An investigation of the expression and adhesin function of H7 flagella in the interaction of<i>Escherichia coli</i>O157 : H7 with bovine intestinal epithelium

Mahajan, Aditya; Currie, Colin; McDermott, Michael; Tree, Jai J.; McAteer, Sean P.; McKendrick, Iain J.; McNeilly, Tom N.; Roe, Andrew J.; Ragione, Roberto M. La; Woodward, Martin J.; Gally, David L.; Smith, David George Emslie

doi:10.1111/j.1462-5822.2008.01244.x

Cited by 128 publications

(126 citation statements)

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“…This transition can be associated with a change in cellular phenotype. For instance, when motile bacteria, such as Escherichia coli, adhere to a substratum (33,82,83), motility ceases, cell multiplication continues (84)(85)(86)(87), and early biofilm-related genes are upregulated, including those that encode additional adhesins (88)(89)(90). Although Karatan and Watnick (91) suggested that bacteria at this point can form either an adherent monolayer biofilm or a multilayer biofilm, the former is not sufficient to encompass some of the main characteristics of a complex biofilm, most notably the formation of ECM and a three-dimensional, controlled microenvironment that facilitates biofilm growth, nutrient acquisition, control of gas and pH, and cell-cell signaling (92)(93)(94)(95)(96)(97).…”

Section: Defining a C Albicans Biofilm: Lessons From Bacteriamentioning

confidence: 99%

Plasticity of Candida albicans Biofilms

Soll

Daniels

2016

Microbiol Mol Biol Rev

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SUMMARYCandida albicans, the most pervasive fungal pathogen that colonizes humans, forms biofilms that are architecturally complex. They consist of a basal yeast cell polylayer and an upper region of hyphae encapsulated in extracellular matrix. However, biofilms formedin vitrovary as a result of the different conditions employed in models, the methods used to assess biofilm formation, strain differences, and, in a most dramatic fashion, the configuration of the mating type locus (MTL). Therefore, integrating data from different studies can lead to problems of interpretation if such variability is not taken into account. Here we review the conditions and factors that cause biofilm variation, with the goal of engendering awareness that more attention must be paid to the strains employed, the methods used to assess biofilm development, every aspect of the model employed, and the configuration of theMTLlocus. We end by posing a set of questions that may be asked in comparing the results of different studies and developing protocols for new ones. This review should engender the notion that not all biofilms are created equal.

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Section: Defining a C Albicans Biofilm: Lessons From Bacteriamentioning

confidence: 99%

Plasticity of Candida albicans Biofilms

Soll

Daniels

2016

Microbiol Mol Biol Rev

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“…Short-chain fatty acids are found in concentrations ranging from 20 to 140 mM in the large bowel, and recognition of this signal, along with the AI-3 and interkingdom signaling molecules, likely contributes to EHEC niche recognition and adaptation. Some evidence also suggests that the flagellum acts as an initial adhesin to epithelial cells from the bovine terminal rectum (25).…”

Section: Motilitymentioning

confidence: 99%

Enterohemorrhagic Escherichia coli Virulence Gene Regulation

Mellies

Lorenzen

2014

Microbiol Spectr

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Coordinated expression of enterohemorrhagic Escherichia coli virulence genes enables the bacterium to cause hemorrhagic colitis and the complication known as hemolytic-uremic syndrome. Horizontally acquired genes and those common to E. coli contribute to the disease process, and increased virulence gene expression is correlated with more severe disease in humans. Researchers have gained considerable knowledge about how the type III secretion system, secreted effectors, adhesin molecules, and the Shiga toxins are regulated by environmental signals and multiple genetic pathways. Also emergent from the data is an understanding of how enterohemorrhagic E. coli regulates response to acid stress, the role of flagellar motility, and how passage through the human host and bovine intestinal tract causes disease and supports carriage in the cattle reservoir, respectively. Particularly exciting areas of discovery include data suggesting how expression of the myriad effectors is coordinately regulated with their cognate type III secretion system and how virulence is correlated with bacterial metabolism and gut physiology.As a species, Escherichia coli is highly successful, adapting to inhabit the lower intestine of warm-blooded animals. Commensal E. coli, part of the normal biota, resides harmlessly in the gut, producing vitamin K. However, E. coli also causes three types of disease in humans: urinary tract infections, sepsis in newborns, and diarrheal disease. Enterohemorrhagic E. coli (EHEC) plays a prominent role in the third type of illness. It has been estimated that, for the pan genome of E. coli, the nonpathogenic and pathogenic strains only contain a core set of genes comprising approximately 20% of any one genome (1, 2). Much of the horizontally acquired genetic information is clustered within genomic islands in pathogens. As for EHEC, this has allowed the organism to not only attach and colonize the large intestine of humans and other animals, to outcompete commensal E. coli and other bacteria at the site of infection, but also to cause serious disease.Horizontally acquired genetic information in EHEC results in evolution into a specific pathotype-genotype dictates phenotype. How this genetic information is controlled is of equal importance for the success and virulence of the organism. Indeed, investigated differences in virulence gene regulation in two distinct EHEC isolate lineages, clade 8 and clade 2. A clade is a group of EHEC isolates with one ancestor and all its descendants. Eight clades of E. coli O157 isolates were defined by single nucleotide polymorphism (SNP) analyses, where clade 8 was a group of hypervirulent bacteria compared to the other seven clades (4). By examining multiple strains per lineage, the investigators found increased expression of horizontally acquired virulence genes in clade 8 versus clade 2. Genes expressed to higher levels in clade 8, which is associated with a greater number of cases of E. coli hemorrhagic

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“…Flagella and motility enhance encounter rates of pathogenic bacteria with host cells or tissues, thus facilitating the spread of infection, and therefore flagellation is advantageous to pathogenic bacteria at the early stages of infection (Ottemann & Miller, 1997;Ramos et al, 2004). In addition, the flagellar filament can act as an adhesin, and thereby increases the frequency and intimacy of early host-pathogen interactions Giró n et al, 2002;Mahajan et al, 2009;Roy et al, 2009). On the other hand, flagella are highly immunostimulatory in the host and recognized by innate immunity defences (Hayashi et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

“…For newborn meningitis-associated E. coli (NMEC), which represents another extraintestinal E. coli pathogroup, the flagellar structure rather than the motility function has been shown to be relevant for bacterial association with and invasion into human brain microvascular endothelial cells (Parthasarathy et al, 2007). Similarly, flagella of diarrhoeagenic E. coli have been demonstrated to be directly involved in the adherence to epithelial cells (Giró n et al, 2002;Mahajan et al, 2009;Roy et al, 2009) and mucins , and also to contribute to host cell invasion (Luck et al, 2006). Thus, flagellation contributes to the pathogenicity of E. coli through motility and adhesive-or invasion-promoting properties.…”

Section: Introductionmentioning

confidence: 99%