson, Zhenfu Han, James W. Janetka, Jeffrey P. Henderson, Michael G. Caparon, and Scott J. Hultgren. "Combinatorial Small-Molecule Therapy Prevents Uropathogenic Escherichia coli Catheter-Associated Urinary Tract Infections in Mice." Antimicrobial Agents and Chemotherapy 56, no. 9 (June 25, 2012): 4738–45. http://dx.doi.org/10.1128/aac.00447-12.

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ABSTRACTCatheter-associated urinary tract infections (CAUTIs) constitute the majority of nosocomial urinary tract infections (UTIs) and pose significant clinical challenges. These infections are polymicrobial in nature and are often associated with multidrug-resistant pathogens, including uropathogenicEscherichia coli(UPEC). Urinary catheterization elicits major histological and immunological alterations in the bladder that can favor microbial colonization and dissemination in the urinary tract. We report that these biological perturbations impact UPEC pathogenesis and that bacterial reservoirs established during a previous UPEC infection, in which bacteriuria had resolved, can serve as a nidus for subsequent urinary catheter colonization. Mannosides, small molecule inhibitors of the type 1 pilus adhesin, FimH, provided significant protection against UPEC CAUTI by preventing bacterial invasion and shifting the UPEC niche primarily to the extracellular milieu and on the foreign body. By doing so, mannosides potentiated the action of trimethoprim-sulfamethoxazole in the prevention and treatment of CAUTI. In this study, we provide novel insights into UPEC pathogenesis in the context of urinary catheterization, and demonstrate the efficacy of novel therapies that target critical mechanisms for this infection. Thus, we establish a proof-of-principle for the development of mannosides to prevent and eventually treat these infections in the face of rising antibiotic-resistant uropathogens.

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Stanford, Kim. "Introduction to the Special Issue “Molecular Basis and the Pathogenesis of Enterohemorrhagic Escherichia coli Infections”." Toxins 12, no. 12 (December 3, 2020): 763. http://dx.doi.org/10.3390/toxins12120763.

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15

Li, Ganwu, Claudia Laturnus, Christa Ewers, and Lothar H. Wieler. "Identification of Genes Required for Avian Escherichia coli Septicemia by Signature-Tagged Mutagenesis." Infection and Immunity 73, no. 5 (May 2005): 2818–27. http://dx.doi.org/10.1128/iai.73.5.2818-2827.2005.

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ABSTRACT Infections with avian pathogenic Escherichia coli (APEC) cause colibacillosis, an acute and largely systemic disease resulting in significant economic losses in poultry industry worldwide. Although various virulence-associated genes have been identified in APEC, their actual role in pathogenesis is still not fully understood, and, furthermore, certain steps of the infection process have not been related to previously identified factors. Here we describe the application of a signature-tagged transposon mutagenesis (STM) approach to identify critical genes required for APEC infections in vivo. Twenty pools of about 1,800 IMT5155 (O2:H5) mutants were screened in an infection model using 5-week-old chickens, and potentially attenuated mutants were subjected to a secondary screen and in vivo competition assays to confirm their attenuation. A total of 28 genes required for E. coli septicemia in chickens were identified as candidates for further characterization. Among these disrupted genes, six encode proteins involved in biosynthesis of extracellular polysaccharides and lipopolysaccharides; two encode iron transporters that have not been previously characterized in APEC in in vivo studies, and four showed similarity to membrane or periplasmic proteins. In addition, several metabolic enzymes, putative proteins with unknown function, and open reading frames with no similarity to other database entries were identified. This genome-wide analysis has identified both novel and previously known factors potentially involved in pathogenesis of APEC infection.

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16

Nataro, James P., and James B. Kaper. "Diarrheagenic Escherichia coli." Clinical Microbiology Reviews 11, no. 1 (January 1, 1998): 142–201. http://dx.doi.org/10.1128/cmr.11.1.142.

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SUMMARY Escherichia coli is the predominant nonpathogenic facultative flora of the human intestine. Some E. coli strains, however, have developed the ability to cause disease of the gastrointestinal, urinary, or central nervous system in even the most robust human hosts. Diarrheagenic strains of E. coli can be divided into at least six different categories with corresponding distinct pathogenic schemes. Taken together, these organisms probably represent the most common cause of pediatric diarrhea worldwide. Several distinct clinical syndromes accompany infection with diarrheagenic E. coli categories, including traveler’s diarrhea (enterotoxigenic E. coli), hemorrhagic colitis and hemolytic-uremic syndrome (enterohemorrhagic E. coli), persistent diarrhea (enteroaggregative E. coli), and watery diarrhea of infants (enteropathogenic E. coli). This review discusses the current level of understanding of the pathogenesis of the diarrheagenic E. coli strains and describes how their pathogenic schemes underlie the clinical manifestations, diagnostic approach, and epidemiologic investigation of these important pathogens.

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Terekhov, Vladimir I., Aleksandr S. Tishchenko, and Anastasiya V. Stepanenko. "Exotoxins of pathogenic Escherichia coli." Veterinaria Kubani, no. 5 (October 30, 2020): 3–7. http://dx.doi.org/10.33861/2071-8020-2020-5-3-7.

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Escherichia coli is a representative of the natural normal microflora of humans and animals. At the same time, some variants may acquire pathogenic properties that contribute to the occurrence of intestinal and extraintestinal infections. In the pathogenesis of these diseases, the main role is played by exotoxins. Currently, along with the well-known and well-studied toxins of Escherichia coli, there is information about new toxoid structures detected in this pathogen, which play an important role in pathologies in humans and animals. Authors summarized current data on the toxigenic properties of Escherichia coli bacteria and established the role of exotoxins of pathogenic Escherichia coli in the mechanism of disease development. Scientific publications of mainly foreign researchers were used as a material for the review. It was found that cyclodomodulating exotoxins that affect the eukaryotic cell cycle were currently identified in Escherichia coli in addition to thermolabile, thermostable, shigalike, necrotizing toxins and hemolysin. Also Escherichia coli has a number of pore-forming toxins that destroy the epithelial barrier and overcome the protection of the host's immune cells due to the formation of pores in their membranes, and so-called repeated toxins, the prototype of which is а-hemolysin. Thus, it can be seen from the review that Escherichia coli, having a wide range of toxoid structures, can cause pathological changes in the human and animal body. The nature of these changes directly depends on the type of E. coli and the type of exotoxin produced by them. Most toxigenic strains of Escherichia coli have the ability to modulate the expression of proinflammatory cytokines, chemokines and other immune cells, which can be further used in the design of effective vaccines and biological products for the treatment and prevention of enterobacterial infections.

