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1
Martinez-Martin, Nadia. "Technologies for Proteome-Wide Discovery of Extracellular Host-Pathogen Interactions." Journal of Immunology Research 2017 (2017): 1–18. http://dx.doi.org/10.1155/2017/2197615.
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Pathogens have evolved unique mechanisms to breach the cell surface barrier and manipulate the host immune response to establish a productive infection. Proteins exposed to the extracellular environment, both cell surface-expressed receptors and secreted proteins, are essential targets for initial invasion and play key roles in pathogen recognition and subsequent immunoregulatory processes. The identification of the host and pathogen extracellular molecules and their interaction networks is fundamental to understanding tissue tropism and pathogenesis and to inform the development of therapeutic strategies. Nevertheless, the characterization of the proteins that function in the host-pathogen interface has been challenging, largely due to the technical challenges associated with detection of extracellular protein interactions. This review discusses available technologies for the high throughput study of extracellular protein interactions between pathogens and their hosts, with a focus on mammalian viruses and bacteria. Emerging work illustrates a rich landscape for extracellular host-pathogen interaction and points towards the evolution of multifunctional pathogen-encoded proteins. Further development and application of technologies for genome-wide identification of extracellular protein interactions will be important in deciphering functional host-pathogen interaction networks, laying the foundation for development of novel therapeutics.
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Chen, Melissa Y., Leah M. Fulton, Ivie Huang, Aileen Liman, Sarzana S. Hossain, Corri D. Hamilton, Siyu Song, Quentin Geissmann, Kayla C. King, and Cara H. Haney. "Order among chaos: High throughput MYCroplanters can distinguish interacting drivers of host infection in a highly stochastic system." PLOS Pathogens 21, no. 2 (February 11, 2025): e1012894. https://doi.org/10.1371/journal.ppat.1012894.
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The likelihood that a host will be susceptible to infection is influenced by the interaction of diverse biotic and abiotic factors. As a result, substantial experimental replication and scalability are required to identify the contributions of and interactions between the host, the environment, and biotic factors such as the microbiome. For example, pathogen infection success is known to vary by host genotype, bacterial strain identity and dose, and pathogen dose. Elucidating the interactions between these factors in vivo has been challenging because testing combinations of these variables quickly becomes experimentally intractable. Here, we describe a novel high throughput plant growth system (MYCroplanters) to test how multiple host, non-pathogenic bacteria, and pathogen variables predict host health. Using an Arabidopsis-Pseudomonas host-microbe model, we found that host genotype and bacterial strain order of arrival predict host susceptibility to infection, but pathogen and non-pathogenic bacterial dose can overwhelm these effects. Host susceptibility to infection is therefore driven by complex interactions between multiple factors that can both mask and compensate for each other. However, regardless of host or inoculation conditions, the ratio of pathogen to non-pathogen emerged as a consistent correlate of disease. Our results demonstrate that high-throughput tools like MYCroplanters can isolate interacting drivers of host susceptibility to disease. Increasing the scale at which we can screen drivers of disease, such as microbiome community structure, will facilitate both disease predictions and treatments for medicine and agricultural applications.
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Burdon, J. J., and P. H. Thrall. "Resistance variation in natural plant populations." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (January 1, 2002): S145—S150. http://dx.doi.org/10.17221/10342-pps.
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The general outcomes of long-term trajectories of coevolutionary interactions between specific hosts and pathogens are<br />set by the interaction of their life histories. However, within those outcomes the speed of co-evolutionary responses and<br />the extent of their expression in the resistance/virulence structure of wild plant and pathogen populations respectively,<br />are highly variable characters changing from place-to-place and time-to-time as a result of the interaction of host and<br />pathogen with the physical environment. As a consequence, understanding of the role of diseases in the evolution of their<br />hosts requires approaches that simultaneously deal with host and pathogen structures over multiple populations within a<br />metapopulation framework.
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Wroth, J. M. "Variation in pathogenicity among and within Mycosphaerella pinodes populations collected from field pea in Australia." Canadian Journal of Botany 76, no. 11 (November 1, 1998): 1955–66. http://dx.doi.org/10.1139/b98-164.
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Ninety-nine single ascospore isolates of Mycosphaerella pinodes (Berk. & Blox.) Vestergr. from widely separated locations in southern Australia varied greatly in their ability to cause disease in leaves and stems of 10 host genotypes when assayed at two inoculum pressures. There were highly significant differences between the infection pressures, isolates, and host genotypes that accounted for most of the variance. A small proportion of the variance included a highly significant host genotype beta isolate interactions in leaves and stems and a highly significant host genotype beta isolate beta environment interaction in leaves. The continuous variation in disease responses among isolates precluded classification into distinct pathotypes. A cluster analysis of the data revealed that many isolates were closely related irrespective of the host cultivar or location from which they were collected. The relationship between mean host resistance and the variation among isolates was assessed, and it was concluded that increasing host resistance was unlikely to increase variation in the pathogen population; therefore, resistance should be relatively stable.Key words: Ascochyta blight, Pisum sativum, host-pathogen interaction, cluster analysis.
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Blaustein, Andrew R., Stephanie S. Gervasi, Pieter T. J. Johnson, Jason T. Hoverman, Lisa K. Belden, Paul W. Bradley, and Gisselle Y. Xie. "Ecophysiology meets conservation: understanding the role of disease in amphibian population declines." Philosophical Transactions of the Royal Society B: Biological Sciences 367, no. 1596 (June 19, 2012): 1688–707. http://dx.doi.org/10.1098/rstb.2012.0011.
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Infectious diseases are intimately associated with the dynamics of biodiversity. However, the role that infectious disease plays within ecological communities is complex. The complex effects of infectious disease at the scale of communities and ecosystems are driven by the interaction between host and pathogen. Whether or not a given host–pathogen interaction results in progression from infection to disease is largely dependent on the physiological characteristics of the host within the context of the external environment. Here, we highlight the importance of understanding the outcome of infection and disease in the context of host ecophysiology using amphibians as a model system. Amphibians are ideal for such a discussion because many of their populations are experiencing declines and extinctions, with disease as an important factor implicated in many declines and extinctions. Exposure to pathogens and the host's responses to infection can be influenced by many factors related to physiology such as host life history, immunology, endocrinology, resource acquisition, behaviour and changing climates. In our review, we discuss the relationship between disease and biodiversity. We highlight the dynamics of three amphibian host–pathogen systems that induce different effects on hosts and life stages and illustrate the complexity of amphibian–host–parasite systems. We then review links between environmental stress, endocrine–immune interactions, disease and climate change.
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Haley, Kathryn P., and Jennifer A. Gaddy. "Helicobacter pylori: Genomic Insight into the Host-Pathogen Interaction." International Journal of Genomics 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/386905.
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The advent of genomic analyses has revolutionized the study of human health. Infectious disease research in particular has experienced an explosion of bacterial genomic, transcriptomic, and proteomic data complementing the phenotypic methods employed in traditional bacteriology. Together, these techniques have revealed novel virulence determinants in numerous pathogens and have provided information for potential chemotherapeutics. The bacterial pathogen,Helicobacter pylori, has been recognized as a class 1 carcinogen and contributes to chronic inflammation within the gastric niche. Genomic analyses have uncovered remarkable coevolution between the human host andH. pylori. Perturbation of this coevolution results in dysregulation of the host-pathogen interaction, leading to oncogenic effects. This review discusses the relationship ofH. pyloriwith the human host and environment and the contribution of each of these factors to disease progression, with an emphasis on features that have been illuminated by genomic tools.
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Gaylord, Elizabeth A., Hau Lam Choy, and Tamara L. Doering. "Dangerous Liaisons: Interactions of Cryptococcus neoformans with Host Phagocytes." Pathogens 9, no. 11 (October 27, 2020): 891. http://dx.doi.org/10.3390/pathogens9110891.
