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Tiny architects: biogenesis of intracellular replicative niches by bacterial pathogens.
Martinez, E, Siadous, FA, Bonazzi, M
FEMS microbiology reviews. 2018;(4):425-447
Abstract
Co-evolution of bacterial pathogens with their hosts led to the emergence of a stunning variety of strategies aiming at the evasion of host defences, colonisation of host cells and tissues and, ultimately, the establishment of a successful infection. Pathogenic bacteria are typically classified as extracellular and intracellular; however, intracellular lifestyle comes in many different flavours: some microbes rapidly escape to the cytosol whereas other microbes remain within vacuolar compartments and harness membrane trafficking pathways to generate their host-derived, pathogen-specific replicative niche. Here we review the current knowledge on a variety of vacuolar lifestyles, the effector proteins used by bacteria as tools to take control of the host cell and the main membrane trafficking signalling pathways targeted by vacuolar pathogens as source of membranes and nutrients. Finally, we will also discuss how host cells have developed countermeasures to sense the biogenesis of the aberrant organelles harbouring bacteria. Understanding the dialogue between bacterial and eukaryotic proteins is the key to unravel the molecular mechanisms of infection and in turn, this may lead to the identification of new targets for the development of new antimicrobials.
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Know your enemy, embrace your friend: using omics to understand how plants respond differently to pathogenic and mutualistic microorganisms.
Plett, JM, Martin, FM
The Plant journal : for cell and molecular biology. 2018;(4):729-746
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Abstract
Microorganisms, or 'microbes', have formed intimate associations with plants throughout the length of their evolutionary history. In extant plant systems microbes still remain an integral part of the ecological landscape, impacting plant health, productivity and long-term fitness. Therefore, to properly understand the genetic wiring of plants, we must first determine what perception systems plants have evolved to parse beneficial from commensal from pathogenic microbes. In this review, we consider some of the most recent advances in how plants respond at the molecular level to different microbial lifestyles. Further, we cover some of the means by which microbes are able to manipulate plant signaling pathways through altered destructiveness and nutrient sinks, as well as the use of effector proteins and micro-RNAs (miRNAs). We conclude by highlighting some of the major questions still to be answered in the field of plant-microbe research, and suggest some of the key areas that are in greatest need of further research investment. The results of these proposed studies will have impacts in a wide range of plant research disciplines and will, ultimately, translate into stronger agronomic crops and forestry stock, with immune perception and response systems bred to foster beneficial microbial symbioses while repudiating pathogenic symbioses.
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Sugar flux and signaling in plant-microbe interactions.
Bezrutczyk, M, Yang, J, Eom, JS, Prior, M, Sosso, D, Hartwig, T, Szurek, B, Oliva, R, Vera-Cruz, C, White, FF, et al
The Plant journal : for cell and molecular biology. 2018;(4):675-685
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Abstract
Plant breeders have developed crop plants that are resistant to pests, but the continual evolution of pathogens creates the need to iteratively develop new control strategies. Molecular tools have allowed us to gain deep insights into disease responses, allowing for more efficient, rational engineering of crops that are more robust or resistant to a greater number of pathogen variants. Here we describe the roles of SWEET and STP transporters, membrane proteins that mediate transport of sugars across the plasma membrane. We discuss how these transporters may enhance or restrict disease through controlling the level of nutrients provided to pathogens and whether the transporters play a role in sugar signaling for disease resistance. This review indicates open questions that require further research and proposes the use of genome editing technologies for engineering disease resistance.
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How Dengue Virus Circumvents Innate Immunity.
Kao, YT, Lai, MMC, Yu, CY
Frontiers in immunology. 2018;:2860
Abstract
In the battle between a virus and its host, innate immunity serves as the first line of defense protecting the host against pathogens. The antiviral actions start with the recognition of pathogen-associated molecular patterns derived from the virus, then ultimately turning on particular transcription factors to generate antiviral interferons (IFNs) or proinflammatory cytokines via fine-tuned signaling cascades. With dengue virus (DENV) infection, its viral RNA is recognized by the host RNA sensors, mainly retinoic acid inducible gene-I (RIG-I)-like receptors (RLRs) and toll-like receptors. DENV infection also activates the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING)-mediated DNA-sensing pathway despite the absence of a DNA stage in the DENV lifecycle. In the last decade, DENV has been considered a weak IFN-inducing pathogen with the evidence that DENV has evolved multiple strategies antagonizing the host IFN system. DENV passively escapes from innate immunity surveillance and also actively subverts the innate immune system at multiple steps. DENV targets both RNA-triggered RLR-mitochondrial antiviral signaling protein (RLR-MAVS) and DNA-triggered cGAS-STING signaling to reduce IFN production in infected cells. It also blocks IFN action by inhibiting IFN regulatory factor- and signal transducer and activator of transcription-mediated signaling. This review explores the current understanding of how DENV escapes the control of the innate immune system by modifying viral RNA and viral protein and by post-translational modification of cellular factors. The roles of the DNA-sensing pathway in DENV infection, and how mitochondrial dynamics participates in innate immunity are also discussed.
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Role of divalent metals in infectious disease susceptibility and outcome.