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Mulvey, Matthew A., Joel D. Schilling, and Scott J. Hultgren. "Establishment of a Persistent Escherichia coli Reservoir during the Acute Phase of a Bladder Infection." Infection and Immunity 69, no. 7 (July 1, 2001): 4572–79. http://dx.doi.org/10.1128/iai.69.7.4572-4579.2001.

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ABSTRACT The vast majority of urinary tract infections are caused by strains of uropathogenic Escherichia coli that encode filamentous adhesive organelles called type 1 pili. These structures mediate both bacterial attachment to and invasion of bladder epithelial cells. However, the mechanism by which type 1 pilus-mediated bacterial invasion contributes to the pathogenesis of a urinary tract infection is unknown. Here we show that type 1-piliated uropathogens can invade the superficial epithelial cells that line the lumenal surface of the bladder and subsequently replicate, forming massive foci of intracellular E. coli termed bacterial factories. In response to infection, superficial bladder cells exfoliate and are removed with the flow of urine. To avoid clearance by exfoliation, intracellular uropathogens can reemerge and eventually establish a persistent, quiescent bacterial reservoir within the bladder mucosa that may serve as a source for recurrent acute infections. These observations suggest that urinary tract infections are more chronic and invasive than generally assumed.

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Jacobsen, S. M., D. J. Stickler, H. L. T. Mobley, and M. E. Shirtliff. "Complicated Catheter-Associated Urinary Tract Infections Due to Escherichia coli and Proteus mirabilis." Clinical Microbiology Reviews 21, no. 1 (January 2008): 26–59. http://dx.doi.org/10.1128/cmr.00019-07.

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SUMMARY Catheter-associated urinary tract infections (CAUTIs) represent the most common type of nosocomial infection and are a major health concern due to the complications and frequent recurrence. These infections are often caused by Escherichia coli and Proteus mirabilis. Gram-negative bacterial species that cause CAUTIs express a number of virulence factors associated with adhesion, motility, biofilm formation, immunoavoidance, and nutrient acquisition as well as factors that cause damage to the host. These infections can be reduced by limiting catheter usage and ensuring that health care professionals correctly use closed-system Foley catheters. A number of novel approaches such as condom and suprapubic catheters, intermittent catheterization, new surfaces, catheters with antimicrobial agents, and probiotics have thus far met with limited success. While the diagnosis of symptomatic versus asymptomatic CAUTIs may be a contentious issue, it is generally agreed that once a catheterized patient is believed to have a symptomatic urinary tract infection, the catheter is removed if possible due to the high rate of relapse. Research focusing on the pathogenesis of CAUTIs will lead to a better understanding of the disease process and will subsequently lead to the development of new diagnosis, prevention, and treatment options.

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Snyder, Jennifer A., Brian J. Haugen, C. Virginia Lockatell, Nathalie Maroncle, Erin C. Hagan, David E. Johnson, Rodney A. Welch, and Harry L. T. Mobley. "Coordinate Expression of Fimbriae in Uropathogenic Escherichia coli." Infection and Immunity 73, no. 11 (November 2005): 7588–96. http://dx.doi.org/10.1128/iai.73.11.7588-7596.2005.

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ABSTRACT Uropathogenic Escherichia coli is the most common etiological agent of urinary tract infections. Bacteria can often express multiple adhesins during infection in order to favor attachment to specific niches within the urinary tract. We have recently demonstrated that type 1 fimbria, a phase-variable virulence factor involved in adherence, was the most highly expressed adhesin during urinary tract infection. Here, we examine whether the expression of type 1 fimbriae can affect the expression of other adhesins. Type 1 fimbrial phase-locked mutants of E. coli strain CFT073, which harbors genes for numerous adhesins, were employed in this study. CFT073-specific DNA microarray analysis of these strains demonstrates that the expression of type 1 fimbriae coordinately affects the expression of P fimbriae in an inverse manner. This represents evidence for direct communication between genes relating to pathogenesis, perhaps to aid the sequential occupation of different urinary tract tissues. While the role of type 1 fimbriae during infection has been clear, the role of P fimbriae must be further defined to assert the relevance of coordinated regulation in vivo. Therefore, we examined the ability of P fimbrial isogenic mutants, constructed in a type 1 fimbrial-negative background, to compete in the murine urinary tract over a period of 168 h. No differences in the colonization of these mutants were observed. However, comparison of these results with previous studies suggests that inversely coordinated expression of adhesin gene clusters does occur in vivo. Interestingly, the mutant that was incapable of expressing either type 1 or P fimbriae compensated by synthesizing F1C fimbriae.

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Pakbin, Babak, Wolfram M. Brück, and John W. A. Rossen. "Virulence Factors of Enteric Pathogenic Escherichia coli: A Review." International Journal of Molecular Sciences 22, no. 18 (September 14, 2021): 9922. http://dx.doi.org/10.3390/ijms22189922.

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Escherichia coli are remarkably versatile microorganisms and important members of the normal intestinal microbiota of humans and animals. This harmless commensal organism can acquire a mixture of comprehensive mobile genetic elements that contain genes encoding virulence factors, becoming an emerging human pathogen capable of causing a broad spectrum of intestinal and extraintestinal diseases. Nine definite enteric E. coli pathotypes have been well characterized, causing diseases ranging from various gastrointestinal disorders to urinary tract infections. These pathotypes employ many virulence factors and effectors subverting the functions of host cells to mediate their virulence and pathogenesis. This review summarizes new developments in our understanding of diverse virulence factors associated with encoding genes used by different pathotypes of enteric pathogenic E. coli to cause intestinal and extraintestinal diseases in humans.

