Anaerobic Conditions Promote Expression of Sfp Fimbriae and Adherence of Sorbitol-Fermenting Enterohemorrhagic
            <i>Escherichia coli</i>
            O157:NM to Human Intestinal Epithelial Cells

Müsken, Anne; Bielaszewska, Martina; Greune, Lilo; Schweppe, Christian Henning; Müthing, Johannes; Schmidt, Herbert; Schmidt, M. Alexander; Karch, Helge; Zhang, Wenlan

doi:10.1128/aem.02496-07

Cited by 51 publications

(47 citation statements)

References 52 publications

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“…In addition, SF E. coli O157:NM strains have been shown to possess a unique fimbrial cluster encoded on their large plasmid, pSFO157, which mediates the expression of Sfp fimbriae (9). Recently published work demonstrates that Sfp fimbriae are expressed by SF STEC O157:NM strains cultured under anaerobic conditions on solid media simulating the colonic environment and that the induction of Sfp fimbriae on wild-type SF STEC O157:NM strains correlated with increased adherence to Caco-2 and HCT-8 cells (38). Single asterisks indicate that, following culture on CFA agar, the CR-positive SF STEC O157:NM strain E02/879 adhered to Caco-2 cells at significantly higher levels than the CR-negative SF STEC O157:NM strains 340/97 and 080/01 (P Ͻ 0.001).…”

Section: Discussionmentioning

confidence: 99%

Pathogenic Potential of Emergent Sorbitol-Fermenting Escherichia coli O157:NM

et al. 2008

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Non-sorbitol-fermenting (NSF) Escherichia coli O157:H7 is the primary Shiga toxin-producing E. coli (STEC) serotype associated with human infection. Since 1988, sorbitol-fermenting (SF) STEC O157:NM strains have emerged and have been associated with a higher incidence of progression to hemolytic-uremic syndrome (HUS) than NSF STEC O157:H7. This study investigated bacterial factors that may account for the increased pathogenic potential of SF STEC O157:NM. While no evidence of toxin or toxin expression differences between the two O157 groups was found, the SF STEC O157:NM strains adhered at significantly higher levels to a human colonic cell line. Under the conditions tested, curli were shown to be the main factor responsible for the increased adherence to Caco-2 cells. Notably, 52 of 66 (79%) European SF STEC O157:NM strains tested bound Congo red at 37 C and this correlated with curli expression. In a subset of strains, curli expression was due to increased expression from the csgBAC promoter that was not always a consequence of increased csgD expression. The capacity of SF STEC O157:NM strains to express curli at 37 C may have relevance to the epidemiology of human infections as curliated strains could promote higher levels of colonization and inflammation in the human intestine. In turn, this could lead to increased toxin exposure and an increased likelihood of progression to HUS.

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Section: Discussionmentioning

confidence: 99%

Pathogenic Potential of Emergent Sorbitol-Fermenting Escherichia coli O157:NM

et al. 2008

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“…In SFO157:NM, the sfp operon is found on the pSFO157 virulence plasmid and was found to be involved in autoagglutination (311). Expression of the sfp under laboratory conditions required anaerobic conditions (312). Although sfp is gen- erally thought to be restricted to SFO157:NM isolates, it has been found in STEC O165:H25/NM (313).…”

Section: Pathogenesismentioning

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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“…The plasmids of STEC are highly variable genetic elements (14), and surveys of STEC strains of various serogroups and other DECs revealed the sfpA and sfpDG regions to be restricted to SF STEC O157:H Ϫ (13, 30). The contribution of Sfp fimbriae to the adherence of SF STEC O157:NM strains to human intestinal epithelial cells has been investigated, and the data showed that the expression of Sfp fimbriae is induced under anaerobic conditions (resembling those of the natural site of infection) and that induction of Sfp fimbriae correlates with increased adherence to Caco-2 and HCT-8 cells (58).…”

Section: Other Stec Fimbriae: Sfp Fimbriaementioning

confidence: 99%

Molecular Mechanisms That Mediate Colonization of Shiga Toxin-Producing Escherichia coli Strains

2012

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Shiga toxin-producing Escherichia coli (STEC) is a group of pathogens which cause gastrointestinal disease in humans and have been associated with numerous food-borne outbreaks worldwide. The intimin adhesin has been considered for many years to be the only colonization factor in these strains. However, the rapid progress in whole-genome sequencing of different STEC serotypes has accelerated the discovery of other adhesins (fimbrial and afimbrial), which have emerged as important contributors to the intestinal colonization occurring during STEC infection. This review summarizes recent progress to identify and characterize, at the molecular level, novel adhesion and colonization factors in STEC strains, with an emphasis on their contribution to virulence traits, their host-pathogen interactions, the regulatory mechanisms controlling their expression, and their role as targets eliciting immune responses in the host. STEC O157:H7 AND NON-O157 STEC Shiga-toxigenic Escherichia coli (STEC) O157:H7 is an important cause of human gastrointestinal disease and the beststudied STEC associated with large outbreaks worldwide (43, 74). STEC O157:H7 strains cause diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS) (59). Disease-associated human isolates of E. coli O157:H7 are characterized for the presence of specific sets of virulence genes, including those encoding Shigatoxins (stx 1 , stx 2 ), intimin (eae), hemolysin (hlyA), and long polar fimbriae (lpf1 and lpf2) (45, 97). The production of Stx is the main virulence feature of STEC associated with the development of HUS (82) but cannot be solely responsible for full pathogenicity. STEC associated with severe human disease is usually capable of colonizing the intestinal mucosa and possesses mobile genetic elements carrying virulence genes, such as plasmids, transposons, phages, and pathogenicity islands (79,92,97). Several important colonization properties are carried by the locus of enterocyte effacement (LEE) pathogenicity island (92), which governs the ability of STEC to colonize the intestinal mucosa of the host and produces a peculiar pathogenic process known as the attachingand-effacing (A/E) lesion (for a review, see reference 59).Most virulence/colonization factors have been described for STEC O157:H7 isolates; however, it is important to identify and determine the virulence traits of other STECs important for disease in humans, the so-called "non-O157 STEC" strains. In addition to diarrhea, these isolates are also associated with severe disease. Several serogroups of non-O157 STEC have been described; however, the serogroups O26, O45, O103, O111, and O145 have been identified as the "big six" non-O157 STEC O serogroups, because they have been associated with increasing frequency in patients with bloody diarrhea and HUS (12,29,41,55). Because the U.S. Food and Drug Administration recognizes that non-O157 STEC serogroups are emerging as an important cause of food-borne disease, these isolates impact both the imported and domestic food supply. Therefor...

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Anaerobic Conditions Promote Expression of Sfp Fimbriae and Adherence of Sorbitol-Fermenting Enterohemorrhagic Escherichia coli O157:NM to Human Intestinal Epithelial Cells

Cited by 51 publications

References 52 publications

Pathogenic Potential of Emergent Sorbitol-Fermenting Escherichia coli O157:NM

Pathogenic Potential of Emergent Sorbitol-Fermenting Escherichia coli O157:NM

Recent Advances in Understanding Enteric Pathogenic Escherichia coli

Molecular Mechanisms That Mediate Colonization of Shiga Toxin-Producing Escherichia coli Strains

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