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[Quorum sensing and quorum quenching: how to disrupt bacterial communication to inhibit virulence?].Medecine Sciences : M/S Jan 2019Most bacteria use a communication system known as quorum sensing which relies on the secretion and perception of small molecules called autoinducers enabling bacteria to... (Review)
Review
Most bacteria use a communication system known as quorum sensing which relies on the secretion and perception of small molecules called autoinducers enabling bacteria to adapt their behavior according to the population size and synchronize the expression of genes involved in virulence, antimicrobial resistance and biofilm formation. Methods have emerged to inhibit bacterial communication and limit their noxious traits. Chemical inhibitors, sequestering antibodies and degrading enzymes have been developed and proved efficient to decrease bacterial virulence both in vitro and in vivo. This strategy, named quorum quenching, also showed synergistic effects with traditional antibacterial treatments by increasing bacterial susceptibility to antibiotics. Thereby quorum quenching constitutes an interesting therapeutic strategy to fight against bacterial infections and limit the consequences of antibiotic resistance.
Topics: Anti-Bacterial Agents; Bacteria; Bacterial Infections; Drug Synergism; Quorum Sensing; Virulence
PubMed: 30672458
DOI: 10.1051/medsci/2018310 -
Microbiology and Immunology 2002Toxigenic Vibrio cholerae is the etiological agent of cholera, an acute dehydrating diarrhea that occurs in epidemic form in many developing countries. Although V.... (Review)
Review
Toxigenic Vibrio cholerae is the etiological agent of cholera, an acute dehydrating diarrhea that occurs in epidemic form in many developing countries. Although V. cholerae is a human pathogen, aquatic ecosystems are major habitats of Vibrio species, which includes both pathogenic and nonpathogenic strains that vary in their virulence gene content. V. cholerae belonging to the 01 and 0139 serogroups is commonly known to carry a set of virulence genes necessary for pathogenesis in humans. Recent studies have indicated that virulence genes or their homologues are also dispersed among environmental strains of V. cholerae belonging to diverse serogroups, which appear to constitute an environmental reservoir of virulence genes. Although the definitive roles of the virulence-associated factors in the environment, and the environmental selection pressures for V. cholerae-carrying virulence genes or their homologues is not clear, the potential for origination of new epidemic strains from environmental progenitors seems real. It is likely that the aquatic environment harbors different virulence-associated genes scattered among environmental vibrios, which possess a lower virulence potential than the epidemic strains. The ecosystem comprising the aquatic environment, V. cholerae, genetic elements mediating gene transfer, and the mammalian host appears to support the clustering of critical virulence genes in a proper combination leading to the origination of new V. cholerae strains with epidemic potential.
Topics: Cholera; Cholera Toxin; Disease Reservoirs; Ecology; Evolution, Molecular; Humans; Vibrio cholerae; Virulence; Water Microbiology
PubMed: 11939579
DOI: 10.1111/j.1348-0421.2002.tb02659.x -
Microbial Genomics Feb 2022is a food-borne pathogen with epidemic potential that causes cholera-like acute gastroenteritis and sometimes extraintestinal infections in humans. However, research on...
is a food-borne pathogen with epidemic potential that causes cholera-like acute gastroenteritis and sometimes extraintestinal infections in humans. However, research on its genetic diversity and pathogenicity-related genetic elements based on whole genome sequences is lacking. In this study, we collected and sequenced 130 strains of from 14 provinces of China, and also determined the susceptibility of 35 of the strains to 30 different antibiotics. Combined with 52 publicly available genomes, we inferred the population structure and investigated the characteristics of pathogenicity-related factors. The strains exhibited high levels of homologous recombination and were assigned to two major populations, VflPop1 and VflPop2, according to the different compositions of their gene pools. VflPop2 was subdivided into groups 2.1 and 2.2. Except for VflPop2.2, which consisted only of Asian strains, the strains in VflPop1 and VflPop2.1 were distributed in the Americas, Asia and Europe. Analysis of the pathogenicity potential of showed that most of the identified virulence-related genes or gene clusters showed high prevalence in , except for three mobile genetic elements: pBD146, ICEInd1 and MGIInd1, which were scattered in only a few strains. A total of 21 antimicrobial resistance genes were identified in the genomes of the 182 strains analysed in this study, and 19 (90%) of them were exclusively present in VflPop2. Notably, the tetracycline resistance-related gene (35) was present in 150 (95%) of the strains in VflPop2, and in only one (4%) strain in VflPop1, indicating it was population-specific. In total, 91% of the 35 selected strains showed resistance to cefazolin, indicating has a high resistance rate to cefazolin. Among the 15 genomes that carried the previously reported drug resistance-related plasmid pBD146, 11 (73%) showed resistance to trimethoprim-sulfamethoxazole, which we inferred was related to the presence of the gene in the plasmid. On the basis of the population genomics analysis, the genetic diversity, population structure and distribution of pathogenicity-related factors of were delineated in this study. The results will provide further clues regarding the evolution and pathogenic mechanisms of , and improve our knowledge for the prevention and control of this pathogen.
