Characterization of Escherichia coli isolated from gut biopsies of newly diagnosed patients with inflammatory bowel disease

Sepehri, Shadi; Khafipour, Ehsan; Bernstein, Çharles N.; Coombes, Brian K.; Pilar, Ana Victoria C.; Karmali, Mohamed A.; Ziebell, Kim; Krause, Denis O.

doi:10.1002/ibd.21509

Cited by 77 publications

(66 citation statements)

References 53 publications

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“…A growing body of work indicates genetic and phenotypic diversity among AIEC isolated from human adults with IBD (7,27,35,44,48), children with Crohn's disease (4,5), and companion animals (49,50). This diversity suggests that host pathways might select for certain AIEC genotypes.…”

Section: Discussionmentioning

confidence: 99%

Host Defense Peptide Resistance Contributes to Colonization and Maximal Intestinal Pathology by Crohn's Disease-Associated Adherent-Invasive Escherichia coli

et al. 2014

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Host defense peptides secreted by colonocytes and Paneth cells play a key role in innate host defenses in the gut. In Crohn's disease, the burden of tissue-associated Escherichia coli commonly increases at epithelial surfaces where host defense peptides concentrate, suggesting that this bacterial population might actively resist this mechanism of bacterial killing. Adherent-invasive E. coli (AIEC) is associated with Crohn's disease; however, the colonization determinants of AIEC in the inflamed gut are undefined. Here, we establish that host defense peptide resistance contributes to host colonization by Crohn's-associated AIEC. We identified a plasmid-encoded genomic island (called PI-6) in AIEC strain NRG857c that confers high-level resistance to ␣-helical cationic peptides and ␣-and ␤-defensins. Deletion of PI-6 sensitized strain NRG857c to these host defense molecules, reduced its competitive fitness in a mouse model of infection, and attenuated its ability to induce cecal pathology. This phenotype is due to two genes in PI-6, arlA, which encodes a Mig-14 family protein implicated in defensin resistance, and arlC, an OmpT family outer membrane protease. Implicit in these findings are new bacterial targets whose inhibition might limit AIEC burden and disease in the gut.

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Section: Discussionmentioning

confidence: 99%

Host Defense Peptide Resistance Contributes to Colonization and Maximal Intestinal Pathology by Crohn's Disease-Associated Adherent-Invasive Escherichia coli

et al. 2014

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“…Multilocus sequence typing (MLST) has become a common method for typing pathogenic E. coli strains (13)(14)(15)(16)(17)(18) and establishing their relatedness. A small number of housekeeping genes are sequenced and assigned a unique allele, and the allelic profile of the housekeeping genes can be used to give an isolate a sequence type (e.g., E. coli O104:H4 is ST678 and many STEC O157:H7 isolates are ST11, based on the MLST databases [see below]).…”

Section: Microbiology Isolation and Typing Of E Colimentioning

confidence: 99%

“…AIEC has been implicated in inflammatory bowel diseases in humans and animals, including CD in humans and granulomatous colitis in boxer dogs, chickens, and turkeys (858,859). Human studies have found that AIEC colonizes the intestinal mucosae of CD patients and is associated with both early and chronic lesions, suggesting that AIEC may initiate disease as well as contribute to chronic inflammation (17,843,860). CD presents with abdominal pain, fever, and bowel obstruction or diarrhea with the presence of blood and/or mucus (861).…”

Section: Clinical Considerationsmentioning

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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“…It has been hypothesized that the LF82 genome has evolved from those of extraintestinal pathogenic E. coli (ExPEC) B2 strains by the acquisition of Salmonella and Yersinia isolated or clustered genes or predicted coding sequences located on plasmids and at various loci on the chromosome (441). Following the isolation of the prototype AIEC LF-82 strain, other CD-and UC-associated AIEC strains have been isolated and characterized (442)(443)(444)(445)(446)(447)(448)(449). The results indicate that AIEC isolated from IBD patients has not evolved from a single ancestral background but corresponds to a group of bacteria that have been able to take advantage of an "IBD microenvironment" and probably share some common genes with ExPEC (446).…”

Section: Cell Interaction Cell Entry and Intracellular Lifestylementioning

confidence: 99%

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Moal

Servin

2013

Microbiol Mol Biol Rev

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SUMMARY Hosts are protected from attack by potentially harmful enteric microorganisms, viruses, and parasites by the polarized fully differentiated epithelial cells that make up the epithelium, providing a physical and functional barrier. Enterovirulent bacteria interact with the epithelial polarized cells lining the intestinal barrier, and some invade the cells. A better understanding of the cross talk between enterovirulent bacteria and the polarized intestinal cells has resulted in the identification of essential enterovirulent bacterial structures and virulence gene products playing pivotal roles in pathogenesis. Cultured animal cell lines and cultured human nonintestinal, undifferentiated epithelial cells have been extensively used for understanding the mechanisms by which some human enterovirulent bacteria induce intestinal disorders. Human colon carcinoma cell lines which are able to express in culture the functional and structural characteristics of mature enterocytes and goblet cells have been established, mimicking structurally and functionally an intestinal epithelial barrier. Moreover, Caco-2-derived M-like cells have been established, mimicking the bacterial capture property of M cells of Peyer's patches. This review intends to analyze the cellular and molecular mechanisms of pathogenesis of human enterovirulent bacteria observed in infected cultured human colon carcinoma enterocyte-like HT-29 subpopulations, enterocyte-like Caco-2 and clone cells, the colonic T84 cell line, HT-29 mucus-secreting cell subpopulations, and Caco-2-derived M-like cells, including cell association, cell entry, intracellular lifestyle, structural lesions at the brush border, functional lesions in enterocytes and goblet cells, functional and structural lesions at the junctional domain, and host cellular defense responses.

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Characterization of Escherichia coli isolated from gut biopsies of newly diagnosed patients with inflammatory bowel disease

Abstract: Adherent invasive E. coli are present at first diagnosis, suggesting that they may have a role in the early stages of disease onset.

Cited by 77 publications

References 53 publications

Host Defense Peptide Resistance Contributes to Colonization and Maximal Intestinal Pathology by Crohn's Disease-Associated Adherent-Invasive Escherichia coli

Host Defense Peptide Resistance Contributes to Colonization and Maximal Intestinal Pathology by Crohn's Disease-Associated Adherent-Invasive Escherichia coli

Recent Advances in Understanding Enteric Pathogenic Escherichia coli

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

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