Type I Secretion System
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12 results
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Metabolism and Pathogenicity of Pseudomonas aeruginosa Infections in the Lungs of Individuals with Cystic Fibrosis
- Authors: Gregory C. Palmer, Marvin Whiteley
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Citation: Palmer G, Whiteley M. 2015. Metabolism and pathogenicity of pseudomonas aeruginosa infections in the lungs of individuals with cystic fibrosis. 3(4): doi:10.1128/microbiolspec.MBP-0003-2014
- DOI 10.1128/microbiolspec.MBP-0003-2014
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Abstract:
Individuals with the genetic disease cystic fibrosis (CF) accumulate mucus or sputum in their lungs. This sputum is a potent growth substrate for a range of potential pathogens, and the opportunistic bacterium Pseudomonas aeruginosa is generally most difficult of these to eradicate. As a result, P. aeruginosa infections are frequently maintained in the CF lung throughout life, and are the leading cause of death for these individuals. While great effort has been expended to better understand and treat these devastating infections, only recently have researchers begun to rigorously examine the roles played by specific nutrients in CF sputum to cue P. aeruginosa pathogenicity. This chapter summarizes the current state of knowledge regarding how P. aeruginosa metabolism in CF sputum affects initiation and maintenance of these infections. It contains an overview of CF lung disease and the mechanisms of P. aeruginosa pathogenicity. Several model systems used to study these infections are described with emphasis on the challenge of replicating the chronic infections observed in humans with CF. Nutrients present in CF sputum are surveyed, and the impacts of these nutrients on the infection are discussed. The chapter concludes by addressing the future of this line of research including the use of next-generation technologies and the potential for metabolism-based therapeutics.
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Mechanisms of Genome Plasticity in Neisseria meningitidis: Fighting Change with Change
- Authors: Roland Schwarz, Biju Joseph, Matthias Frosch, Christoph Schoen
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Source: Genome Plasticity and Infectious Diseases , pp 103-124
Publication Date :
January 2012
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Abstract:
This chapter on mechanisms of genome plasticity in Neisseria meningitidis initially gives a short overview over the genetic variability at the population level and some peculiarities of meningococcal genome organization as revealed by genome sequencing projects. Later, the focus is on genetic mechanisms and genomic features that are paramount for the generation of genomic flexibility, and a brief account of the genetic basis of virulence in Neisseria meningitidis as far as it is known today. Exogenous and endogenous stress induces DNA damage in the meningococcal genome that must be repaired, and DNA repair mechanisms are therefore likely to have a key role in meningococcal genome dynamics. So far, Escherichia coli has served as the prime model organism for DNA repair systems in other microorganisms such as N. meningitidis. The majority of strong mutators found in a number of bacterial species have a defective MMR pathway due to the inactivation of mutS or mutL genes. In addition to global mutation and phase variation, intragenomic as well as intergenomic recombination is of pivotal importance for the generation of genome flexibility in N. meningitidis, and one of the most striking characteristics of the meningococcal genomes is the abundance and diversity of repetitive DNA serving as potential target sites for homologous recombination or replication slippage.
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Uropathogenic Escherichia coli
- Authors: Harry L. T. Mobley, Michael S. Donnenberg, and Erin C. Hagan
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Citation: Mobley H, Donnenberg M, Hagan E. 2009. Uropathogenic Escherichia coli, EcoSal Plus 2009; doi:10.1128/ecosalplus.8.6.1.3
- DOI 10.1128/ecosalplus.8.6.1.3
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Abstract:
The urinary tract is among the most common sites of bacterial infection, and Escherichia coli is by far the most common species infecting this site. Individuals at high risk for symptomatic urinary tract infection (UTI) include neonates, preschool girls, sexually active women, and elderly women and men. E. coli that cause the majority of UTIs are thought to represent only a subset of the strains that colonize the colon. E. coli strains that cause UTIs are termed uropathogenic E. coli (UPEC). In general, UPEC strains differ from commensal E. coli strains in that the former possess extragenetic material, often on pathogenicity-associated islands (PAIs), which code for gene products that may contribute to bacterial pathogenesis. Some of these genes allow UPEC to express determinants that are proposed to play roles in disease. These factors include hemolysins, secreted proteins, specific lipopolysaccharide and capsule types, iron acquisition systems, and fimbrial adhesions. The current dogma of bacterial pathogenesis identifies adherence, colonization, avoidance of host defenses, and damage to host tissues as events vital for achieving bacterial virulence. These considerations, along with analysis of the E. coli CFT073, UTI89, and 536 genomes and efforts to identify novel virulence genes should advance the field significantly and allow for the development of a comprehensive model of pathogenesis for uropathogenic E. coli.Further study of the adaptive immune response to UTI will be especially critical to refine our understanding and treatment of recurrent infections and to develop vaccines.