Topics: Anti-Bacterial Agents; Cefazolin; Humans; Metagenomics; Vibrio; Virulence; Virulence Factors
PubMed: 35212619
DOI: 10.1099/mgen.0.000769 -
Medical Mycology Feb 2010Over the past two decades, the incidence of fungal infections has dramatically increased. This is primarily due to increases in the population of immunocompromised... (Review)
Review
Over the past two decades, the incidence of fungal infections has dramatically increased. This is primarily due to increases in the population of immunocompromised individuals attributed to the HIV/AIDS pandemic and immunosuppression therapies associated with organ transplantation, cancer, and other diseases where new immunomodulatory therapies are utilized. Significant advances have been made in understanding how fungi cause disease, but clearly much remains to be learned about the pathophysiology of these often lethal infections. Fungal pathogens face numerous environmental challenges as they colonize and infect mammalian hosts. Regardless of a pathogen's complexity, its ability to adapt to environmental changes is critical for its survival and ability to cause disease. For example, at sites of fungal infections, the significant influx of immune effector cells and the necrosis of tissue by the invading pathogen generate hypoxic microenvironments to which both the pathogen and host cells must adapt in order to survive. However, our current knowledge of how pathogenic fungi adapt to and survive in hypoxic conditions during fungal pathogenesis is limited. Recent studies have begun to observe that the ability to adapt to various levels of hypoxia is an important component of the virulence arsenal of pathogenic fungi. In this review, we focus on known oxygen sensing mechanisms that non-pathogenic and pathogenic fungi utilize to adapt to hypoxic microenvironments and their possible relation to fungal virulence.
Topics: Adaptation, Physiological; Anaerobiosis; Animals; Fungi; Gene Expression Regulation, Fungal; Humans; Hypoxia; Mycoses; Oxygen; Stress, Physiological; Virulence
PubMed: 19462332
DOI: 10.3109/13693780902947342 -
Surgical Infections 2018Bacterial virulence is a dynamic property of pathogens that is expressed in a context-dependent manner. For a bacterial pathogen, the expression of virulence is a... (Review)
Review
Bacterial virulence is a dynamic property of pathogens that is expressed in a context-dependent manner. For a bacterial pathogen, the expression of virulence is a tradeoff, as there is an energy cost that can disturb other functions. As a result, virulence is activated only when bacteria sense the need for it. Recent work from our laboratory has identified many of the local cues in the environmental context that activate bacterial virulence during surgical injury, resulting in bacterial invasion, tissue inflammation, and, in some cases, lethal sepsis. After surgical injury, cytokines, opioids, and end-products of ischemia can activate bacterial virulence circuits, such as the quorum-sensing signaling system, directly. However, when key ions are present, such as phosphate and iron, certain pathogenic bacteria become insensitive to these incoming host cues. In this review, we provide molecular insight into the process by which certain surgical infections may be prevented by ionic modulation of the local microenvironment.
Topics: Animals; Bacteria; Bacterial Infections; Gene Expression Regulation, Bacterial; Humans; Iron; Phosphates; Surgical Wound Infection; Virulence
PubMed: 30359172
DOI: 10.1089/sur.2018.224 -
Molecular Plant-microbe Interactions :... Jun 2021This article is part of the Top 10 Unanswered Questions in MPMI invited review series.We consider the state of knowledge on pathogen evolution of novel virulence...
This article is part of the Top 10 Unanswered Questions in MPMI invited review series.We consider the state of knowledge on pathogen evolution of novel virulence activities, broadly defined as anything that increases pathogen fitness with the consequence of causing disease in either the qualitative or quantitative senses, including adaptation of pathogens to host immunity and physiology, host species, genotypes, or tissues, or the environment. The evolution of novel virulence activities as an adaptive trait is based on the selection exerted by hosts on variants that have been generated de novo or arrived from elsewhere. In addition, the biotic and abiotic environment a pathogen experiences beyond the host may influence pathogen virulence activities. We consider host-pathogen evolution, host range expansion, and external factors that can mediate pathogen evolution. We then discuss the mechanisms by which pathogens generate and recombine the genetic variation that leads to novel virulence activities, including DNA point mutation, transposable element activity, gene duplication and neofunctionalization, and genetic exchange. In summary, if there is an (epi)genetic mechanism that can create variation in the genome, it will be used by pathogens to evolve virulence factors. Our knowledge of virulence evolution has been biased by pathogen evolution in response to major gene resistance, leaving other virulence activities underexplored. Understanding the key driving forces that give rise to novel virulence activities and the integration of evolutionary concepts and methods with mechanistic research on plant-microbe interactions can help inform crop protection.[Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
Topics: Adaptation, Physiological; Host-Pathogen Interactions; Phenotype; Virulence
PubMed: 33522842
DOI: 10.1094/MPMI-09-20-0258-IA -
The Plant Journal : For Cell and... Feb 2018Fungi represent an ecologically diverse group of microorganisms that includes plant pathogenic species able to cause considerable yield loses in crop production systems... (Review)
Review
Fungi represent an ecologically diverse group of microorganisms that includes plant pathogenic species able to cause considerable yield loses in crop production systems worldwide. In order to establish compatible interactions with their hosts, pathogenic fungi rely on the secretion of molecules of diverse nature during host colonization to modulate host physiology, manipulate other environmental factors or provide self-defence. These molecules, collectively known as effectors, are typically small secreted cysteine-rich proteins, but may also comprise secondary metabolites and sRNAs. Here, we discuss the most common strategies that fungal plant pathogens employ to subvert their host plants in order to successfully complete their life cycle and secure the release of abundant viable progeny.
