Mucosal Reactive Oxygen Species Decrease Virulence by Disrupting Campylobacter jejuni Phosphotyrosine Signaling

Corcionivoschi, Nicolae; Álvarez, Luis; Sharp, Thomas H.; Strengert, Monika; Alemka, Abofu; Mantell, Judith; Verkade, Paul; Knaus, Ulla G.; Bourke, Billy

doi:10.1016/j.chom.2012.05.018

Cited by 110 publications

(129 citation statements)

References 45 publications

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“…In addition, differences between chicken and cattle husbandry may apply different selection pressures to genes associated with survival of oxygen-intolerant Campylobacter outside the host. For example, depletion of the hypothetical protein Cj1169c and the protein Cj1170c (OMP50) in C. jejuni mutants has been shown to result in reduced colonization of chicken and higher sensitivity to oxygen (42,46). Considering the cause of sequence variation at host-segregating loci is purely speculative in this study, but it is interesting to note that many of these loci are within the core (soft-core) genome.…”

Section: Source Attribution In C Jejuni Using Novel Markersmentioning

confidence: 80%

“…Multiple factors associated with differences in animal husbandry and host physiology make it difficult to assign a biological basis for host segregation of alleles among the marker loci. However, some of the genes are involved in acid stress response (groES) (41) or are organized in the same operon as flagellar proteins (flgJ) or as proteins involved in oxidative stress response (Cj1169c) (42). While it is not necessary to define epidemiological markers based on functional differences, it is interesting to speculate how host colonization factors may have influenced genomic signatures of host association.…”

Section: Source Attribution In C Jejuni Using Novel Markersmentioning

confidence: 99%

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Genome-Wide Identification of Host-Segregating Epidemiological Markers for Source Attribution in Campylobacter jejuni

Thépault

Méric

Rivoal

et al. 2017

Appl Environ Microbiol

110

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Campylobacter is among the most common worldwide causes of bacterial gastroenteritis. This organism is part of the commensal microbiota of numerous host species, including livestock, and these animals constitute potential sources of human infection. Molecular typing approaches, especially multilocus sequence typing (MLST), have been used to attribute the source of human campylobacteriosis by quantifying the relative abundance of alleles at seven MLST loci among isolates from animal reservoirs and human infection, implicating chicken as a major infection source. The increasing availability of bacterial genomes provides data on allelic variation at loci across the genome, providing the potential to improve the discriminatory power of data for source attribution. Here we present a source attribution approach based on the identification of novel epidemiological markers among a reference pan-genome list of 1,810 genes identified by gene-by-gene comparison of 884 genomes of Campylobacter jejuni isolates from animal reservoirs, the environment, and clinical cases. Fifteen loci involved in metabolic activities, protein modification, signal transduction, and stress response or coding for hypothetical proteins were selected as host-segregating markers and used to attribute the source of 42 French and 281 United Kingdom clinical C. jejuni isolates. Consistent with previous studies of British campylobacteriosis, analyses performed using STRUCTURE software attributed 56.8% of British clinical cases to chicken, emphasizing the importance of this host reservoir as an infection source in the United Kingdom. However, among French clinical isolates, approximately equal proportions of isolates were attributed to chicken and ruminant reservoirs, suggesting possible differences in the relative importance of animal host reservoirs and indicating a benefit for further nationalscale attribution modeling to account for differences in production, behavior, and food consumption.IMPORTANCE Accurately quantifying the relative contribution of different host reservoirs to human Campylobacter infection is an ongoing challenge. This study, based on the development of a novel source attribution approach, provides the first results of source attribution in Campylobacter jejuni in France. A systematic analysis using gene-by-gene comparison of 884 genomes of C. jejuni isolates, with a pan-genome list of genes, identified 15 novel epidemiological markers for source attribution. The different proportions of French and United Kingdom clinical isolates attributed to

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Section: Source Attribution In C Jejuni Using Novel Markersmentioning

confidence: 80%

Section: Source Attribution In C Jejuni Using Novel Markersmentioning

confidence: 99%

Genome-Wide Identification of Host-Segregating Epidemiological Markers for Source Attribution in Campylobacter jejuni