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Biernbaum, Erika N., and Indira T. Kudva. "AB5 Enterotoxin-Mediated Pathogenesis: Perspectives Gleaned from Shiga Toxins." Toxins 14, no. 1 (January 16, 2022): 62. http://dx.doi.org/10.3390/toxins14010062.

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Foodborne diseases affect an estimated 600 million people worldwide annually, with the majority of these illnesses caused by Norovirus, Vibrio, Listeria, Campylobacter, Salmonella, and Escherichia coli. To elicit infections in humans, bacterial pathogens express a combination of virulence factors and toxins. AB5 toxins are an example of such toxins that can cause various clinical manifestations, including dehydration, diarrhea, kidney damage, hemorrhagic colitis, and hemolytic uremic syndrome (HUS). Treatment of most bacterial foodborne illnesses consists of fluid replacement and antibiotics. However, antibiotics are not recommended for infections caused by Shiga toxin-producing E. coli (STEC) because of the increased risk of HUS development, although there are conflicting views and results in this regard. Lack of effective treatment strategies for STEC infections pose a public health threat during outbreaks; therefore, the debate on antibiotic use for STEC infections could be further explored, along with investigations into antibiotic alternatives. The overall goal of this review is to provide a succinct summary on the mechanisms of action and the pathogenesis of AB5 and related toxins, as expressed by bacterial foodborne pathogens, with a primary focus on Shiga toxins (Stx). The role of Stx in human STEC disease, detection methodologies, and available treatment options are also briefly discussed.

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Kim, Kwang S. "Current concepts on the pathogenesis of Escherichia coli meningitis." Current Opinion in Infectious Diseases 25, no. 3 (June 2012): 273–78. http://dx.doi.org/10.1097/qco.0b013e3283521eb0.

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24

Raj, Pushker. "Pathogenesis and laboratory diagnosis of Escherichia coli—associated enteritis." Clinical Microbiology Newsletter 15, no. 12 (June 1993): 89–93. http://dx.doi.org/10.1016/0196-4399(93)90012-c.

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Thachil, A. J., B. T. Velayudhan, D. P. Shaw, D. A. Halvorson, and K. V. Nagaraja. "Pathogenesis of Ornithobacterium rhinotracheale in egg-laying hens with coexisting infectious bronchitis virus and Escherichia coli infections." Journal of Applied Poultry Research 18, no. 4 (December 2009): 780–88. http://dx.doi.org/10.3382/japr.2009-00039.

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Cusumano, Corinne K., Chia S. Hung, Swaine L. Chen, and Scott J. Hultgren. "Virulence Plasmid Harbored by Uropathogenic Escherichia coli Functions in Acute Stages of Pathogenesis." Infection and Immunity 78, no. 4 (February 1, 2010): 1457–67. http://dx.doi.org/10.1128/iai.01260-09.

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ABSTRACT Urinary tract infections (UTIs), the majority of which are caused by uropathogenic Escherichia coli (UPEC), afflict nearly 60% of women within their lifetimes. Studies in mice and humans have revealed that UPEC strains undergo a complex pathogenesis cycle that involves both the formation of intracellular bacterial communities (IBC) and the colonization of extracellular niches. Despite the commonality of the UPEC pathogenesis cycle, no specific urovirulence genetic profile has been determined; this is likely due to the fluid nature of the UPEC genome as the result of horizontal gene transfer and numerous genes of unknown function. UTI89 has a large extrachromosomal element termed pUTI89 with many characteristics of UPEC pathogenicity islands and that likely arose due to horizontal gene transfer. The pUTI89 plasmid has characteristics of both F plasmids and other known virulence plasmids. We sought to determine whether pUTI89 is important for virulence. Both in vitro and in vivo assays were used to examine the function of pUTI89 using plasmid-cured UTI89. No differences were observed between UTI89 and plasmid-cured UTI89 based on growth, type 1 pilus expression, or biofilm formation. However, in a mouse model of UTI, a significant decrease in bacterial invasion, CFU and IBC formation of the pUTI89-cured strain was observed at early time points postinfection compared to the wild type. Through directed deletions of specific operons on pUTI89, the cjr operon was partially implicated in this observed defect. Our findings implicate pUTI89 in the early aspects of infection.

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Predojević, Luka, Darja Keše, Darja Žgur Bertok, Taja Železnik Ramuta, Peter Veranič, Mateja Erdani Kreft, and Marjanca Starčič Erjavec. "A Biomimetic Porcine Urothelial Model for Assessing Escherichia coli Pathogenicity." Microorganisms 10, no. 4 (April 7, 2022): 783. http://dx.doi.org/10.3390/microorganisms10040783.

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Urinary tract infections can be severe, sometimes fatal, diseases whose etiological pathogens are predominantly uropathogenic strains of E. coli (UPEC). To investigate the UPEC pathogenesis, several models have already been established with minor or major disadvantages. The aim was to develop a simple, fast, and inexpensive biomimetic in vitro model based on normal porcine urothelial (NPU) cells that are genetically and physiologically similar to human bladder urothelium and to perform basic studies of E. coli pathogenicity. Initially, the model was tested using a set of control E. coli strains and, subsequently, with human E. coli strains isolated either from patients with urinary infections or from the feces of healthy individuals. A drop in viability of NPU cells was used as a measure of the pathogenicity of the individual strain tested. To visualize the subcellular events, transmission and scanning electron microscopy was performed. The strains were tested for the presence of different virulence-associated genes, phylogroup, type of core lipid, O-serotype, and type of lipopolysaccharide and a statistical analysis of possible correlations between strains’ characteristics and the effect on the model was performed. Results showed that our model has the discriminatory power to distinguish pathogenic from non-pathogenic E. coli strains, and to identify new, potentially pathogenic strains.

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Hagiwara, Shin-ichiro, Hisako Tobayama, and Seiichi Kagimoto. "Successful colonoscopic approach in a child with intussusception associated with enterohemorrhagic Escherichia coli O157 infection." Pediatric Reports 4, no. 4 (December 19, 2012): 33. http://dx.doi.org/10.4081/pr.2012.e33.