Topics: Biological Evolution; Fungi; Host-Pathogen Interactions; Hydrogen-Ion Concentration; Plant Diseases; Plants; Reactive Oxygen Species; Secondary Metabolism; Virulence
PubMed: 29277938
DOI: 10.1111/tpj.13810 -
Frontiers in Immunology 2018The central dogma of molecular biology describes the flow of genetic information from DNA to protein via an RNA intermediate. For many years, RNA has been considered... (Review)
Review
The central dogma of molecular biology describes the flow of genetic information from DNA to protein via an RNA intermediate. For many years, RNA has been considered simply as a messenger relaying information between DNA and proteins. Recent advances in next generation sequencing technology, bioinformatics, and non-coding RNA biology have highlighted the many important roles of RNA in virtually every biological process. Our understanding of RNA biology has been further enriched by a number of significant advances in probing RNA structures. It is now appreciated that many cellular and viral biological processes are highly dependent on specific RNA structures and/or sequences, and such reliance will undoubtedly impact on the evolution of both hosts and viruses. As a contribution to this special issue on host immunity and virus evolution, it is timely to consider how RNA sequences and structures could directly influence the co-evolution between hosts and viruses. In this manuscript, we begin by stating some of the basic principles of RNA structures, followed by describing some of the critical RNA structures in both viruses and hosts. More importantly, we highlight a number of available new tools to predict and to evaluate novel RNA structures, pointing out some of the limitations readers should be aware of in their own analyses.
Topics: Animals; Base Sequence; Evolution, Molecular; Host-Pathogen Interactions; Humans; Nucleic Acid Conformation; RNA; Virulence; Virus Diseases; Viruses
PubMed: 30283444
DOI: 10.3389/fimmu.2018.02097 -
Microbiology and Molecular Biology... Mar 2003Agrobacterium tumefaciens and related Agrobacterium species have been known as plant pathogens since the beginning of the 20th century. However, only in the past two... (Review)
Review
Agrobacterium tumefaciens and related Agrobacterium species have been known as plant pathogens since the beginning of the 20th century. However, only in the past two decades has the ability of Agrobacterium to transfer DNA to plant cells been harnessed for the purposes of plant genetic engineering. Since the initial reports in the early 1980s using Agrobacterium to generate transgenic plants, scientists have attempted to improve this "natural genetic engineer" for biotechnology purposes. Some of these modifications have resulted in extending the host range of the bacterium to economically important crop species. However, in most instances, major improvements involved alterations in plant tissue culture transformation and regeneration conditions rather than manipulation of bacterial or host genes. Agrobacterium-mediated plant transformation is a highly complex and evolved process involving genetic determinants of both the bacterium and the host plant cell. In this article, I review some of the basic biology concerned with Agrobacterium-mediated genetic transformation. Knowledge of fundamental biological principles embracing both the host and the pathogen have been and will continue to be key to extending the utility of Agrobacterium for genetic engineering purposes.
Topics: Biotechnology; Gene Expression Regulation; Gene Silencing; Gene Transfer Techniques; Genes, Plant; Genetic Engineering; Plants, Genetically Modified; Rhizobium; Transformation, Genetic; Transgenes; Virulence
PubMed: 12626681
DOI: 10.1128/MMBR.67.1.16-37.2003 -
Infection and Immunity Jun 2020Bacterial populations are phenotypically heterogeneous, which allows subsets of cells to survive and thrive following changes in environmental conditions. For bacterial... (Review)
Review
Bacterial populations are phenotypically heterogeneous, which allows subsets of cells to survive and thrive following changes in environmental conditions. For bacterial pathogens, changes within the host environment occur over the course of the immune response to infection and can result in exposure to host-derived, secreted antimicrobials or force direct interactions with immune cells. Many recent studies have shown host cell interactions promote virulence factor expression, forcing subsets of bacterial cells to battle the host response, while other bacteria reap the benefits of this pacification. It still remains unclear whether virulence factor expression is truly energetically costly within host tissues and whether expression is sufficient to impact the growth kinetics of virulence factor-expressing cells. However, it is clear that slow-growing subsets of bacteria emerge during infection and that these subsets are particularly difficult to eliminate with antibiotics. This minireview will focus on our current understanding of heterogenous virulence factor expression and discuss the evidence that supports or refutes the hypothesis that virulence factor expression is linked to slowed growth and antibiotic tolerance.
Topics: Bacteria; Bacterial Infections; Gene Expression Regulation, Bacterial; Genetic Heterogeneity; Host-Pathogen Interactions; Virulence; Virulence Factors
PubMed: 32041785
DOI: 10.1128/IAI.00911-19