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Cryptococcus neoformans is an opportunistic fungal pathogen and a leading cause of death in immunocompromised individuals. The interactions of this yeast with host phagocytes are critical to disease outcome, and C. neoformans is equipped with an array of factors to modulate these processes. Cryptococcal infection begins with the deposition of infectious particles into the lungs, where the fungal cells deploy various antiphagocytic factors to resist internalization by host cells. If the cryptococci are still engulfed, they can survive and proliferate within host cells by modulating the phagolysosome environment in which they reside. Lastly, cryptococcal cells may escape from phagocytes by host cell lysis, nonlytic exocytosis, or lateral cell-to-cell transfer. The interactions between C. neoformans and host phagocytes also influence the dissemination of this pathogen to the brain, where it may cross the blood-brain barrier and cause an often-fatal meningoencephalitis. In this review, we highlight key cryptococcal factors involved in various stages of cryptococcal-host interaction and pathogenesis.
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Tung, Pham X., Eufemio T. Rasco, Peter Vander Zaag, and Peter Schmiediche. "Resistance to Pseudomonas solanacearum in the potato: II. Aspects of host-pathogen-environment interaction." Euphytica 45, no. 3 (February 1990): 211–15. http://dx.doi.org/10.1007/bf00032988.
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Tamir-Ariel, Dafna, Naama Navon, and Saul Burdman. "Identification of Genes in Xanthomonas campestris pv. vesicatoria Induced during Its Interaction with Tomato." Journal of Bacteriology 189, no. 17 (June 15, 2007): 6359–71. http://dx.doi.org/10.1128/jb.00320-07.
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ABSTRACT Xanthomonas campestris pv. vesicatoria is the causal agent of bacterial spot disease of tomato and pepper. The disease process is interactive and very intricate and involves a plethora of genes in the pathogen and in the host. In the pathogen, different genes are activated in response to the changing environment to enable it to survive, adapt, evade host defenses, propagate, and damage the host. To understand the disease process, it is imperative to broaden our understanding of the gene machinery that participates in it, and the most reliable way is to identify these genes in vivo. Here, we have adapted a recombinase-based in vivo expression technology (RIVET) to study the genes activated in X. campestris pv. vesicatoria during its interaction with one of its hosts, tomato. This is the first study that demonstrates the feasibility of this approach for identifying in vivo induced genes in a plant pathogen. RIVET revealed 61 unique X. campestris pv. vesicatoria genes or operons that delineate a picture of the different processes involved in the pathogen-host interaction. To further explore the role of some of these genes, we generated knockout mutants for 13 genes and characterized their ability to grow in planta and to cause disease symptoms. This analysis revealed several genes that may be important for the interaction of the pathogen with its host, including a citH homologue gene, encoding a citrate transporter, which was shown to be required for wild-type levels of virulence.
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Mehta, Sahil, Amrita Chakraborty, Amit Roy, Indrakant K. Singh, and Archana Singh. "Fight Hard or Die Trying: Current Status of Lipid Signaling during Plant–Pathogen Interaction." Plants 10, no. 6 (May 30, 2021): 1098. http://dx.doi.org/10.3390/plants10061098.
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Plant diseases pose a substantial threat to food availability, accessibility, and security as they account for economic losses of nearly $300 billion on a global scale. Although various strategies exist to reduce the impact of diseases, they can introduce harmful chemicals to the food chain and have an impact on the environment. Therefore, it is necessary to understand and exploit the plants’ immune systems to control the spread of pathogens and enable sustainable agriculture. Recently, growing pieces of evidence suggest a functional myriad of lipids to be involved in providing structural integrity, intracellular and extracellular signal transduction mediators to substantial cross-kingdom cell signaling at the host–pathogen interface. Furthermore, some pathogens recognize or exchange plant lipid-derived signals to identify an appropriate host or development, whereas others activate defense-related gene expression. Typically, the membrane serves as a reservoir of lipids. The set of lipids involved in plant–pathogen interaction includes fatty acids, oxylipins, phospholipids, glycolipids, glycerolipids, sphingolipids, and sterols. Overall, lipid signals influence plant–pathogen interactions at various levels ranging from the communication of virulence factors to the activation and implementation of host plant immune defenses. The current review aims to summarize the progress made in recent years regarding the involvement of lipids in plant–pathogen interaction and their crucial role in signal transduction.
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Labarthe, Simon, Béatrice Laroche, Thi Nhu Tao Nguyen, Bastien Polizzi, Florian Patout, Magali Ribot, and Tabea Stegmaier. "A multi-scale epidemic model of Salmonella infection with heterogeneous shedding." ESAIM: Proceedings and Surveys 67 (2020): 261–84. http://dx.doi.org/10.1051/proc/202067015.
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Salmonella strains colonize the digestive tract of farm livestock, such as chickens or pigs, without affecting them, and potentially infect food products, representing a threat for human health ranging from food poisoning to typhoid fever. It has been shown that the ability to excrete the pathogen in the environment and contaminate other animals is variable. This heterogeneity in pathogen carriage and shedding results from interactions between the host’s immune response, the pathogen and the commensal intestinal microbiota. In this paper we propose a novel generic multiscale modeling framework of heterogeneous pathogen transmission in an animal population. At the intra-host level, the model describes the interaction between the commensal microbiota, the pathogen and the inflammatory response. Random fluctuations in the ecological dynamics of the individual microbiota and transmission at between-host scale are added to obtain a drift-diffusion PDE model of the pathogen distribution at the population level. The model is further extended to represent transmission between several populations. The asymptotic behavior as well as the impact of control strategies including cleaning and antimicrobial administration are investigated through numerical simulation.
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Dubljanin, Eleonora, Jelena Zunic, Isidora Vujcic, Ivana Colovic Calovski, Sandra Sipetic Grujicic, Stefan Mijatovic, and Aleksandar Dzamic. "Host-Pathogen Interaction and Resistance Mechanisms in Dermatophytes." Pathogens 13, no. 8 (August 4, 2024): 657. http://dx.doi.org/10.3390/pathogens13080657.
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Dermatophytes are widely distributed in the environment, with an estimated prevalence of 20–25% of the the global population yearly. These fungi are keratinophilic and keratinolytic and cause the infection of keratin-rich structures such as skin, hair, and nails. The pattern of this infectious disease covers a wide spectrum from exposed individuals without symptoms to those with acutely inflammatory or non-inflammatory, chronic to invasive, and even life-threatening symptoms. This review summarizes current information on the pathogenicity, virulence factors, and drug resistance mechanisms associated with dermatophytes. A greater number of virulence factors of these fungi are important for the occurrence of infection and the changes that occur, including those regarding adhesins, the sulfite efflux pump, and proteolytic enzymes. Other virulence factors include mechanisms of evading the host defense, while the development of resistance to antifungal drugs is increasing, resulting in treatment failure. The investigation of host-pathogen interactions is essential for developing a more complete understanding of the mechanisms underlying dermatophyte pathogenesis and host response to inform the use of diagnostics methods and antifungal therapeutics to minimize the high fungal burden caused by dermatophytes and to control the spread of resistance.
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Schulte, Marc, and Michael Hensel. "Models of intestinal infection by Salmonella enterica: introduction of a new neonate mouse model." F1000Research 5 (June 24, 2016): 1498. http://dx.doi.org/10.12688/f1000research.8468.1.
