Role of F1C Fimbriae, Flagella, and Secreted Bacterial Components in the Inhibitory Effect of Probiotic Escherichia coli Nissle 1917 on Atypical Enteropathogenic E. coli Infection (original) (raw)
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Probiotic and enterohemorrhagic Escherichia coli: An effective strategy against a deadly enemy?
Critical reviews in microbiology, 2017
Enterohemorrhagic Escherichia coli (EHEC) are major food-borne pathogens that constitute a serious public health threat. Currently, there is no specific treatment available for EHEC infections in human creating an urgent need for the development of alternative therapeutic strategies. Among them, one of the most promising approaches is the use of probiotic microorganisms. Even if many studies have shown the antagonistic effects of probiotic bacteria or yeast on EHEC survival, virulence, adhesion on intestinal epithelium or pathogen-induced inflammatory responses, mechanisms mediating their beneficial effects remain unclear. This review describes EHEC pathogenesis and novel therapeutic strategies, with a particular emphasis on probiotics. The interests and limits of a probiotic-based approach and the way it might be incorporated into global health strategies against EHEC infections will be discussed.
Journal of Infectious Diseases, 2012
Background. Enteroaggregative Escherichia coli (EAEC) are increasingly recognized as an important agent of inflammatory and often persistent diarrhea. Although previous studies report on the inflammatory aspects of EAEC pathogenesis, the mechanisms by which EAEC trigger these events are not well understood. Methods. EAEC strains harboring mutations in known EAEC virulence determinants were tested in an in vitro model of transepithelial migration of polymorphonuclear neutrophils (PMNs) and in human intestinal xenografts in severe-combined immunodeficient (SCID-HU-INT) mice, a novel model for studying EAEC disease in vivo. Results. Expression of aggregative adherence fimbriae (AAFs), the principal adhesins of EAEC, was required for EAEC-induced PMN transepithelial migration in vitro. Moreover, constructed plasmids encoding AAF gene clusters demonstrated that the AAF adhesins are sufficient for triggering this event in a nonpathogenic E. coli background. Furthermore, with use of the SCID-HU-INT mouse model, severe tissue damage and infiltration of inflammatory cells was observed in the human tissue after EAEC infection. These pathological marks were strongly related to AAF expression, thus clearly confirming our in vitro findings. Conclusions. The present work establishes EAEC as an important inflammatory pathogen and the AAF adhesins as inducers of potentially detrimental immune responses.
Developmental & Comparative Immunology, 2010
Infections with F4 + enterotoxigenic Escherichia coli (ETEC) causes severe diarrhoea in piglets, resulting in morbidity and mortality. F4 fimbriae are the key virulence factors mediating the attachment of F4 + ETEC to the intestinal epithelium. Intestinal epithelial cells (IEC) are recently being recognized as important regulators of the intestinal immune system through the secretion of cytokines, however, data on how F4 + ETEC affect this cytokine secretion are scarce. By using ETEC strains expressing either polymeric, monomeric or F4 fimbriae with a reduced polymeric stability, we demonstrated that polymeric fimbriae are essential for adhesion to porcine IEC and the secretion of IL-6 and IL-8 by IEC. Remarkably, this cytokine secretion was not abrogated following stimulation with an F4-negative strain. Since this strain expresses flagellin, TLR5 mediated signalling could be involved. Indeed, porcine IEC express TLR5 and purified flagellin induced IL-6 and IL-8 secretion, indicating that, as for other pathogens, flagellin is the dominant virulence factor involved in the induction of proinflammatory responses in IEC. These results indicate a potential mucosal adjuvant capacity of ETEC-derived flagellin and may improve rational vaccine design against F4 + ETEC infections.
Adherence of Diarrheagenic Escherichia coli Strains to Epithelial Cells
Infection and Immunity, 2005
An important early step in the colonization of the human gastrointestinal tract by bacteria is the adhesion of the organism to the host surface. Although adhesion is essential to maintain members of the normal microflora in the intestine, it is also the critical early phase in all diarrheal infections caused by pathogenic Escherichia coli strains. It is important, therefore, to fully understand the mechanisms underlying E. coli adhesion and in that way to be able to develop methods of maintaining the intestinal normal microflora and to prevent pathogenic E. coli from initiating an infectious process. Great progress has been made in recent years in the identification of the adherence factors of different diarrheagenic E. coli strains (Table 1). These protein structures are associated with the bacterial surface and can be subdivided into fimbrial and nonfimbrial adhesins (Fig. 1). In this minireview, we will discuss recent advances in the identification and characterization of previously known and novel adhesion factors from the six major categories of diarrheagenic E. coli strains: enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli (EHEC), enterotoxigenic E. coli (ETEC), enteroaggregative E. coli (EAEC), enteroinvasive E. coli (EIEC), and diffusely adhering E. coli (DAEC).
