Intracellular pathogenic bacteria
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Scooped by Damien Meyer
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PLOS Pathogens: Bringing Culture to the Uncultured: Coxiella burnetii and Lessons for Obligate Intracellular Bacterial Pathogens

PLOS Pathogens: Bringing Culture to the Uncultured: Coxiella burnetii and Lessons for Obligate Intracellular Bacterial Pathogens | Intracellular pathogenic bacteria | Scoop.it
Obligate intracellular bacteria that replicate in the cytoplasm of host endothelial cells include Rickettsia prowazekii, Rickettsia rickettsii, and Orientia tsutsugamushi (etiologic agents of epidemic typhus, Rocky Mountain spotted fever, and scrub typhus, respectively). Residing in specialized vacuolar compartments are Anaplasma phagocyophilum and Ehrlichia chaffensis (agents of febrile illnesses that have tropisms for neutrophils and monocytes, respectively) and Chlamydia trachomatis, which targets mucosal epithelia and causes blinding trachoma and sexually transmitted diseases.... The absolute reliance of obligates on a eucaryotic host cell for growth imposes significant experimental constraints, not the least of which is difficulty in establishing pathogen genetic systems. However, C. burnetii was recently liberated from its host cell by a medium that supports axenic (host cell–free) growth
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Rescooped by Damien Meyer from Plants and Microbes
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Trends in Microbiology: Pseudomonas syringae type III effector repertoires: last words in endless arguments (2012)

Trends in Microbiology: Pseudomonas syringae type III effector repertoires: last words in endless arguments (2012) | Intracellular pathogenic bacteria | Scoop.it

Many plant pathogens subvert host immunity by injecting compositionally diverse but functionally similar repertoires of cytoplasmic effector proteins. The bacterial pathogenPseudomonas syringae is a model for exploring the functional structure of such repertoires. The pangenome of P. syringae encodes 57 families of effectors injected by the type III secretion system. Distribution of effector genes among phylogenetically diverse strains reveals a small set of core effectors targeting antimicrobial vesicle trafficking and a much larger set of variable effectors targeting kinase-based recognition processes. Complete disassembly of the 28-effector repertoire of a model strain and reassembly of a minimal functional repertoire reveals the importance of simultaneously attacking both processes. These observations, coupled with growing knowledge of effector targets in plants, support a model for coevolving molecular dialogs between effector repertoires and plant immune systems that emphasizes mutually-driven expansion of the components governing recognition.


Via Kamoun Lab @ TSL
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last paper of one of my best friend

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Rescooped by Damien Meyer from Effectors and Plant Immunity
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Pseudomonas syringae pv. tomato DC3000: A Model Pathogen for Probing Disease Susceptibility and Hormone Signaling in Plants

Pseudomonas syringae pv. tomato DC3000: A Model Pathogen for Probing Disease Susceptibility and Hormone Signaling in Plants | Intracellular pathogenic bacteria | Scoop.it

Scooped from: Annual Review of Phytopathology, 2013
Authors: Xiu-Fang Xin and Sheng Yang He

Summary: Since the early 1980s, various strains of the gram-negative bacterial pathogen Pseudomonas syringae have been used as models for understanding plant-bacterial interactions. In 1991, a P. syringae pathovar tomato (Pst) strain, DC3000, was reported to infect not only its natural host tomato but also Arabidopsis in the laboratory, a finding that spurred intensive efforts in the subsequent two decades to characterize the molecular mechanisms by which this strain causes disease in plants. Genomic analysis shows that Pst DC3000 carries a large repertoire of potential virulence factors, including proteinaceous effectors that are secreted through the type III secretion system and a polyketide phytotoxin called coronatine, which structurally mimics the plant hormone jasmonate ( JA). Study of Pst DC3000 pathogenesis has not only provided several conceptual advances in understanding how a bacterial pathogen employs type III effectors to suppress plant immune responses and promote disease susceptibility but has also facilitated the discovery of the immune function of stomata and key components of JA signaling in plants. The concepts derived from the study of Pst DC3000 pathogenesis may prove useful in understanding pathogenesis mechanisms of other plant pathogens.


Via Freddy Monteiro, Nicolas Denancé
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remarkable review

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Subversion of trafficking, apoptosis, and innate immunity by type III secretion system effectors

Subversion of trafficking, apoptosis, and innate immunity by type III secretion system effectors | Intracellular pathogenic bacteria | Scoop.it
Publication date: Available online 16 July 2013 Source:Trends in Microbiology Author(s): Benoit Raymond , Joanna C. Young , Mitchell Pallett , Robert G.
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Rescooped by Damien Meyer from of Plants & Bacteria (and sometimes other fellows too)
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Microbial quest for food in vivo: ‘Nutritional virulence’ as an emerging paradigm

Microbial quest for food in vivo: ‘Nutritional virulence’ as an emerging paradigm | Intracellular pathogenic bacteria | Scoop.it

Scooped from: Cellular Microbiology, 2013.

Authors: Yousef Abu Kwaik and Dirk Bumann

 

Summary:

Microbial access to host nutrients is a fundamental aspect of infectious diseases. Pathogens face complex dynamic nutritional host microenvironments that change with increasing inflammation and local hypoxia. Since the host can actively limit microbial access to nutrient supply, pathogens have evolved various metabolic adaptations to successfully exploit available host nutrients for proliferation. Recent studies have unraveled an emerging paradigm that we propose to designate as ‘nutritional virulence’. This paradigm is based on specific virulence mechanisms that target major host biosynthetic and degradation pathways (proteasomes, autophagy and lysosomes) or nutrient-rich sources, such as glutathione, to enhance host supply of limiting nutrients, such as cysteine. Although Cys is the most limiting cellular amino acid, it is a metabolically favourable source of carbon and energy for various pathogens that are auxotrophic for Cys but utilize idiosyncratic nutritional virulence strategies to generate a gratuitous supply of host Cys. Therefore, proliferation of some intracellular pathogens is restricted by a host nutritional rheostat regulated by certain limiting amino acids, and pathogens have evolved idiosyncratic strategies to short circuit the host nutritional rheostat. Deciphering mechanisms of microbial ‘nutritional virulence’ and metabolism in vivo will facilitate identification of novel microbialand host targets for treatment and prevention of infectious diseases. Host–pathogen synchronization of amino acid auxotrophy indicates that this nutritional synchronization has been a major driving force in the evolution of many intracellular bacterial pathogens.


Via Freddy Monteiro
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Freddy Monteiro's curator insight, May 15, 2013 5:47 AM

'Nutritional Virulence' is first introduced, to my knowledge, in this review to define the set of virulence strategies evolved by pathogens to "directly manipulate host nutrient supply".

 

I'll try to kickstart a discussion here by asking if such effectors are known in plant pathogens. We are talking about thinking out of the "host immunity suppression" box, and rather concentrate on effectors acting on metabolism pathways, sugar or amino acid biosynthesis, from which the pathogen clearly (data available) benefits.

To put it in other words, how many "classical pathogen virulence mechanisms that result in manipulation of host cellular processes", as the authors state, may have a role in nutrien gathering during infection!? How many others are we missing? And how important this function during the intectaion of pathogens with plants?