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Quorum Sensing in the Soft-Rot Erwinias
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Source: Chemical Communication among Bacteria , pp 185-199
Publication Date :
January 2008
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Abstract:
One of the first bacterial species for which N-acylhomoserine lactone (AHL) quorum sensing (QS) was described was Erwinia carotovora. Since then, QS has been well studied in the soft-rot erwinias, where, as described in this chapter, QS plays a key role in the regulation of secreted plant cell wall-degrading enzymes (PCWDEs) production and hence in virulence. In certain strains, a well-defined AHL QS system also controls production of β-lactam antibiotic, carbapenem. In addition, it must be emphasized that QS is only one of many regulatory inputs into virulence factor production in Erwinia. The majority of the key secreted virulence factors of E. carotovora and E. chrysanthemi, including multiple Pels, Peh, Cel, and Svx, are secreted by a type II secretion system known as the Out system. There have been two reports describing the existence of AHL QS in E. amylovora. First, production of a single AHL, most likely 3-oxo-C6-HSL, was described for several Italian strains of E. amylovora; for one strain, production of AHL was observed in planta. Second, AHL activity was detected in the culture supernatant of a Swiss strain of E. amylovora. Both reports describe the detection and partial sequencing of pairs of convergent luxIR homologues, named eamIR.
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Cell-to-Cell Communication in Rhizobia: Quorum Sensing and Plant Signaling
- Authors: J. Allan Downie, Juan E. González
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Source: Chemical Communication among Bacteria , pp 213-232
Publication Date :
January 2008
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Abstract:
This chapter briefly describes the nodulation process and some of the quorum-sensing regulatory systems that rhizobia use to monitor their population density. Conjugation is common among Rhizobiaceae, and there are very strong selection pressures to optimize growth in the rhizosphere and nodulation competitiveness. The regulation of gene transfer by quorum-sensing regulation is common among rhizobia. Individual rhizobial strains can contain up to four different LuxI-type acyl-homoserine lactone (AHL) synthases and associated regulators plus several other LuxR-type regulators lacking dedicated AHL synthases. Mutations in cinI and cinR delayed and decreased the growth rate of Rhizobium etli; because such altered growth was not observed in R. leguminosarum cinI or cinR mutants, this suggests that different sets of genes are induced via this quorum-sensing regulon in these two Rhizobium species. Bradyoxetin activity was found in extracts of all α-proteobacteria tested. This suggests that compounds similar to bradyoxetin may play an important role, not only in rhizobial symbiosis, but also in other plant- and animal-bacterial interactions. Elegant studies by researchers suggest that quorum sensing modulates both intra- and inter-species cell-cell communications. It was demonstrated that the halogenated furanones modulate LuxR activity through accelerated degradation of the transcriptional activator, rather than by blocking or displacing the binding of the AHL signal. Another potential way to interfere with quorum sensing is through the degradation or inactivation of the AHL signal molecules.