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The pathogenesis of intussusception caused by enterohemorrhagic <em>Escherichia coli</em> (<em>E. coli</em>) O157 infection is unknown. In our case, colonoscopy was useful for confirming O157 infection. The intussusception was caused by focally damaged edematous mucosa in the cecum. This case helped in elucidating the pathogenesis of the disease.

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Regev-Shoshani, Gilly, Mary Ko, Chris Miller, and Yossef Av-Gay. "Slow Release of Nitric Oxide from Charged Catheters and Its Effect on Biofilm Formation by Escherichia coli." Antimicrobial Agents and Chemotherapy 54, no. 1 (November 2, 2009): 273–79. http://dx.doi.org/10.1128/aac.00511-09.

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ABSTRACT Catheter-associated urinary tract infection is the most prevalent cause of nosocomial infections. Bacteria associated with biofilm formation play a key role in the morbidity and pathogenesis of these infections. Nitric oxide (NO) is a naturally produced free radical with proven bactericidal effect. In this study, Foley urinary catheters were impregnated with gaseous NO. The catheters demonstrated slow release of nitric oxide over a 14-day period. The charged catheters were rendered antiseptic, and as such, were able to prevent bacterial colonization and biofilm formation on their luminal and exterior surfaces. In addition, we observed that NO-impregnated catheters were able to inhibit the growth of Escherichia coli within the surrounding media, demonstrating the ability to eradicate a bacterial concentration of up to 104 CFU/ml.

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Rosen, David A., Jerome S. Pinkner, Jennifer N. Walker, Jennifer Stine Elam, Jennifer M. Jones, and Scott J. Hultgren. "Molecular Variations in Klebsiella pneumoniae and Escherichia coli FimH Affect Function and Pathogenesis in the Urinary Tract." Infection and Immunity 76, no. 7 (May 12, 2008): 3346–56. http://dx.doi.org/10.1128/iai.00340-08.

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ABSTRACT Type 1 pili mediate binding, invasion, and biofilm formation of uropathogenic Escherichia coli (UPEC) in the host urothelium during urinary tract infection (UTI) via the adhesin FimH. In this study, we characterized the molecular basis of functional differences between FimH of the UPEC isolate UTI89 and the Klebsiella pneumoniae cystitis isolate TOP52. Type 1 pili characteristically mediate mannose-sensitive hemagglutination of guinea pig erythrocytes. Although the adhesin domain of K. pneumoniae TOP52 FimH (FimH52) is highly homologous to that of E. coli, with an identical mannose binding pocket and surrounding hydrophobic ridge, it lacks the ability to agglutinate guinea pig erythrocytes. In addition, FimH-dependent biofilm formation in K. pneumoniae is inhibited by heptyl mannose, but not methyl mannose, suggesting the need for contacts outside of the mannose binding pocket. The binding specificity differences observed for FimH52 resulted in significant functional differences seen in the pathogenesis of K. pneumoniae UTI compared to E. coli UTI. Infections in a murine model of UTI demonstrated that although the K. pneumoniae strain TOP52 required FimH52 for invasion and IBC formation in the bladder, FimH52 was not essential for early colonization. This work reveals that a limited amount of sequence variation between the FimH of E. coli and K. pneumoniae results in significant differences in function and ability to colonize the urinary tract.

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Kong, Haishen, Xiaoping Hong, and Xuefen Li. "Current perspectivesin pathogenesis and antimicrobial resistance of enteroaggregative Escherichia coli." Microbial Pathogenesis 85 (August 2015): 44–49. http://dx.doi.org/10.1016/j.micpath.2015.06.002.

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32

Shikunova, Ya V., A. V. Gudkov, V. S. Boshchenko, S. P. Selivanov, and S. N. Isayeva. "Etiology and pathogenesis of acute pyelonephritis in children." Experimental and Сlinical Urology 14, no. 1 (March 25, 2021): 135–39. http://dx.doi.org/10.29188/2222-8543-2021-14-1-135-139.

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Introduction. Acute pyelonephritis in children takes a leading place among the reasons for hospitalization. Objective. To study the epidemiological, anamnestic, diagnostic and clinical features of the course of pyelonephritis in children. Materials and methods. We have carried out a retrospective study of case histories of 142 children admitted to the urology department of the Emergency hospital №2 (Tomsk) with a diagnosis of acute pyelonephritis. Results. According to the results of our study, children of both sexes of young age (up to 1 year оf age) suffer from acute complicated pyelonephritis, whereas acute uncomplicated pyelonephritis is typical for girls over 3 years old. The sensitivity of ultrasound examination of the kidneys in acute pyelonephritis was 76.8%. The vast majority (96,8%) of acute uncomplicated pyelonephritis were caused by Escherichia coli. Escherichia coli was the cause of acute complicated pyelonephrities only in 30.8% of patients, Pseudomonas aeruginosa was ranked in second in frequency (15.4%), and Enteroccoccus faecalis was ranked third (11.5%). The following antibiotics retained their effectiveness among all the identified causative flora of uncomplicated pyelonephritis: fosfomycin, furagin, gentamicin, amikacin. Only amikacin showed absolute efficiency (100%) in the group of complicated pyelonephritis. 90% of bacteria showed sensitivity to fosfomycin, and 88.5% to cefepime and ertapenem. For children with acute pyelonephritis, the acute phase process of cytomegalovirus, Ebstein-Barr viral infections, previous herpes simplex virus infection, as well as contact with Chlamydia trachomatis, Ureaplasma urealуticum and Mycoplasma hominis are specific. Conclusion. The results of the study indicate the dynamics in the etiology and pathogenesis of acute pyelonephritis in children and a need for an annual monitoring in order to correct therapy.

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Mctaggart, L. A., R. C. Rigby, and T. S. J. Elliott. "The pathogenesis of urinary tract infections associated with Escherichia coli, Staphylococcus saprophyticus and S. epidermidis." Journal of Medical Microbiology 32, no. 2 (June 1, 1990): 135–41. http://dx.doi.org/10.1099/00222615-32-2-135.