Thépault

Méric

Rivoal

et al. 2017

Appl Environ Microbiol

110

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“…This IVOC system has been used mainly to study the mechanisms of virulence of ETEC (839), EPEC (840)(841)(842)(843)(844)(845)(846)(847)(848)(849)(850)(851), EHEC (852)(853)(854)(855)(856)(857), EAEC (507,858), and Salmonella (392) and the action of Stx toxins (641). Other IVOCs have been used for studies on C. jejuni (859), EPEC (692,860,861), EAEC (645,(862)(863)(864), and Shigella (865) pathogenesis. Moreover, IVOCs from colonic biopsy specimens from CD patients have been used to show the adhesion of AIEC (444,866).…”

Section: Discussionmentioning

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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“…This has been used to examine both enteropathogenic Escherichia coli and C. jejuni pathogenicity. 31,32 In addition several groups have made recombinant proteins consisting of mucin domains. [33][34][35][36] While recombinant production of full-length gel-forming human mucins has not been reported to date, murine Muc5ac has been cloned in its entirety and a murine model of MUC5AC overexpression established 37 suggesting that this approach should be feasible in the future to modulate cellular mucin production.…”

Section: Use Of Novel Tools To Assess the Interactions Of Bacteria Wimentioning

confidence: 99%

Interaction of microbes with mucus and mucins

et al. 2013

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Due to the recent rapid expansion in our understanding of the composition of the gut microflora and the consequences of altering that composition the question of how bacteria colonise mucus layers and interact with components of mucus, such as mucin, is now receiving widespread attention. Using a combination of mucus secreting cells, and a novel mucin microarray platform containing purified native mucins from different sources we recently demonstrated that two gastrointestinal pathogens, Helicobacter pylori and Campylobacter jejuni, colonise mucus by different mechanisms. This result emphasizes the potential for even closely related bacteria to interact with mucus in divergent ways to establish successful infection. Expanding the use of the mucin arrays described in the study to other microorganisms, both pathogenic and commensal, should lead to the discovery of biologically important motifs in bacterial-host interactions and complement the use of novel in vitro cell models, such as mucus secreting cell lines. IntroductionMucosal surfaces serve as a portal of entry for the majority of infections that occur in humans and animals. All mucosal surfaces are covered in a layer of mucus. In the gastrointestinal tract this mucus is colonised by tens of trillions of commensal organisms, essential for the development and health of the host. Mucus in the murine colon and the stomach has been shown to consist of an inner closely adherent mucus layer and an outer less dense, loosely adherent layer. 1,2The small intestine has a single loosely adherent layer.2 In the colon the outer mucus layer is colonised by commensal bacteria while the inner mucus layer is devoid of microbiota.1 The protective function of the inner mucus layer can be disrupted in disease, allowing access of organisms to the underlying epithelium. For example, the mucus layer has been shown to be depleted in animal models of colitis, and also in humans with ulcerative colitis resulting in bacterial penetration of the inner layer. 3A complex, mutually dependent relationship is established between the gut microbiota and the human host from birth which persists throughout life. 4 Initial cross talk between the host and gut microbiota influences postnatal intestinal epithelial differentiation by altering gene expression and improves immune tolerance. 5-7The microbiota also provides other benefits to the host including priming of the immune system and protection of the mucosal surface by competing with invading pathogens for space, nutrients, and binding receptors. Recent advances in sequencing technology and metagenomics have revealed changes in the microbial population of the gut in both health and disease. Strikingly, these studies have shown that alterations in the composition of the gut microflora, sometimes referred to as dysbiosis, are associated with a number of chronic diseases including obesity, diabetes and inflammatory disease. 8-10 Interaction of microbes with mucus and mucins Recent developmentsJulie Naughton, 1,2 Gina Duggan, 1, 2 Billy Bourke, 1,...

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Mucosal Reactive Oxygen Species Decrease Virulence by Disrupting Campylobacter jejuni Phosphotyrosine Signaling

Cited by 110 publications

References 45 publications

Genome-Wide Identification of Host-Segregating Epidemiological Markers for Source Attribution in Campylobacter jejuni

Genome-Wide Identification of Host-Segregating Epidemiological Markers for Source Attribution in Campylobacter jejuni

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

Interaction of microbes with mucus and mucins

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