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Genomic Analysis of Plant Pathogenic Bacteria
- Authors: Gail M. Preston, David S. Guttman, Ian Toth
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Source: Bacterial Pathogenomics , pp 392-418
Publication Date :
January 2007
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Abstract:
This chapter provides an overview of how genome sequence data are changing our understanding of the mechanisms and evolution of plant pathogenesis, and discusses the opportunities and challenges genome data present for future research. The majority of plant pathogenic bacteria contain large numbers of genomic islands, and it is clear that in many cases they play an essential role in disease. Genes encoding the P. syringae phytotoxins coronatine and syringomycin reside on PIs, as do their recently discovered counterparts in E. carotovora subsp. atroseptica SCR1043. Pathogenicity and virulence factors have received the greatest focus in the genomic analysis of plant pathogens. Protein secretion systems are essential for pathogenesis in most plant pathogenic bacteria and have been extensively studied, particularly in proteobacterial pathogens. The phytohormones indole-3-acetic acid (IAA or auxin) is produced by many phytopathogenic bacteria. IAA production has been shown to contribute to in planta and epiphytic growth, virulence, and the regulation of syringomycin in P. syringae. Genome analyses of plant pathogens have highlighted three aspects of physiological adaptation to life on plants: specialization, innovation, and flexibility. A largely uninvestigated element in understanding the content and function of plant pathogen genomes, particularly the genomes of facultative plant pathogens, rests on understanding what plant pathogenic bacteria do when not causing disease.
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INDEX
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Source: Bacterial Pathogenomics
Publication Date :
January 2007
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No descriptions available.
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Identification of Target Proteins of the Lss Secretion System of Legionella pneumophila Corby
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Source: Legionella , pp 221-223
Publication Date :
January 2006
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Abstract:
This chapter describes a first putative type I secretion system (Lss) of Legionella pneumophila which is encoded by the lssXYZABD locus. In order to identify substrates of this Lss secretion system, the authors performed comparative two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) analysis of extracellular proteins of L. pneumophila Corby wild type, Corby lssB mutant, and complemented lssB mutant strain. In this study it was shown that the identified VirK protein of L. pneumophila is secreted in an LssB- but not a TatC-dependent manner. Referring to the results, it is implied that the Lss secretion system is also linked to the Lsp type II secretion system in L. pneumophila. It is speculated that VirK and p14 are secreted via a concerted action of the Lss and the Lsp system which includes cleavage of the signal sequences during secretion. In Agrobacterium and Rhizobium VirK is associated with the vir-regulon, and it was postulated that VirK should have a function in the interaction of the bacteria with the host cells. Therefore, the authors started to generate a virK mutant strain of L. pneumophila Corby and an antibody against VirK to further characterize the expression, secretion, and function of VirK of L. pneumophila.
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Vibrio cholerae: the Genetics of Pathogenesis and Environmental Persistence
- Authors: Michael G. Prouty, Karl E. Klose
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Source: The Biology of Vibrios , pp 311-339
Publication Date :
January 2006
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Abstract:
Cholera is acquired through the consumption of contaminated water or food. After passing through the acid barrier of the stomach, the bacteria penetrate the mucous lining of the small intestine and adhere to intestinal epithelial cells to establish an infection. During colonization of the small intestine, the bacteria begin to express several key virulence factors, including cholera toxin (CT). The action of CT on intestinal epithelial cells is responsible for the massive diarrhea associated with cholera. Key to the ability of Vibrio cholerae to cause disease is the virulence factors that it produces. Extensive research efforts involving innovative techniques have been directed at understanding the mechanisms involved in V. cholerae’s establishing a successful infection. The two most important virulence factors required for the ability of the organism to cause cholera are the CT and the toxin-coregulated pilus (TCP). The evolution of the pathogenic potential of V. cholerae has clearly occurred through the acquisition of several mobile genetic elements. A number of different genetic techniques have been utilized to identify V. cholerae genes important for virulence. Several in vivo transcriptome studies have also shed light on aspects of V. cholerae pathogenesis. Transcriptome profiling of V. cholerae isolated from human stools using microarray analysis has provided the closest understanding of gene expression relevant to the natural host. Considering the severe global impact of cholera, much effort has been directed at vaccine development.