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Salmonella entericaserovar Typhimurium is a foodborne pathogen causing inflammatory disease in the intestine following diarrhea and is responsible for thousands of deaths worldwide. Manyin vitroinvestigations using cell culture models are available, but these do not represent the real natural environment present in the intestine of infected hosts. Severalin vivoanimal models have been used to study the host-pathogen interaction and to unravel the immune responses and cellular processes occurring during infection. An animal model forSalmonella-induced intestinal inflammation relies on the pretreatment of mice with streptomycin. This model is of great importance but still shows limitations to investigate the host-pathogen interaction in the small intestinein vivo. Here, we review the use of mouse models forSalmonellainfections and focus on a new small animal model using 1-day-old neonate mice. The neonate model enables researchers to observe infection of both the small and large intestine, thereby offering perspectives for new experimental approaches, as well as to analyze theSalmonella-enterocyte interaction in the small intestinein vivo.
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Kogut, Michael H., and Mariano Enrique Fernandez Miyakawa. "Phenotype Alterations in the Cecal Ecosystem Involved in the Asymptomatic Intestinal Persistence of Paratyphoid Salmonella in Chickens." Animals 13, no. 18 (September 6, 2023): 2824. http://dx.doi.org/10.3390/ani13182824.
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The gastrointestinal ecosystem involves interactions between the host, gut microbiota, and external environment. To colonize the gut of poultry, Salmonella must surmount barriers levied by the intestine including mucosal innate immune responses and microbiota-mediated niche restrictions. Accordingly, comprehending Salmonella intestinal colonization in poultry requires an understanding of how the pathogen interacts with the intestinal ecosystem. In chickens, the paratyphoid Salmonella have evolved the capacity to survive the initial immune response and persist in the avian ceca for months without triggering clinical signs. The persistence of a Salmonella infection in the avian host involves both host defenses and tolerogenic defense strategies. The initial phase of the Salmonella–gut ecosystem interaction is characteristically an innate pro-inflammatory response that controls bacterial invasion. The second phase is initiated by an expansion of the T regulatory cell population in the cecum of Salmonella-infected chickens accompanied by well-defined shifts in the enteric neuro-immunometabolic pathways that changes the local phenotype from pro-inflammatory to an anti-inflammatory environment. Thus, paratyphoid Salmonella in chickens have evolved a unique survival strategy that minimizes the inflammatory response (disease resistance) during the initial infection and then induces an immunometabolic reprogramming in the cecum that alters the host defense to disease tolerance that provides an environment conducive to drive asymptomatic carriage of the bacterial pathogen.
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Páez, David J., Rachel L. Powers, Peng Jia, Natalia Ballesteros, Gael Kurath, Kerry A. Naish, and Maureen K. Purcell. "Temperature Variation and Host Immunity Regulate Viral Persistence in a Salmonid Host." Pathogens 10, no. 7 (July 7, 2021): 855. http://dx.doi.org/10.3390/pathogens10070855.
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Environmental variation has important effects on host–pathogen interactions, affecting large-scale ecological processes such as the severity and frequency of epidemics. However, less is known about how the environment interacts with host immunity to modulate virus fitness within hosts. Here, we studied the interaction between host immune responses and water temperature on the long-term persistence of a model vertebrate virus, infectious hematopoietic necrosis virus (IHNV) in steelhead trout (Oncorhynchus mykiss). We first used cell culture methods to factor out strong host immune responses, allowing us to test the effect of temperature on viral replication. We found that 15 ∘C water temperature accelerated IHNV replication compared to the colder 10 and 8 ∘C temperatures. We then conducted in vivo experiments to quantify the effect of 6, 10, and 15 ∘C water temperatures on IHNV persistence over 8 months. Fish held at 15 and 10 ∘C were found to have higher prevalence of neutralizing antibodies compared to fish held at 6 ∘C. We found that IHNV persisted for a shorter time at warmer temperatures and resulted in an overall lower fish mortality compared to colder temperatures. These results support the hypothesis that temperature and host immune responses interact to modulate virus persistence within hosts. When immune responses were minimized (i.e., in vitro) virus replication was higher at warmer temperatures. However, with a full potential for host immune responses (i.e., in vivo experiments) longer virus persistence and higher long-term virulence was favored in colder temperatures. We also found that the viral RNA that persisted at later time points (179 and 270 days post-exposure) was mostly localized in the kidney and spleen tissues. These tissues are composed of hematopoietic cells that are favored targets of the virus. By partitioning the effect of temperature on host and pathogen responses, our results help to better understand environmental drivers of host–pathogen interactions within hosts, providing insights into potential host–pathogen responses to climate change.
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Ramakrishnan, Gayatri, Narayanaswamy Srinivasan, Ponnan Padmapriya, and Vasant Natarajan. "Homology-Based Prediction of Potential Protein-Protein Interactions between Human Erythrocytes and Plasmodium falciparum." Bioinformatics and Biology Insights 9 (January 2015): BBI.S31880. http://dx.doi.org/10.4137/bbi.s31880.
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Plasmodium falciparum, a causative agent of malaria, is a well-characterized obligate intracellular parasite known for its ability to remodel host cells, particularly erythrocytes, to successfully persist in the host environment. However, the current levels of understanding from the laboratory experiments on the host-parasite interactions and the strategies pursued by the parasite to remodel host erythrocytes are modest. Several computational means developed in the recent past to predict host-parasite/pathogen interactions have generated testable hypotheses on feasible protein-protein interactions. We demonstrate the utility of protein structure-based protocol in the recognition of potential interacting proteins across P. falciparum and host erythrocytes. In concert with the information on the expression and subcellular localization of host and parasite proteins, we have identified 208 biologically feasible interactions potentially brought about by 59 P. falciparum and 30 host erythrocyte proteins. For selected cases, we have evaluated the physicochemical viability of the predicted interactions in terms of surface complementarity, electrostatic complementarity, and interaction energies at protein interface regions. Such careful inspection of molecular and mechanistic details generates high confidence on the predicted host-parasite protein-protein interactions. The predicted host-parasite interactions generate many experimentally testable hypotheses that can contribute to the understanding of possible mechanisms undertaken by the parasite in host erythrocyte remodeling. Thus, the key protein players recognized in P. falciparum can be explored for their usefulness as targets for chemotherapeutic intervention.
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Bourouiba, Lydia. "Fluid Dynamics of Respiratory Infectious Diseases." Annual Review of Biomedical Engineering 23, no. 1 (July 13, 2021): 547–77. http://dx.doi.org/10.1146/annurev-bioeng-111820-025044.
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The host-to-host transmission of respiratory infectious diseases is fundamentally enabled by the interaction of pathogens with a variety of fluids (gas or liquid) that shape pathogen encapsulation and emission, transport and persistence in the environment, and new host invasion and infection. Deciphering the mechanisms and fluid properties that govern and promote these steps of pathogen transmission will enable better risk assessment and infection control strategies, and may reveal previously underappreciated ways in which the pathogens might actually adapt to or manipulate the physical and chemical characteristics of these carrier fluids to benefit their own transmission. In this article, I review our current understanding of the mechanisms shaping the fluid dynamics of respiratory infectious diseases.
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Oyesola, Oyebola Oluwakemi, Alexander E. Downie, Ramya Smithaveni Barre, Ying-Han Chen, Kasalina N. Kiwanuka, Kimberly Zaldana, Nina Howard, et al. "Interactions between the Environment and Genetics determines immune variation in rewilded mice." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 115.23. http://dx.doi.org/10.4049/jimmunol.208.supp.115.23.