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Bessaiah, Hicham, Carole Anamalé, Jacqueline Sung, and Charles M. Dozois. "What Flips the Switch? Signals and Stress Regulating Extraintestinal Pathogenic Escherichia coli Type 1 Fimbriae (Pili)." Microorganisms 10, no. 1 (December 21, 2021): 5. http://dx.doi.org/10.3390/microorganisms10010005.

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Pathogens are exposed to a multitude of harmful conditions imposed by the environment of the host. Bacterial responses against these stresses are pivotal for successful host colonization and pathogenesis. In the case of many E. coli strains, type 1 fimbriae (pili) are an important colonization factor that can contribute to diseases such as urinary tract infections and neonatal meningitis. Production of type 1 fimbriae in E. coli is dependent on an invertible promoter element, fimS, which serves as a phase variation switch determining whether or not a bacterial cell will produce type 1 fimbriae. In this review, we present aspects of signaling and stress involved in mediating regulation of type 1 fimbriae in extraintestinal E. coli; in particular, how certain regulatory mechanisms, some of which are linked to stress response, can influence production of fimbriae and influence bacterial colonization and infection. We suggest that regulation of type 1 fimbriae is potentially linked to environmental stress responses, providing a perspective for how environmental cues in the host and bacterial stress response during infection both play an important role in regulating extraintestinal pathogenic E. coli colonization and virulence.

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Luck, Shelley N., Luminita Badea, Vicki Bennett-Wood, Roy Robins-Browne, and Elizabeth L. Hartland. "Contribution of FliC to Epithelial Cell Invasion by Enterohemorrhagic Escherichia coli O113:H21." Infection and Immunity 74, no. 12 (September 18, 2006): 6999–7004. http://dx.doi.org/10.1128/iai.00435-06.

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ABSTRACT Enterohemorrhagic Escherichia coli (EHEC) O113:H21 can invade epithelial cells. In this study, we found that invasion but not adherence was inhibited by anti-FliCH21 specific antibodies. In addition, deletion of fliCH21 from EHEC O113:H21 resulted in an eightfold decrease in invasion that was restored upon transcomplementation with fliCH21 but not with fliCH6 . These results suggested that FliC plays an important role in the pathogenesis of infections caused by EHEC O113:H21 by allowing bacteria to penetrate the intestinal epithelium.

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Washington, Casandra, Josep Bassaganya-Riera, Monica Viladomiu, Mireia Pedragosa-Marin, Richard Guerrant, James Roche та Raquel Hontecillas. "Th17 responses driven via PPARγ blockade lead to faster recovery from enteroaggregative Escherichia coli infection (49.13)". Journal of Immunology 188, № 1_Supplement (1 травня 2012): 49.13. http://dx.doi.org/10.4049/jimmunol.188.supp.49.13.

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Abstract Enteroaggregative Escherichia coli (EAEC) is a recognized cause of enteric disease in diverse clinical settings. Mucosal immunity towards EAEC infections is poorly understood. To better characterize immunoregulatory mechanisms underlying EAEC infections we constructed a computational model mimicking host responses to EAEC at the gut mucosa. Preliminary model calibration efforts demonstrated remarkable fitting to experimental data. Nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) has been targeted to modulate mucosal immune responses to EAEC. Wild type and conditional knockout mice lacking PPARγ in T cells were fed protein-deficient diets at weaning and challenged with 5x109cfu EAEC strain JM221. Quantitative RT-PCR data reveal that administration of GW9662, a potent PPARγ antagonist, for 7 days post infection or the deletion of PPARγ in T cells results in upregulation of pro-inflammatory cytokines including IL-6, TNF-α, and IL-1β when compared to non-treated infected animals. Histological analysis of colons divulges lower leukocyte infiltration and decreased mucosal thickness 14 days following EAEC infection after pharmacological blockade of PPARγ or deletion of PPARγ in T cells. These findings were accompanied by faster clearance of colonic EAEC in tissue-specific PPARγ null mice. In conclusion, we present a fully integrated approach to study host responses to EAEC that provides new insights on the pathogenesis and treatment of enteric infections.

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Allen, Kenneth P., Mildred M. Randolph, and James M. Fleckenstein. "Importance of Heat-Labile Enterotoxin in Colonization of the Adult Mouse Small Intestine by Human Enterotoxigenic Escherichia coli Strains." Infection and Immunity 74, no. 2 (February 2006): 869–75. http://dx.doi.org/10.1128/iai.74.2.869-875.2006.

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ABSTRACT Enterotoxigenic Escherichia coli (ETEC) infections are a significant cause of diarrheal disease and infant mortality in developing countries. Studies of ETEC pathogenesis relevant to vaccine development have been greatly hampered by the lack of a suitable small-animal model of infection with human ETEC strains. Here, we demonstrate that adult immunocompetent outbred mice can be effectively colonized with the prototypical human ETEC H10407 strain (colonization factor antigen I; heat-labile and heat-stable enterotoxin positive) and that production of heat-labile holotoxin provides a significant advantage in colonization of the small intestine in this model.

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Riff, Jason D., John W. Callahan, and Philip M. Sherman. "Cholesterol-Enriched Membrane Microdomains Are Required for Inducing Host Cell Cytoskeleton Rearrangements in Response to Attaching-Effacing Escherichia coli." Infection and Immunity 73, no. 11 (November 2005): 7113–25. http://dx.doi.org/10.1128/iai.73.11.7113-7125.2005.

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ABSTRACT The diarrheal pathogens enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain CL56 and enteropathogenic Escherichia coli (EPEC) O127:H6 strain E2348/69 adhere intimately to epithelial cells through attaching-effacing lesions, which are characterized by rearrangements of the host cytoskeleton, intimate adherence, and destruction of microvilli. These cytoskeletal responses require activation of host signal transduction pathways. Lipid rafts are signaling microdomains enriched in sphingolipid and cholesterol in the plasma membrane. The effect of perturbing plasma membrane cholesterol on bacterial intimate adherence was assessed. Infection of both HEp-2 cells and primary skin fibroblasts with strains CL56 and E2348/69 caused characteristic rearrangements of the cytoskeleton at sites of bacterial adhesion. CL56- and E2348/69-induced cytoskeletal rearrangements were inhibited following cholesterol depletion. Addition of exogenous cholesterol to depleted HEp-2 cells restored cholesterol levels and rescued bacterially induced α-actinin mobilization. Quantitative bacterial adherence assays showed that EPEC adherence to HEp-2 cells was dramatically reduced following cholesterol depletion, whereas the adherence of EHEC remained high. Cytoskeletal rearrangements on skin fibroblasts obtained from children with Niemann-Pick type C disease were markedly reduced. These findings indicate that host membrane cholesterol contained in lipid rafts is necessary for the cytoskeletal rearrangements following infection with attaching-effacing Escherichia coli. Differences in initial adherence indicate divergent roles for host membrane cholesterol in the pathogenesis of EHEC and EPEC infections.