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The Escherichia coli Hemolysin
- Author: Rodney A. Welch
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Citation: Welch R. 2005. The Escherichia coli Hemolysin, EcoSal Plus 2005; doi:10.1128/ecosalplus.8.7.2
- DOI 10.1128/ecosalplus.8.7.2
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Abstract:
The Escherichia coli hemolysin, earlier referred to as the hemolysin, is the best-characterized repeats in toxin (RTX) secreted by a type I exoprotein secretion system. The E. coli hemolysin is a significant virulence factor in murine models of peritonitis and ascending urinary tract infection, which suggests it is likely to be an important cytotoxin in human, extraintestinal E. coli diseases. Among E. coli or Salmonella strains there are no known examples of strict RTX leukotoxins in which lytic activity is limited to white blood cells. The general gene organization of the Vibrio cholerae RTX locus is similar to that seen with either of the E. coli hly and ehx loci with C, B, and D RTX homologs, clearly indicating it is a member of the RTX family. The hemolysin occurs less frequently in cystitis strains and only rarely among normal fecal strains. Among the extraintestinal E. coli isolates, the hlyCABDgenes were among the first virulence factors localized to unique, tRNA-associated segments of E. coli chromosomes. The hemolysin genes were eventually linked to P-type pilin and cytotoxic necrotizing factor-1 genes. Recent progress with its study has slowed down because of the difficulty in deriving the physical structure of the hemolysin protein or other RTX toxins and establishing its precise cytotoxic mechanism and role in pathogenesis of extraintestinal E. coli disease. Genomic sequencing has revealed that there are additional RTX-like genes found among many different pathogens; perhaps new efforts to discover their functions will aid progress in the RTX toxin field.
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Yersinia
- Author: Robert D. Perry
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Source: Iron Transport in Bacteria , pp 219-240
Publication Date :
January 2004
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Abstract:
The genus Yersinia is part of the Enterobacteriaceae family and consists of environmental species (Yersinia aldovae, Y. bercovieri, Y. frederiksenii, Y. intermedia, Y. kristensenii, Y. mollaretii, and Y. rohdei), a primary fish pathogen (Y. ruckeri), two enteropathogenic species (Y. enterocolitica and Y. pseudotuberculosis), and the plague bacillus (Y. pestis). The virulence properties of the human pathogenic Yersinia species include iron acquisition systems. The Y. pestis genome encodes three potential siderophore biosynthesis systems, two of which are nonribosomal peptide synthetase (NRPS) systems. Only one of these has been demonstrated to produce a siderophore, yersiniabactin (Ybt). Genes iucA through iucD, which are required for non-NRPS-mediated synthesis of the hydroxamate siderophore aerobactin, are also present in the Y. pestis genome. The Y. pestis genome encodes a number of ABC transport systems with significant similarities to iron or siderophore transport systems. Since none of these systems is associated with genes encoding biosynthetic enzymes for siderophores and since the ligands for most of these systems have not been experimentally determined, they are included in the topic on siderophore-independent iron transport systems. Heme transport systems, including the Hmu/Hem heme uptake system, and the Has hemophore system, and iron regulation and storage are discussed in this chapter.
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Type III Secretion Systems
- Authors: Gregory V. Plano, Kurt Schesser, Matthew L. Nilles
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Source: Bacterial Protein Toxins , pp 95-114
Publication Date :
January 2003
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Abstract:
Type III secretion system (TTSS) is believed to have originally evolved from the flagellar export system and is now dispersed among a number of both animal- and plant-interacting gram-negative bacteria. The aim of much current research on TTSS is to understand the mechanisms involved in effector secretion/injection and what the effectors are doing inside the host cell. Bacterial pathogens use several different protein secretion pathways to export virulence proteins from the bacterial cytoplasm to their site of action. Chaperones bind to effector proteins in the bacterial cytosol and remain cytosolic following export of their cognate substrate. Secreted proteins exhibiting significant structural similarities to YopB and YopD are present in all TTSSs of animal pathogens but not plant pathogens. Secretion of LcrQ upon cell contact depletes LcrQ from the cytoplasmic compartment and triggers increased transcription of type III genes. Secretion and polymerization of PrgI are required to complete the assembly of the needle complex and type III export apparatus. Two flagellar components, FlhB, an inner membrane protein with a substantial C-terminal cytoplasmic domain, and FliK, the secreted hook-length control protein, are proposed to be involved in switches substrate specificity process. An important question is how far knowledge of flagellar biogenesis can be extrapolated to understand the structure and function of the type III export apparatus. It is obvious that there will be features unique to each system; however, the basic process of transporting substrates across the bacterial membranes appears to be relatively well conserved.