Weiss, G, Carver, PL
Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases. 2018;(1):16-23
Abstract
BACKGROUND Divalent metals play important roles in maintaining metabolism and cellular growth of both eukaryotic hosts and invading microbes. Both metal deficiency and overload can result in abnormal cellular function or damage. Given its central role in host-pathogen interactions, subtle alterations of divalent metal homeostasis can occur in the course of infectious diseases which aim, from the host perspective, either to reduce the availability of respective metals to microbes or to use toxic metal accumulation to eliminate pathogens. AIMS To provide the reader with background information and clinical data on divalent metal homeostasis in host-pathogen interactions, how this affects the course of infectious disease and whether correction of metal disturbances has shown benefit in infections. SOURCES An in-depth analysis of PubMed articles related to the topic of this review published in English between 1970 and 2016 was performed. CONTENT From the microbial perspective, divalent metals are essential for growth and pathogenicity and to mount effective protection against antimicrobial host responses, including toxic radical formation. Microbes have evolved multiple strategies to control their access to divalent metals. From the clinical perspective, alterations of divalent metal levels may result in increased or decreased susceptibility to infection and often occur in response to infections. However, keeping in mind the strategies underlying such alterations, for which the term 'nutritional immunity' was coined, the uncritical correction of such divalent metal imbalances may cause harm to patients. This review addresses the role of the divalent metals iron, selenium, zinc, manganese and copper in infectious diseases from a mechanistic and clinical perspective. IMPLICATIONS We point out areas of research needed to expand our limited knowledge, hoping to improve the clinical management of patients with infections and to identify promising new targets for treatment by modulation of host or microbe divalent metal metabolism.
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Mycobacterial extracellular vesicles and host pathogen interactions.
Gupta, S, Rodriguez, GM
Pathogens and disease. 2018;(4)
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Abstract
Mycobacteria, like other bacteria, archaea and eukaryotic cells, naturally release extracellular vesicles (EVs) to interact with their environment. EVs produced by pathogenic bacteria are involved in many activities including cell-cell communication, immunomodulation, virulence and cell survival. Although EVs released by thick cell wall microorganisms like mycobacteria were recognized only recently, studies of Mycobacterium tuberculosis EVs already point to their important roles in host pathogen interactions, opening exciting new areas of investigation. This minireview will summarize the current understanding of mycobacterial EV biology and roles in pathogenesis and will discuss their potential therapeutic applications.
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Iron at the Centre of Candida albicans Interactions.
Fourie, R, Kuloyo, OO, Mochochoko, BM, Albertyn, J, Pohl, CH
Frontiers in cellular and infection microbiology. 2018;:185
Abstract
Iron is an absolute requirement for both the host and most pathogens alike and is needed for normal cellular growth. The acquisition of iron by biological systems is regulated to circumvent toxicity of iron overload, as well as the growth deficits imposed by iron deficiency. In addition, hosts, such as humans, need to limit the availability of iron to pathogens. However, opportunistic pathogens such as Candida albicans are able to adapt to extremes of iron availability, such as the iron replete environment of the gastrointestinal tract and iron deficiency during systemic infection. C. albicans has developed a complex and effective regulatory circuit for iron acquisition and storage to circumvent iron limitation within the human host. As C. albicans can form complex interactions with both commensal and pathogenic co-inhabitants, it can be speculated that iron may play an important role in these interactions. In this review, we highlight host iron regulation as well as regulation of iron homeostasis in C. albicans. In addition, the review argues for the need for further research into the role of iron in polymicrobial interactions. Lastly, the role of iron in treatment of C. albicans infection is discussed.
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[Host-microbiota crosstalk and cardiovascular diseases].
Amar, J
Presse medicale (Paris, France : 1983). 2018;(9):775-779
Abstract
When analyzing the microbiota-host crosstalk, we have to consider three participants in this dialogue: the gut microbiota, the intestinal barrier and bacterial translocation. Experimental data demonstrate that host microbiota crosstalk plays a causal on the regulation of blood pressure, glucose metabolism and the development of atherosclerosis. Host microbiota crosstalk is associated in humans with main cardiovascular risk factors notably hypertension and type 2 diabetes. Host microbiota crosstalk is associated in humans with the onset of cardiovascular diseases. The Mediterranean diet has proven as proven to be an effective strategy in improving cardiovascular prognosis and in changing gut microbiota.
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Modulation of plant autophagy during pathogen attack.
Leary, AY, Sanguankiattichai, N, Duggan, C, Tumtas, Y, Pandey, P, Segretin, ME, Salguero Linares, J, Savage, ZD, Yow, RJ, Bozkurt, TO
Journal of experimental botany. 2018;(6):1325-1333
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Abstract
In plants, the highly conserved catabolic process of autophagy has long been known as a means of maintaining cellular homeostasis and coping with abiotic stress conditions. Accumulating evidence has linked autophagy to immunity against invading pathogens, regulating plant cell death, and antimicrobial defences. In turn, it appears that phytopathogens have evolved ways not only to evade autophagic clearance but also to modulate and co-opt autophagy for their own benefit. In this review, we summarize and discuss the emerging discoveries concerning how pathogens modulate both host and self-autophagy machineries to colonize their host plants, delving into the arms race that determines the fate of interorganismal interaction.
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RNA Thermometers in Bacterial Pathogens.
Loh, E, Righetti, F, Eichner, H, Twittenhoff, C, Narberhaus, F
Microbiology spectrum. 2018;(2)
Abstract
Temperature variation is one of the multiple parameters a microbial pathogen encounters when it invades a warm-blooded host. To survive and thrive at host body temperature, human pathogens have developed various strategies to sense and respond to their ambient temperature. An instantaneous response is mounted by RNA thermometers (RNATs), which are integral sensory structures in mRNAs that modulate translation efficiency. At low temperatures outside the host, the folded RNA blocks access of the ribosome to the translation initiation region. The temperature shift upon entering the host destabilizes the RNA structure and thus permits ribosome binding. This reversible zipper-like mechanism of RNATs is ideally suited to fine-tune virulence gene expression when the pathogen enters or exits the body of its host. This review summarizes our present knowledge on virulence-related RNATs and discusses recent developments in the field.