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Abstract Immune responses to pathogens and vaccination can be varied with some individuals inducing optimal responses while others do not. The host genetic profile, environment and previous microbial experience could influence an individual’s response, but the relative contribution, and interactions of these different factors remains largely unknown. Here, using various multi-omics, ecological and single cell approaches, we show that release of genetic inbred strains of mice, 129-SL, PWK and C57/B6 mice, to a rewilded environment and exposure of these rewilded and laboratory specific pathogen free control mice to a helminth parasite, Trichuris muris allowed us to assess the contribution and interaction of host genotype and environment to the immune cell landscape in the blood and secondary lymphoid organs. Critically, we find that the environment has the greatest effect on circulating blood immune cells while the genetic profile has the greatest effect on the mesenteric lymph node. We also observed significant interactions between the host genetic profile, environment, and infection status in their contribution to immune cell composition, with most of the effect driven by the cells of the adaptive immune system. These findings provide a model for contribution and interactions between genetics, environment, and helminth infection in the inter-individual variation of immune responses.
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Nasher, Fauzy, Burhan Lehri, Megan F. Horney, Richard A. Stabler, and Brendan W. Wren. "Survival of Campylobacter jejuni 11168H in Acanthamoebae castellanii Provides Mechanistic Insight into Host Pathogen Interactions." Microorganisms 10, no. 10 (September 23, 2022): 1894. http://dx.doi.org/10.3390/microorganisms10101894.
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Campylobacter jejuni is the leading cause of bacterial foodborne gastroenteritis worldwide but is rarely transferred between human hosts. Although a recognized microaerophile, the majority of C. jejuni are incapable of growing in an aerobic environment. The persistence and transmission of this pathogen outside its warm-blooded avian and mammalian hosts is poorly understood. Acanthamoebae species are predatory protists and form an important ecological niche with several bacterial species. Here, we investigate the interaction of C. jejuni 11168H and Acanthamoebae castellanii at the single-cell level. We observe that a subpopulation of C. jejuni cells can resist killing by A. castellanii, and non-digested bacteria are exocytosed into the environment where they can persist. In addition, we observe that A. castellanii can harbor C. jejuni 11168H even upon encystment. Transcriptome analyses of C. jejuni interactions revealed similar survival mechanisms when infecting both A. castellanii and warm-blooded hosts. In particular, nitrosative stress defense mechanisms and flagellum function are important as confirmed by mutational analyses of C. jejuni 11168H. This study describes a new host–pathogen interaction for C. jejuni and confirms that amoebae are transient hosts for the persistence, adaptability, and potential transmission of C. jejuni.
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Rajashekara, Gireesh, Linda Eskra, Angie Mathison, Erik Petersen, Qiqi Yu, Jerome Harms, and Gary Splitter. "Brucella: functional genomics and host–pathogen interactions." Animal Health Research Reviews 7, no. 1-2 (June 2006): 1–11. http://dx.doi.org/10.1017/s146625230700117x.
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Brucellosis is a zoonotic disease caused by a number ofBrucellaspecies and is characterized by chronic macrophage infection. However, genes that may contribute to intracellular survival of theBrucellaspecies are not well studied. This review presents, first, genomic islands that are present or absent in variousBrucellaspecies that may help establishBrucellainfection and survival strategies. Second, the alteration in macrophage transcription byBrucellato permit its long-term survival within this hostile intracellular environment. A large number of macrophage gene transcripts are altered followingBrucellainfection indicating thatBrucellais not a silent invader of host cells. Macrophage transcript levels associated with inflammation, apoptosis, signal transduction and vesicular intracellular trafficking are altered duringBrucellainfection, and likely contribute to intracellular survival ofBrucella. Lastly, the host–pathogen interaction events associated withBrucellainfection in living mice visualized in real-time using biophotonic imaging. Mice are often used to evaluateBrucellainfections; however,Brucelladissemination and pathogenesis is poorly understood in mice. Biophotonic imaging ofBrucellainfections revealed sites of bacterial localization similar to human infections and different patterns of infection by attenuated or virulentBrucella.
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Shlykova, D. S., V. M. Pisarev, A. M. Gaponov, and A. V. Tutelyan. "Interaction of bacterial extracellular microvesicles with eukaryotic cells." Medical Immunology (Russia) 22, no. 6 (January 10, 2021): 1065–84. http://dx.doi.org/10.15789/1563-0625-iob-2079.
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Bacterial extracellular microvesicles (BMV) are formed by nonpathogenic, pathogenic and opportunistic bacteria. BMV are spherical bilayer-membrane organelles containing different cargoes: lipopolysaccharides, pathogen associated molecular patterns (PUMP), DNA, RNA, signal molecules, proteins, antibiotic resistance factors, virulence factors, toxins providing various immune response options and conducive to the survival and pathogen dissemination in the human body. BMVs secretion play an important role in the ability of microorganisms to cause various diseases. BMV are involved in biofilms formation, help bacteria to obtain nutrition in a nutrient-poor conditions, to evade the host's immune response, provide communication and surviving in a stressful environment during infection inside the host. The heterogeneity of the biogenesis mechanisms causes differences in the BMV and their characteristics including virulence rate. BMVs host cells entering is mediated by several mechanisms and helps to activate innate and adaptive immune reactions. This review focuses on interaction study of BMV with various eukaryotic cells types including neutrophils, dendritic cells, macrophages, epithelial, endothelial cells. This interaction depends on bacteria species, type of target cell and number of vesicles and can lead to different responses: non-immunogenic, pro-inflammatory, cytotoxic. Subcellular and molecular mechanisms related to the involvement of extracellular microvesicles in host's immune response modulation are presented. Stimulation of immune response is provided by increased secretion of proinflammatory cytokines and chemokines. In some cases BMV use mechanisms to evade immune surveillance: anti-inflammatory cytokines secretion, alterations of phagocytosis and chemotaxis of macrophages, increasing the proteolytic cleavage of CD14 on the macrophage surface, alterations of antigen-presenting function of dendritic cells, T-cell proliferation suppression, reducing the pro-inflammatory cytokines secretion, evasion of host-immune cells direct interactions, destruction of neutrophilic traps. These features allow bacterial cells to survive in the human body, increase their invasive potential, and reduce the excessive inflammatory reactions leading to death of the pathogen itself and life-threatening damage of tissues and organs of the host. Further studies of these mechanisms will improve existing therapeutic approaches to the infectious diseases treatment.
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Cuomo, Paola, Rosanna Capparelli, Marco Alifano, Antonio Iannelli, and Domenico Iannelli. "Gut Microbiota Host–Gene Interaction." International Journal of Molecular Sciences 23, no. 22 (November 8, 2022): 13717. http://dx.doi.org/10.3390/ijms232213717.
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Studies carried out in the last ten years have shown that the metabolites made up from the gut microbiota are essential for multiple functions, such as the correct development of the immune system of newborns, interception of pathogens, and nutritional enrichment of the diet. Therefore, it is not surprising that alteration of the gut microbiota is the starting point of gastrointestinal infection, obesity, type 2 diabetes, inflammatory bowel disease, colorectal cancer, and lung cancer. Diet changes and antibiotics are the major factors damaging the gut microbiota. Early exposure of the newborns to antibiotics may prevent their correct development of the immune system, exposing them to pathogen infections, allergies, and chronic inflammatory diseases. We already know much on how host genes, microbiota, and the environment interact, owing to experiments in several model animals, especially in mice; advances in molecular technology; microbiota transplantation; and comparative metagenomic analysis. However, much more remains to be known. Longitudinal studies on patients undergoing to therapy, along with the identification of bacteria prevalent in responding patients may provide valuable data for improving therapies.
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Gai, Yunpeng, Qichen Niu, Jinchao Kong, Lei Li, Xingxing Liang, Yuwei Cao, Xianqi Zhou, et al. "Genomic and Transcriptomic Characterization of Alternaria alternata during Infection." Agronomy 13, no. 3 (March 10, 2023): 809. http://dx.doi.org/10.3390/agronomy13030809.