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39

Menge, Christian. "Molecular Biology of Escherichia coli Shiga Toxins’ Effects on Mammalian Cells." Toxins 12, no. 5 (May 23, 2020): 345. http://dx.doi.org/10.3390/toxins12050345.

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Shiga toxins (Stxs), syn. Vero(cyto)toxins, are potent bacterial exotoxins and the principal virulence factor of enterohemorrhagic Escherichia coli (EHEC), a subset of Shiga toxin-producing E. coli (STEC). EHEC strains, e.g., strains of serovars O157:H7 and O104:H4, may cause individual cases as well as large outbreaks of life-threatening diseases in humans. Stxs primarily exert a ribotoxic activity in the eukaryotic target cells of the mammalian host resulting in rapid protein synthesis inhibition and cell death. Damage of endothelial cells in the kidneys and the central nervous system by Stxs is central in the pathogenesis of hemolytic uremic syndrome (HUS) in humans and edema disease in pigs. Probably even more important, the toxins also are capable of modulating a plethora of essential cellular functions, which eventually disturb intercellular communication. The review aims at providing a comprehensive overview of the current knowledge of the time course and the consecutive steps of Stx/cell interactions at the molecular level. Intervention measures deduced from an in-depth understanding of this molecular interplay may foster our basic understanding of cellular biology and microbial pathogenesis and pave the way to the creation of host-directed active compounds to mitigate the pathological conditions of STEC infections in the mammalian body.

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BRAGA, Ricardo Luís Lopes, Ana Claudia Machado PEREIRA, Paula Azevedo dos SANTOS, Angela Corrêa FREITAS-ALMEIDA, and Ana Cláudia de Paula ROSA. "EX VIVO MODEL OF RABBIT INTESTINAL EPITHELIUM APPLIED TO THE STUDY OF COLONIZATION BY ENTEROAGGREGATIVE ESCHERICHIA COLI." Arquivos de Gastroenterologia 54, no. 2 (March 16, 2017): 130–34. http://dx.doi.org/10.1590/s0004-2803.201700000-12.

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ABSTRACT BACKGROUND The diarrheal syndrome is considered a serious public health problem all over the world and is considered a major cause of morbidity and mortality in developing countries. The high incidence of enteroaggregative Escherichia coli in diarrheal syndromes classified as an emerging pathogen of gastrointestinal infections. After decades of study, your pathogenesis remains uncertain and has been investigated mainly using in vitro models of adhesion in cellular lines. OBJECTIVE The present study investigated the interaction of enteroaggregative Escherichia coli strains isolated from childhood diarrhea with rabbit ileal and colonic mucosa ex vivo, using the in vitro organ culture model. METHODS The in vitro adhesion assays using cultured tissue were performed with the strains co-incubated with intestinal fragments of ileum and colon over a period of 6 hours. Each strain was tested with three intestinal fragments for each region. The fragments were analysed by scanning electron microscopy. RESULTS Through scanning electron microscopy we observed that all strains adhered to rabbit ileal and colonic mucosa, with the typical aggregative adherence pattern of “stacked bricks” on the epithelium. However, the highest degree of adherence was observed on colonic mucosa. Threadlike structures were found in greater numbers in the ileum compared to the colon. CONCLUSION These data showed that enteroaggregative Escherichia coli may have a high tropism for the human colon, which was ratified by the higher degree of adherence on the rabbit colonic mucosa. Finally, data indicated that in vitro organ culture of intestinal mucosa from rabbit may be used to elucidate the enteroaggregative Escherichia coli pathogenesis.

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Ortega-Hernandez, Oscar-Danilo, Nancy-Agmon Levin, Arie Altman, and Yehuda Shoenfeld. "Infectious Agents in the Pathogenesis of Primary Biliary Cirrhosis." Disease Markers 29, no. 6 (2010): 277–86. http://dx.doi.org/10.1155/2010/923928.

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Primary biliary cirrhosis (PBC) is a chronic progressive cholestatic liver disease which is characterized by the breakdown of self-tolerance to the highly conserved pyruvate dehydrogenase complex, specially the pyruvate dehydrogenase E2 complex (PDC-E2). The breakdown of the tolerance to such antigens leads to an autoimmune process characterized by portal inflammation and immune-mediated destruction of the intrahepatic bile ducts. Epidemiological studies have suggested that infections agents can trigger or even exacerbate the disease. Among other gram negative bacteria,Escherichia Coli, andNosphingobium aromaticivoransare the most associated agents reported hitherto. Epidemiological and molecular evidence points towards molecular mimicry between some components of these microorganisms and specific amino-acid sequences that are present in proteins on normal cells of the biliary tract. In this review, we revisit all reports suggesting that infectious agents might be associated with the autoimmune pathogenesis of PBC. We also retrieve the immune molecular mimicry mechanisms that are likely involved with the autoimmune process in PBC.

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Clarke, S. C., R. D. Haigh, P. P. E. Freestone, and P. H. Williams. "Virulence of Enteropathogenic Escherichia coli, a Global Pathogen." Clinical Microbiology Reviews 16, no. 3 (July 2003): 365–78. http://dx.doi.org/10.1128/cmr.16.3.365-378.2003.