Veterinary Microbiology, 2008
Enterotoxigenic Escherichia coli (ETEC) infections result in large economic losses in the swine industry worldwide. The organism causes diarrhea by adhering to and colonizing enterocytes in the small intestines. While much progress has been made in understanding the pathogenesis of ETEC, no homologous intestinal epithelial cultures suitable for studying porcine ETEC pathogenesis have been described prior to this report. In the current study, we investigated the adherence of various porcine ETEC strains to two porcine (IPEC-1 and IPEC-J2) and one human (INT-407) small intestinal epithelial cell lines. Each cell line was assessed for its ability to support the adherence of E. coli expressing fimbrial adhesins K88ab, K88ac, K88ad, K99, F41, 987P, and F18. Wild-type ETEC expressing K88ab, K88ac, and K88ad efficiently bound to both IPEC-1 and IPEC-J2 cells. An ETEC strain expressing both K99 and F41 bound heavily to both porcine cell lines but an E. coli strain expressing only K99 bound very poorly to these cells. E. coli expressing F18 adhesin strongly bound to IPEC-1 cells but did not adhere to IPEC-J2 cells. The E. coli strains G58-1 and 711 which express no fimbrial adhesins and those that express 987P fimbriae failed to bind to either porcine cell line. Only strains B41 and K12:K99 bound in abundance to INT-407 cells. The binding of porcine ETEC to IPEC-J2, IPEC-1 and INT-407 with varying affinities, together with lack of binding of 987P ETEC and non-fimbriated E. coli strains, suggests strain-specific E. coli binding to these cell lines. These findings suggest the potential usefulness of porcine intestinal cell lines for studying ETEC pathogenesis.
Diarrheagenic Escherichia Coli and Probiotic Activity against Foodborne Pathogens: A Brief Review
2017
E. coli strains are naturally commensal bacteria that live in intestinal tract of humans and other mammals. Some strains are pathogenic and can cause disease, especially intestinal [2]. Diarrheagenic E. coli strains are classified into six categories, based in clinical syndromes, symptoms, epidemiology, O:H serotypes, virulence factors and interaction with in vitro cultivated cells [3]. All enteropathogenic E. coli types cause generally watery diarrhea as a common symptom. Most episodes of intestinal dysfunction are auto limited and solved in a few days, but some rare cases can progress to more severe disease [2,3].
ABSTRACTEnteropathogenic E. coli (EPEC) are recognized as one of the leading bacterial causes of infantile diarrhea worldwide. Weaned C57BL/6 mice pretreated with antibiotics were challenged orally with wild-type EPEC or escN mutant (lacking type 3 secretion system) to determine colonization, inflammatory responses and clinical outcomes during infection. Antibiotic disruption of intestinal microbiota enabled efficient colonization by wild-type EPEC resulting in growth impairment and diarrhea. Increase in inflammatory biomarkers, chemokines, cellular recruitment and pro-inflammatory cytokines were observed in intestinal tissues. Metabolomic changes were also observed in EPEC infected mice with changes in TCA cycle intermediates, increased creatine excretion and shifts in gut microbial metabolite levels. In addition, by 7 days after infection, although weights were recovering, EPEC-infected mice had increased intestinal permeability and decreased colonic claudin-1 levels. The escN mut...
Interactions Between Enteropathogenic Escherichia coli and Epithelial Cells
Clinical Infectious Diseases, 1999
Enteropathogenic Escherichia coli (EPEC) may be considered a paradigm for a multistage interaction between pathogen and host cell. EPEC strains produce a type IV pilus that is associated with initial adherence to host cells, and these strains possess a type III secretion apparatus that is necessary for transducing signals to host cells. Secretion of three Esp proteins is required for activation of a phosphotyrosine-containing receptor that allows EPEC to bind intimately to host cells via the bacterial outer membrane protein intimin. Intimately attached bacteria rest upon a pedestal composed of host cytoskeletal proteins in an arrangement recognized as the attaching and effacing phenotype. The precise molecular interactions that lead to these dramatic alterations in the host cell cytoskeleton remain to be elucidated.