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Host-pathogen interactions are the result of the continuously evolving dynamics of the genomic interphases between pathogens and the host plants. Alternaria brown spot (ABS) caused by the pathogen Alternaria alternata is a serious threat to tangerine production. Although recent studies have made significant advances in the characterization of A. alternata virulence factors, a gap exists in the regulation of virulent genes throughout the course of A. alternata infection on host plants. To gain a better understanding of the dynamic defense transcriptome in Alternaria alternata during Infection, we performed a comparative transcriptome approach. After inoculation on citrus, we found that 2142, 1964, 2359 genes were up-regulated, and 1948, 1434, 1996 genes were down-regulated at 12 hours-post-inoculation (hpi), 24 hpi and 48 hpi, respectively. Among these genes, 1333 genes were up-regulated at three time points, and 1054 genes were down-regulated, indicating that most of the differentially expressed genes at the early stage of infection tended to remain differentially expressed at the later stage of infection. In addition to the genes that are known to be part of the infection network in plant-pathogen interactions, many novel genes related to plant-pathogen interaction were identified. Interestingly, our results indicate that A. alternata is able to rapidly alter its gene expression pattern during infection process, which is vital for the successful colonization of the pathogen. Moreover, this rapid alteration of gene expression is likely to be an adaptive mechanism, enabling the pathogen to quickly respond to any changes in the environment and adapt to the host’s defense system. This ability to modify gene expression quickly in the face of environmental changes could play a critical role in the successful establishment of infection. RT-qPCR analysis confirmed that the expression pattern of nine randomly selected genes from the peroxisome pathway were consistent with the RNA-seq data. Our study provided a comprehensive study of the expression of genes during A. alternata infection of citrus, which may facilitate the understanding of host-plant interactions in A. alternata.
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Chan, Marion M., Nagasuresh Adapala, and Cui Chen. "Peroxisome Proliferator-Activated Receptor-γ-Mediated Polarization of Macrophages inLeishmaniaInfection." PPAR Research 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/796235.
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Infection is the outcome of a contest between a pathogen and its host. In the disease leishmaniasis, the causative protozoan parasites are harbored inside the macrophages.Leishmaniaspecies adapt strategies to make the infection chronic, keeping a balance between their own and the host's defense so as to establish an environment that is favorable for survival and propagation. Activation of peroxisome proliferator-activated receptor (PPAR) is one of the tactics used. This ligand-activated nuclear factor curbs inflammation to protect the host from excessive injuries by setting a limit to its destructive force. In this paper, we report the interaction of host PPARs and the pathogen for visceral leishmaniasis,Leishmania donovani,in vivoandin vitro. PPAR expression is induced by parasitic infection. Leishmanial activation of PPARγpromotes survival, whereas blockade of PPARγfacilitates removal of the parasite. Thus,Leishmaniaparasites harness PPARγto increase infectivity.
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Kawka, Malwina, Anna Brzostek, Katarzyna Dzitko, Jakub Kryczka, Radosław Bednarek, Renata Płocińska, Przemysław Płociński, et al. "Mycobacterium tuberculosis Binds Human Serum Amyloid A, and the Interaction Modulates the Colonization of Human Macrophages and the Transcriptional Response of the Pathogen." Cells 10, no. 5 (May 20, 2021): 1264. http://dx.doi.org/10.3390/cells10051264.
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As a very successful pathogen with outstanding adaptive properties, Mycobacterium tuberculosis (Mtb) has developed a plethora of sophisticated mechanisms to subvert host defenses and effectively enter and replicate in the harmful environment inside professional phagocytes, namely, macrophages. Here, we demonstrated the binding interaction of Mtb with a major human acute phase protein, namely, serum amyloid A (SAA1), and identified AtpA (Rv1308), ABC (Rv2477c), EspB (Rv3881c), TB 18.6 (Rv2140c), and ThiC (Rv0423c) membrane proteins as mycobacterial effectors responsible for the pathogen-host protein interplay. SAA1-opsonization of Mtb prior to the infection of human macrophages favored bacterial entry into target phagocytes accompanied by a substantial increase in the load of intracellularly multiplying and surviving bacteria. Furthermore, binding of human SAA1 by Mtb resulted in the up- or downregulation of the transcriptional response of tubercle bacilli. The most substantial changes were related to the increased expression level of the genes of two operons encoding mycobacterial transporter systems, namely, mmpL5/mmpS5 (rv0676c), and rv1217c, rv1218c. Therefore, we postulate that during infection, Mtb-SAA1 binding promotes the infection of host macrophages by tubercle bacilli and modulates the functional response of the pathogen.
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Biernat, Monika Maria, and Tomasz Wróbel. "Bacterial Infection and Non-Hodgkin B-Cell Lymphoma: Interactions between Pathogen, Host and the Tumor Environment." International Journal of Molecular Sciences 22, no. 14 (July 9, 2021): 7372. http://dx.doi.org/10.3390/ijms22147372.
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Non-Hodgkin B-cell lymphomas (NHL) are a heterogeneous group of lymphoid neoplasms with complex etiopathology, rich symptomatology, and a variety of clinical courses, therefore requiring different therapeutic approaches. The hypothesis that an infectious agent may initiate chronic inflammation and facilitate B lymphocyte transformation and lymphogenesis has been raised in recent years. Viruses, like EBV, HTLV-1, HIV, HCV and parasites, like Plasmodium falciparum, have been linked to the development of lymphomas. The association of chronic Helicobacter pylori (H. pylori) infection with mucosa-associated lymphoid tissue (MALT) lymphoma, Borrelia burgdorferi with cutaneous MALT lymphoma and Chlamydophila psittaci with ocular adnexal MALT lymphoma is well documented. Recent studies have indicated that other infectious agents may also be relevant in B-cell lymphogenesis such as Coxiella burnettii, Campylobacter jejuni, Achromobacter xylosoxidans, and Escherichia coli. The aim of the present review is to provide a summary of the current literature on infectious bacterial agents associated with B-cell NHL and to discuss its role in lymphogenesis, taking into account the interaction between infectious agents, host factors, and the tumor environment.
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Arenas, Ailan F., Nicolás Arango-Plaza, Juan Camilo Arenas, and Gladys E. Salcedo. "Time-Frequency Approach Applied to Finding Interaction Regions in Pathogenic Proteins." Bioinformatics and Biology Insights 13 (January 2019): 117793221985017. http://dx.doi.org/10.1177/1177932219850172.
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Protein-protein interactions govern all molecular processes for living organisms, even those involved in pathogen infection. Pathogens such as virus, bacteria, and parasites contain proteins that help the pathogen to attach, penetrate, and settle inside the target cell. Thus, it is necessary to know the regions in pathogenic proteins that interact with host cell receptors. Currently, powerful pathogen databases are available and many pathogenic proteins have been recognized, but many pathogenic proteins have not been characterized. This work developed a program in MATLAB environment based on the time-frequency analysis to recognize important sites in proteins. Our program highlights the highest energy patches in proteins from their time-frequency distribution and matches the corresponding frequency. We sought to know if this approach is able to recognize stretches residues related to interaction. Our approach was applied to five study cases from pathogenic co-crystallized structures that have been well characterized. We searched the frequencies that characterize interaction regions in pathogenic proteins and with this information tried to identify new interaction patches in either paralogs or orthologs. We found that our program generates a well-interpretable graphic under several descriptors that can show important regions in proteins even those related to interaction. We propose that this MATLAB program could be used as a tool to explore outstanding regions in uncharacterized proteins.
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Mayer, François L., and James W. Kronstad. "The Spectrum of Interactions between Cryptococcus neoformans and Bacteria." Journal of Fungi 5, no. 2 (April 12, 2019): 31. http://dx.doi.org/10.3390/jof5020031.