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SUMMARY Enteropathogenic Escherichia coli (EPEC) remains an important cause of diarrheal disease worldwide. Research into EPEC is intense and provides a good virulence model of other E. coli infections as well as other pathogenic bacteria. Although the virulence mechanisms are now better understood, they are extremely complex and much remains to be learnt. The pathogenesis of EPEC depends on the formation of an ultrastructural lesion in which the bacteria make intimate contact with the host apical enterocyte membrane. The formation of this lesion is a consequence of the ability of EPEC to adhere in a localized manner to the host cell, aided by bundle-forming pili. Tyrosine phosphorylation and signal transduction events occur within the host cell at the lesion site, leading to a disruption of the host cell mechanisms and, consequently, to diarrhea. These result from the action of highly regulated EPEC secreted proteins which are released via a type III secretion system, many genes of which are located within a pathogenicity island known as the locus of enterocyte effacement. Over the last few years, dramatic increases in our knowledge of EPEC virulence have taken place. This review therefore aims to provide a broad overview of and update to the virulence aspects of EPEC.

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Barbieri, Nicolle L., Bryon Nicholson, Ashraf Hussein, Wentong Cai, Yvonne M. Wannemuehler, Giuseppe Dell'Anna, Catherine M. Logue, Fabiana Horn, Lisa K. Nolan, and Ganwu Li. "FNR Regulates Expression of Important Virulence Factors Contributing to Pathogenicity of Uropathogenic Escherichia coli." Infection and Immunity 82, no. 12 (September 22, 2014): 5086–98. http://dx.doi.org/10.1128/iai.02315-14.

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ABSTRACTUropathogenicEscherichia coli(UPEC) is responsible for the majority of urinary tract infections (UTIs), which are some of the world's most common bacterial infections of humans. Here, we examined the role of FNR (fumarate andnitratereduction), a well-known global regulator, in the pathogenesis of UPEC infections. We constructed anfnrdeletion mutant of UPEC CFT073 and compared it to the wild type for changes in virulence, adherence, invasion, and expression of key virulence factors. Compared to the wild type, thefnrmutant was highly attenuated in the mouse model of human UTI and showed severe defects in adherence to and invasion of bladder and kidney epithelial cells. Our results showed that FNR regulates motility and multiple virulence factors, including expression of type I and P fimbriae, modulation of hemolysin expression, and expression of a novel pathogenicity island involved in α-ketoglutarate metabolism under anaerobic conditions. Our results demonstrate that FNR is a key global regulator of UPEC virulence and controls expression of important virulence factors that contribute to UPEC pathogenicity.

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Zhang, Hongwei, David W. Niesel, Johnny W. Peterson, and Gary R. Klimpel. "Lipoprotein Release by Bacteria: Potential Factor in Bacterial Pathogenesis." Infection and Immunity 66, no. 11 (November 1, 1998): 5196–201. http://dx.doi.org/10.1128/iai.66.11.5196-5201.1998.

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ABSTRACT Lipoprotein (LP) is a major component of the outer membrane of bacteria in the family Enterobacteriaceae. LP induces proinflammatory cytokine production in macrophages and lethal shock in LPS-responsive and -nonresponsive mice. In this study, the release of LP from growing bacteria was investigated by immuno-dot blot analysis. An immuno-dot blot assay that could detect LP at levels as low as 100 ng/ml was developed. By using this assay, significant levels of LP were detected in culture supernatants of growing Escherichia coli cells. During mid-logarithmic growth, approximately 1 to 1.5 μg of LP per ml was detected in culture supernatants from E. coli. In contrast, these culture supernatants contained 5 to 6 μg/ml of lipopolysaccharide (LPS). LP release was not unique toE. coli. Salmonella typhimurium, Yersinia enterocolitica, and two pathogenic E. coli strains also released LP during in vitro growth. Treatment of bacteria with the antibiotic ceftazidime significantly enhanced LP release. Culture supernatants from 5-h cultures of E. coli were shown to induce in vitro production of interleukin-6 (IL-6) by macrophages obtained from LPS-nonresponsive C3H/HeJ mice. In contrast, culture supernatants from an E. coli LP-deletion mutant were significantly less efficient at inducing IL-6 production in C3H/HeJ macrophages. These results suggest, for the first time, that LP is released from growing bacteria and that this released LP may play an important role in the induction of cytokine production and pathologic changes associated with gram-negative bacterial infections.

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Tu, Jian, Ting Xue, Kezong Qi, Ying Shao, Boyan Huang, Xueyan Wang, and Xiuhong Zhou. "The irp2 and fyuA genes in High Pathogenicity Islands are involved in the pathogenesis of infections caused by avian pathogenic Escherichia coli (APEC)." Polish Journal of Veterinary Sciences 19, no. 1 (March 1, 2016): 21–29. http://dx.doi.org/10.1515/pjvs-2016-0004.

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Abstract Avian pathogenic Escherichia coli (APEC) is a major bacterial infectious disease that may lead to local or systemic infections in chickens with clinical manifestations. The irp2-fyuA gene cluster has been confirmed to be the main genes involved in the synthesis of HPI. The objective of this study was to determine the influence of the irp2 and fyuA genes in the high pathogenicity island (HPI) of avian pathogenic Escherichia coli (APEC) on its pathogenicity by knocking out these genes. The ΔAE17 (lacking irp2) and ΔΔAE17 (lacking irp2 and fyuA) strains of APEC were constructed. The ΔAE17 and ΔΔAE17 strains showed significantly impaired capacity to adhere onto DF-1 cells. The LD50 results indicated that the virulence of the ΔAE17 and ΔΔAE17 strains was decreased in comparison with that of the AE17 strain. We concluded that the knock-out of the core HPI genes weakened APEC adhesion onto DF-1 cells, inhibited transcription of virulence genes, and reduced pathogenicity in chicks. The effects of genetic deletion of irp2 and fyuA on APEC were more severe than those produced by deletion of irp2 only, indicating that irp2 and fyuA co-regulate APEC pathogenicity.

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Tuntufye, Huruma Nelwike, Sarah Lebeer, Paul Simon Gwakisa, and Bruno Maria Goddeeris. "Identification of Avian Pathogenic Escherichia coli Genes That Are InducedIn Vivoduring Infection in Chickens." Applied and Environmental Microbiology 78, no. 9 (February 17, 2012): 3343–51. http://dx.doi.org/10.1128/aem.07677-11.

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ABSTRACTAvian pathogenicEscherichia coli(APEC) is associated with extraintestinal infections in poultry causing a variety of diseases collectively known as colibacillosis. The host and bacterial factors influencing and/or responsible for carriage and systemic translocation of APEC inside the host are poorly understood. Identification of such factors could help in the understanding of its pathogenesis and in the subsequent development of control strategies. Recombination-basedin vivoexpression technology (RIVET) was used to identify APEC genes specifically expressed during infection in chickens. A total of 21 clones within vivo-induced promoters were isolated from chicken livers and spleens, indicative of systemic infection. DNA sequencing of the cloned fragments revealed that 12 of the genes were conservedE. coligenes (metH,lysA,pntA,purL,serS,ybjE,ycdK[rutC],wcaJ,gspL,sdsR,ylbE, andyjiY), 6 of the genes were phage related/associated, and 3 genes were pathogen specific (tkt1,irp2, andeitD). These genes are involved in various cellular functions, such as metabolism, cell envelope and integrity, transport systems, and virulence. Others were phage related or have yet-unknown functions.

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Wang, Haixiu, Zifu Zhong, Yu Luo, Eric Cox, and Bert Devriendt. "Heat-Stable Enterotoxins of Enterotoxigenic Escherichia coli and Their Impact on Host Immunity." Toxins 11, no. 1 (January 8, 2019): 24. http://dx.doi.org/10.3390/toxins11010024.

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Enterotoxigenic Escherichia coli (ETEC) are an important diarrhea-causing pathogen and are regarded as a global threat for humans and farm animals. ETEC possess several virulence factors to infect its host, including colonization factors and enterotoxins. Production of heat-stable enterotoxins (STs) by most ETEC plays an essential role in triggering diarrhea and ETEC pathogenesis. In this review, we summarize the heat-stable enterotoxins of ETEC strains from different species as well as the molecular mechanisms used by these heat-stable enterotoxins to trigger diarrhea. As recently described, intestinal epithelial cells are important modulators of the intestinal immune system. Thus, we also discuss the impact of the heat-stable enterotoxins on this role of the intestinal epithelium and how these enterotoxins might affect intestinal immune cells. Finally, the latest developments in vaccination strategies to protect against infections with ST secreting ETEC strains are discussed. This review might inform and guide future research on heat-stable enterotoxins to further unravel their molecular pathogenesis, as well as to accelerate vaccine design.

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PADHYE, NISHA V., and MICHAEL P. DOYLE. "Escherichia coli O157:H7: Epidemiology, Pathogenesis, and Methods for Detection in Food." Journal of Food Protection 55, no. 7 (July 1, 1992): 555–65. http://dx.doi.org/10.4315/0362-028x-55.7.555.

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Escherichia coli O157:H7 is now recognized as an important human pathogen. Illnesses caused by E. coli O157:H7 infection can range from self-limited, watery diarrhea to life-threatening manifestations such as hemolytic uremic syndrome or thrombotic thrombocytopenic purpura. The mode of transmission is primarily through food; however, person-to-person transmission also has been identified in some day-care center and nursing home out-breaks. Studies to date indicate that cattle are an important reservoir of the organism. Although adhesion to intestinal epithelial cells and verotoxins are considered important virulence factors in the pathogenesis of the organism, more research is are necessary to determine the exact mechanism of pathogenicity. There is need for a rapid diagnostic test for the detection of E. coli O157:H7 in food and in clinical samples. Several useful research reagents have been developed for detecting E. coli O157:H7; however, they must be applied to a procedure that is specific, sensitive, rapid, easy to use, and commercially available so that microbiological laboratories can readily use them.

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., Shahin Najar Peerayeh, Narges Nooritalab ., and Mortaza Sattari . "Roles of Uropathogenic Escherichia coli Pili in Pathogenesis of Urinary Tract Infection." Research Journal of Microbiology 3, no. 3 (March 1, 2008): 175–80. http://dx.doi.org/10.3923/jm.2008.175.180.

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Brumbaugh, Ariel R., Sara N. Smith, Sargurunathan Subashchandrabose, Stephanie D. Himpsl, Tracy H. Hazen, David A. Rasko, and Harry L. T. Mobley. "Blocking Yersiniabactin Import Attenuates Extraintestinal Pathogenic Escherichia coli in Cystitis and Pyelonephritis and Represents a Novel Target To Prevent Urinary Tract Infection." Infection and Immunity 83, no. 4 (January 26, 2015): 1443–50. http://dx.doi.org/10.1128/iai.02904-14.

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The emergence and spread of extended-spectrum beta-lactamases and carbapenemases among common bacterial pathogens are threatening our ability to treat routine hospital- and community-acquired infections. With the pipeline for new antibiotics virtually empty, there is an urgent need to develop novel therapeutics. Bacteria require iron to establish infection, and specialized pathogen-associated iron acquisition systems like yersiniabactin, common among pathogenic species in the familyEnterobacteriaceae, including multidrug-resistantKlebsiella pneumoniaeand pathogenicEscherichia coli, represent potentially novel therapeutic targets. Although the yersiniabactin system was recently identified as a vaccine target for uropathogenicE. coli(UPEC)-mediated urinary tract infection (UTI), its contribution to UPEC pathogenesis is unknown. Using anE. colimutant (strain 536ΔfyuA) unable to acquire yersiniabactin during infection, we established the yersiniabactin receptor as a UPEC virulence factor during cystitis and pyelonephritis, a fitness factor during bacteremia, and a surface-accessible target of the experimental FyuA vaccine. In addition, we determined through transcriptome sequencing (RNA-seq) analyses of RNA fromE. colicausing cystitis in women that iron acquisition systems, including the yersiniabactin system, are highly expressed by bacteria during natural uncomplicated UTI. Given that yersiniabactin contributes to the virulence of several pathogenic species in the familyEnterobacteriaceae, including UPEC, and is frequently associated with multidrug-resistant strains, it represents a promising novel target to combat antibiotic-resistant infections.

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