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Cryptococcus neoformans is a major fungal pathogen that infects immunocompromised people and causes life-threatening meningoencephalitis. C. neoformans does not occur in isolation either in the environment or in the human host, but is surrounded by other microorganisms. Bacteria are ubiquitously distributed in nature, including soil, and make up the dominant part of the human microbiota. Pioneering studies in the 1950s demonstrated antifungal activity of environmental bacteria against C. neoformans. However, the mechanisms and implications of these interactions remain largely unknown. Recently, interest in polymicrobial interaction studies has been reignited by the development of improved sequencing methodologies, and by the realization that such interactions may have a huge impact on ecology and human health. In this review, we summarize our current understanding of the interaction of bacteria with C. neoformans.
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Liu, Rui, Zheng-Xue Bao, Pei-Ji Zhao, and Guo-Hong Li. "Advances in the Study of Metabolomics and Metabolites in Some Species Interactions." Molecules 26, no. 11 (May 31, 2021): 3311. http://dx.doi.org/10.3390/molecules26113311.
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In the natural environment, interactions between species are a common natural phenomena. The mechanisms of interaction between different species are mainly studied using genomic, transcriptomic, proteomic, and metabolomic techniques. Metabolomics is a crucial part of system biology and is based on precision instrument analysis. In the last decade, the emerging field of metabolomics has received extensive attention. Metabolomics not only provides a qualitative and quantitative method for studying the mechanisms of interactions between different species, but also helps clarify the mechanisms of defense between the host and pathogen, and to explore new metabolites with various biological activities. This review focuses on the methods and progress of interspecies metabolomics. Additionally, the prospects and challenges of interspecies metabolomics are discussed.
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Kutama, A. S., M. Adamu, H. U. Baita, S. Zafar, and M. M. Hadiza. "Review on the contributions of some human cultural practices to plant disease epidemiology." Dutse Journal of Pure and Applied Sciences 8, no. 2b (June 25, 2022): 12–20. http://dx.doi.org/10.4314/dujopas.v8i2b.2.
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An epidemy of a disease usually occurs when there is an interaction of the three (3) major factors of disease development popularly called disease triangle. The disease triangle consists of a susceptible host, virulent pathogen, and a suitable environment that favors the growth of the pathogen. When the two other factors interact with the pathogen, disease can reach epidemic condition referred to as epiphytotic stage. However, apart from these factors, many activities of human have a direct or indirect effect on plant disease epidemics, some of them favors and some reducing the frequency and the rate of epidemics. It has been established that some on-farm cultural practices such as selection of planting site, tillage, continues mono cropping and monoculture, inter cropping, spacing between plants/ plant density, weeding, crop rotation, fertilizer application and many others when misused or used carelessly may tend to allow or favor the development of epidemy by creating a suitable environment optimum for pathogen growth and development and sometimes making the host plant vulnerable to some peculiar diseases. This when human cultural practices are considered appropriately together with the disease triangle, could change the triangle shaped factors to a tetrahedral structure necessary for disease development. In this paper, major on-farm cultural practices that contribute to the epidemy of disease and the need to incorporate these factors as the fourth item in the disease factors are discussed.
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Lewis, Matthew S., Lia Danelishvili, Sasha J. Rose, and Luiz E. Bermudez. "MAV_4644 Interaction with the Host Cathepsin Z Protects Mycobacterium avium subsp. hominissuis from Rapid Macrophage Killing." Microorganisms 7, no. 5 (May 21, 2019): 144. http://dx.doi.org/10.3390/microorganisms7050144.
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Mycobacterium avium subspecies hominissuis (MAH) is an opportunistic pathogen that is ubiquitous in the environment and often isolated from faucets and showerheads. MAH mostly infects humans with an underlying disease, such as chronic pulmonary disorder, cystic fibrosis, or individuals that are immunocompromised. In recent years, MAH infections in patients without concurrent disease are increasing in prevalence as well. This pathogen is resistant to many antibiotics due to the impermeability of its envelope and due to the phenotypic resistance established within the host macrophages, making difficult to treat MAH infections. By screening a MAH transposon library for mutants that are susceptible to killing by reactive nitrogen intermediaries, we identified the MAV_4644 (MAV_4644:Tn) gene knockout clone that was also significantly attenuated in growth within the host macrophages. Complementation of the mutant restored the wild-type phenotype. The MAV_4644 gene encodes a dual-function protein with a putative pore-forming function and ADP-ribosyltransferase activity. Protein binding assay suggests that MAV_4644 interacts with the host lysosomal peptidase cathepsin Z (CTSZ), a key regulator of the cell signaling and inflammation. Pathogenic mycobacteria have been shown to suppress the action of many cathepsins to establish their intracellular niche. Our results demonstrate that knocking-down the cathepsin Z in human macrophages rescues the attenuated phenotype of MAV_4644:Tn clone. Although, the purified cathepsin Z by itself does not have any killing effect on MAH, it contributes to bacterial killing in the presence of the nitric oxide (NO). Our data suggest that the cathepsin Z is involved in early macrophage killing of MAH, and the virulence factor MAV_4644 protects the pathogen from this process.
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Dühring, Sybille, Jan Ewald, Sebastian Germerodt, Christoph Kaleta, Thomas Dandekar, and Stefan Schuster. "Modelling the host–pathogen interactions of macrophages and Candida albicans using Game Theory and dynamic optimization." Journal of The Royal Society Interface 14, no. 132 (July 2017): 20170095. http://dx.doi.org/10.1098/rsif.2017.0095.
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The release of fungal cells following macrophage phagocytosis, called non-lytic expulsion, is reported for several fungal pathogens. On one hand, non-lytic expulsion may benefit the fungus in escaping the microbicidal environment of the phagosome. On the other hand, the macrophage could profit in terms of avoiding its own lysis and being able to undergo proliferation. To analyse the causes of non-lytic expulsion and the relevance of macrophage proliferation in the macrophage– Candida albicans interaction, we employ Evolutionary Game Theory and dynamic optimization in a sequential manner. We establish a game-theoretical model describing the different strategies of the two players after phagocytosis. Depending on the parameter values, we find four different Nash equilibria and determine the influence of the systems state of the host upon the game. As our Nash equilibria are a direct consequence of the model parameterization, we can depict several biological scenarios. A parameter region, where the host response is robust against the fungal infection, is determined. We further apply dynamic optimization to analyse whether macrophage mitosis is relevant in the host–pathogen interaction of macrophages and C. albicans . For this, we study the population dynamics of the macrophage– C. albicans interactions and the corresponding optimal controls for the macrophages, indicating the best macrophage strategy of switching from proliferation to attacking fungal cells.
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Bojang, Ebrima, Harlene Ghuman, Pizga Kumwenda, and Rebecca A. Hall. "Immune Sensing of Candida albicans." Journal of Fungi 7, no. 2 (February 6, 2021): 119. http://dx.doi.org/10.3390/jof7020119.
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Candida albicans infections range from superficial to systemic and are one of the leading causes of fungus-associated nosocomial infections. The innate immune responses during these various infection types differ, suggesting that the host environment plays a key role in modulating the host–pathogen interaction. In addition, C. albicans is able to remodel its cell wall in response to environmental conditions to evade host clearance mechanisms and establish infection in niches, such as the oral and vaginal mucosa. Phagocytes play a key role in clearing C. albicans, which is primarily mediated by Pathogen Associated Molecular Pattern (PAMP)–Pattern Recognition Receptor (PRR) interactions. PRRs such as Dectin-1, DC-SIGN, and TLR2 and TLR4 interact with PAMPs such as β-glucans, N-mannan and O-mannan, respectively, to trigger the activation of innate immune cells. Innate immune cells exhibit distinct yet overlapping repertoires of PAMPs, resulting in the preferential recognition of particular Candida morphotypes by them. The role of phagocytes in the context of individual infection types also differs, with neutrophils playing a prominent role in kidney infections, and dendritic cells playing a prominent role in skin infections. In this review, we provide an overview of the key receptors involved in the detection of C. albicans and discuss the differential innate immune responses to C. albicans seen in different infection types such as vulvovaginal candidiasis (VVC) and oral candidiasis.
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Di Pietro, Marisa, Simone Filardo, Silvio Romano, and Rosa Sessa. "Chlamydia trachomatis and Chlamydia pneumoniae Interaction with the Host: Latest Advances and Future Prospective." Microorganisms 7, no. 5 (May 16, 2019): 140. http://dx.doi.org/10.3390/microorganisms7050140.
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Research in Chlamydia trachomatis and Chlamydia pneumoniae has gained new traction due to recent advances in molecular biology, namely the widespread use of the metagenomic analysis and the development of a stable genomic transformation system, resulting in a better understanding of Chlamydia pathogenesis. C. trachomatis, the leading cause of bacterial sexually transmitted diseases, is responsible of cervicitis and urethritis, and C. pneumoniae, a widespread respiratory pathogen, has long been associated with several chronic inflammatory diseases with great impact on public health. The present review summarizes the current evidence regarding the complex interplay between C. trachomatis and host defense factors in the genital micro-environment as well as the key findings in chronic inflammatory diseases associated to C. pneumoniae.
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Yang, Huai, and Peigao Luo. "Changes in Photosynthesis Could Provide Important Insight into the Interaction between Wheat and Fungal Pathogens." International Journal of Molecular Sciences 22, no. 16 (August 18, 2021): 8865. http://dx.doi.org/10.3390/ijms22168865.
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Photosynthesis is a universal process for plant survival, and immune defense is also a key process in adapting to the growth environment. Various studies have indicated that these two processes are interconnected in a complex network. Photosynthesis can influence signaling pathways and provide both materials and energy for immune defense, while the immune defense process can also have feedback effects on photosynthesis. Pathogen infection inevitably leads to changes in photosynthesis parameters, including Pn, Gs, and Ci; biochemical materials such as SOD and CAT; signaling molecules such as H2O2 and hormones; and the expression of genes involved in photosynthesis. Some researchers have found that changes in photosynthesis activity are related to the resistance level of the host, the duration after infection, and the infection position (photosynthetic source or sink). Interactions between wheat and the main fungal pathogens, such as Puccinia striiformis, Blumeria graminis, and Fusarium graminearum, constitute an ideal study system to elucidate the relationship between changes in host photosynthesis and resistance levels, based on the accessibility of methods for artificially controlling infection and detecting changes in photosynthesis, the presence of multiple pathogens infecting different positions, and the abundance of host materials with various resistance levels. This review is written only from the perspective of plant pathologists, and after providing an overview of the available data, we generally found that changes in photosynthesis in the early stage of pathogen infection could be a causal factor influencing acquired resistance, while those in the late stage could be the result of resistance formation.
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Castro, Sarah L., Mayra Nelman-Gonzalez, Cheryl A. Nickerson, and C. Mark Ott. "Induction of Attachment-Independent Biofilm Formation and Repression ofhfqExpression by Low-Fluid-Shear Culture of Staphylococcus aureus." Applied and Environmental Microbiology 77, no. 18 (July 29, 2011): 6368–78. http://dx.doi.org/10.1128/aem.00175-11.
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ABSTRACTThe opportunistic pathogenStaphylococcus aureusencounters a wide variety of fluid shear levels within the human host, and they may play a key role in dictating whether this organism adopts a commensal interaction with the host or transitions to cause disease. By using rotating-wall vessel bioreactors to create a physiologically relevant, low-fluid-shear environment,S. aureuswas evaluated for cellular responses that could impact its colonization and virulence.S. aureuscells grown in a low-fluid-shear environment initiated a novel attachment-independent biofilm phenotype and were completely encased in extracellular polymeric substances. Compared to controls, low-shear-cultured cells displayed slower growth and repressed virulence characteristics, including decreased carotenoid production, increased susceptibility to oxidative stress, and reduced survival in whole blood. Transcriptional whole-genome microarray profiling suggested alterations in metabolic pathways. Further genetic expression analysis revealed downregulation of the RNA chaperone Hfq, which parallels low-fluid-shear responses of certain Gram-negative organisms. This is the first study to report an Hfq association with fluid shear in a Gram-positive organism, suggesting an evolutionarily conserved response to fluid shear among structurally diverse prokaryotes. Collectively, our results suggestS. aureusresponds to a low-fluid-shear environment by initiating a biofilm/colonization phenotype with diminished virulence characteristics, which could lead to insight into key factors influencing the divergence between infection and colonization during the initial host-pathogen interaction.
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Barbosa, Roneres Deniz, Jânia Lília da Silva Bentes, and Ana Francisca Tiburcia Amorim Ferreira e. Ferreira. "Manejo da nutrição mineral e doenças de plantas – uma revisão." Revista Agraria Academica 6, no. 5 (September 1, 2023): 10–26. http://dx.doi.org/10.32406/v6n5/2023/10-26/agrariacad.
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Plant diseases are responsible for significant reductions in agricultural production. The ability of the plant to express resistance to a given phytopathogen is strongly affected by mineral nutrition. The mechanisms leading to these mineral nutrient-induced changes in disease development are complex and include effects directly on the pathogen, the host and the environment. In the present review, studies on the effect of macro- and micronutrients on plant disease intensity are presented, showing the need for understanding this interaction for the correct establishment of integrated management measures.
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Li, Ting, Zhaohong Zhan, Yunuan Lin, Maojuan Lin, Qingbiao Xie, Yinhua Chen, Chaozu He, Jun Tao, and Chunxia Li. "Biosynthesis of Amino Acids in Xanthomonas oryzae pv. oryzae Is Essential to Its Pathogenicity." Microorganisms 7, no. 12 (December 13, 2019): 693. http://dx.doi.org/10.3390/microorganisms7120693.
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Xanthomonas oryzae pv. oryzae (Xoo) is the causal agent of rice bacterial blight disease, which causes a large reduction in rice production. The successful interaction of pathogens and plants requires a particular nutrient environment that allows pathogen growth and the initiation of both pathogen and host responses. Amino acid synthesis is essential for bacterial growth when bacteria encounter amino acid-deficient environments, but the effects of amino acid synthesis on Xoo pathogenicity are unclear. Here, we systemically deleted the essential genes (leuB, leuC, leuD, ilvC, thrC, hisD, trpC, argH, metB, and aspC) involved in the synthesis of different amino acids and analyzed the effects of these mutations on Xoo virulence. Our results showed that leucine, isoleucine, valine, histidine, threonine, arginine, tryptophan, and cysteine syntheses are essential to Xoo infection. We further studied the role of leucine in the interaction between pathogens and hosts and found that leucine could stimulate some virulence-related responses and regulate Xoo pathogenicity. Our findings highlight that amino acids not only act as nutrients for bacterial growth but also play essential roles in the Xoo and rice interaction.
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Young, Vincent B. "Old and new models for studying host-microbe interactions in health and disease:C. difficileas an example." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 6 (June 1, 2017): G623—G627. http://dx.doi.org/10.1152/ajpgi.00341.2016.
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There has been an explosion of interest in studying the indigenous microbiota, which plays an important role in human health and disease. Traditionally, the study of microbes in relationship to human health involved consideration of individual microbial species that caused classical infectious diseases. With the interest in the human microbiome, an appreciation of the influence that complex communities of microbes can have on their environment has developed. When considering either individual pathogenic microbes or a symbiotic microbial community, researchers have employed a variety of model systems with which they can study the host-microbe interaction. With the use of studies of infections with the toxin-producing bacterium Clostridium difficile as a model for both a pathogen and beneficial bacterial communities as an example, this review will summarize and compare various model systems that can be used to gain insight into the host-microbe interaction.
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Chang, Che-Kang, Min-Chi Yang, Hsueh-Fen Chen, Yi-Ling Liao, and Chung-Yu Lan. "The Role of Sfp1 in Candida albicans Cell Wall Maintenance." Journal of Fungi 8, no. 11 (November 13, 2022): 1196. http://dx.doi.org/10.3390/jof8111196.
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The cell wall is the first interface for Candida albicans interaction with the surrounding environment and the host cells. Therefore, maintenance of cell wall integrity (CWI) is crucial for C. albicans survival and host-pathogen interaction. In response to environmental stresses, C. albicans undergoes cell wall remodeling controlled by multiple signaling pathways and transcription regulators. Here, we explored the role of the transcription factor Sfp1 in CWI. A deletion of the SFP1 gene not only caused changes in cell wall properties, cell wall composition and structure but also modulated expression of cell wall biosynthesis and remodeling genes. In addition, Cas5 is a known transcription regulator for C. albicans CWI and cell wall stress response. Interestingly, our results indicated that Sfp1 negatively controls the CAS5 gene expression by binding to its promoter element. Together, this study provides new insights into the regulation of C. albicans CWI and stress response.
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Giuffrè, Mauro, Rita Moretti, Giuseppina Campisciano, Alexandre Barcelos Morais da Silveira, Vincenzo Maria Monda, Manola Comar, Stefano Di Bella, Roberta Maria Antonello, Roberto Luzzati, and Lory Saveria Crocè. "You Talking to Me? Says the Enteric Nervous System (ENS) to the Microbe. How Intestinal Microbes Interact with the ENS." Journal of Clinical Medicine 9, no. 11 (November 18, 2020): 3705. http://dx.doi.org/10.3390/jcm9113705.
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Mammalian organisms form intimate interfaces with commensal and pathogenic gut microorganisms. Increasing evidence suggests a close interaction between gut microorganisms and the enteric nervous system (ENS), as the first interface to the central nervous system. Each microorganism can exert a different effect on the ENS, including phenotypical neuronal changes or the induction of chemical transmitters that interact with ENS neurons. Some pathogenic bacteria take advantage of the ENS to create a more suitable environment for their growth or to promote the effects of their toxins. In addition, some commensal bacteria can affect the central nervous system (CNS) by locally interacting with the ENS. From the current knowledge emerges an interesting field that may shape future concepts on the pathogen–host synergic interaction. The aim of this narrative review is to report the current findings regarding the inter-relationships between bacteria, viruses, and parasites and the ENS.
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Silva, Karla Christina Sousa, Lana O’Hara Souza Silva, Guilherme Algusto Alves Silva, Clayton Luiz Borges, Evandro Novaes, Juliano Domiraci Paccez, Wagner Fontes, Marcia Giambiagi-deMarval, Célia Maria de Almeida Soares, and Juliana Alves Parente-Rocha. "Staphylococcus saprophyticus Proteomic Analyses Elucidate Differences in the Protein Repertories among Clinical Strains Related to Virulence and Persistence." Pathogens 9, no. 1 (January 19, 2020): 69. http://dx.doi.org/10.3390/pathogens9010069.
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Staphylococcus saprophyticus is a Gram-positive and coagulase negative cocci that composes the skin microbiota and can act as an opportunistic agent causing urinary tract infections, being more frequent in sexually active young women. The ability of a pathogen to cause infection in the host is associated to its ability to adhere to host cells and to survive host immune defenses. In this work, we presented the comparative proteomic profile of three S. saprophyticus strains. It was possible to characterize differences in the proteome content, specially related to expression of virulence factors. We compiled this data and previous data and we detected one strain (9325) possessing higher production and secretion of proteins related to virulence. Our results show that phenotypic, genotypic, and proteomic differences reflect in the ability to survive during interaction with host cells, since the 9325 strain presented a higher survival rate after macrophage interaction. In counterpart, the 7108 strain that possesses lower content of proteins related to virulence presented higher ability to form biofilm suggesting that this strain can be better adapted to persist in the host and in the environment. Our work describes, for the first time, proteomic flexibility among S. saprophyticus strains, reflecting in virulence and persistence.
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Diéguez-Uribeondo, J., H. Förster, and J. E. Adaskaveg. "Visualization of Localized Pathogen-Induced pH Modulation in Almond Tissues Infected by Colletotrichum acutatum Using Confocal Scanning Laser Microscopy." Phytopathology® 98, no. 11 (November 2008): 1171–78. http://dx.doi.org/10.1094/phyto-98-11-1171.
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Modulation of pH within the host during infection of almond by the anthracnose pathogen Colletotrichum acutatum was studied using confocal scanning laser microscopy and the dual emission fluorescence indicator SNARF-1. This highly sensitive method allowed visualization of the spatial distribution of localized pathogen-induced pH modulation within and in proximity to fungal infection structures in host tissue at the cellular level. Ratiometric measurement of fluorescence at two emission wavelengths and in situ calibration allowed the quantification of pH ranges. After incubation of leaf epidermal tissue with SNARF-1, distinct alkaline (pH 8 to ≥9), red-spectrum (650 nm wave length) fluorescent zones developed as partial or complete halos around many fungal appressoria and in infection vesicles at 24 to 36 h after inoculation. In samples taken after 48 to 72 h, colonizing hyphae in the biotrophic phase and subsequently in the necrotrophic phase were also emitting the red fluorescence that extended into the surrounding host tissue, as also verified by depth analyses. Host epidermal cells were intact and apparently alive during the fungal alkalization process, with no visible disruption of cell structure. Generally, the pH of epidermal cells in noninoculated samples or in areas away from the infection in inoculated samples was lower than pH 7 with green (i.e., 500 to 550 nm wave length) fluorescence detected. Using standard electrodes, a significant increase in pH and ammonia concentration in leaf and fruit tissue was also measured but only at advanced stages of disease. In contrast, hyphae of the pathogen Alternaria alternata were mostly acidic and no change in fluorescence was found inside invaded host cells. The sequence of events in the C. acutatum–almond interaction includes penetration, production of ammonia by C. acutatum, and subsequent pH modulation within almond epidermal tissue to an alkaline environment that leads to further colonization of the host.
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Connolly, James PR, Robert J. Goldstone, Karl Burgess, Richard J. Cogdell, Scott A. Beatson, Waldemar Vollmer, David GE Smith, and Andrew J. Roe. "The host metabolite D-serine contributes to bacterial niche specificity through gene selection." ISME Journal 9, no. 4 (December 19, 2014): 1039–51. http://dx.doi.org/10.1038/ismej.2014.242.
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Abstract Escherichia coli comprise a diverse array of both commensals and niche-specific pathotypes. The ability to cause disease results from both carriage of specific virulence factors and regulatory control of these via environmental stimuli. Moreover, host metabolites further refine the response of bacteria to their environment and can dramatically affect the outcome of the host–pathogen interaction. Here, we demonstrate that the host metabolite, D-serine, selectively affects gene expression in E. coli O157:H7. Transcriptomic profiling showed exposure to D-serine results in activation of the SOS response and suppresses expression of the Type 3 Secretion System (T3SS) used to attach to host cells. We also show that concurrent carriage of both the D-serine tolerance locus (dsdCXA) and the locus of enterocyte effacement pathogenicity island encoding a T3SS is extremely rare, a genotype that we attribute to an ‘evolutionary incompatibility’ between the two loci. This study demonstrates the importance of co-operation between both core and pathogenic genetic elements in defining niche specificity.
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Jang, Sung, Kiwan Kim, and Gap Lee. "Cyclo(L-phe-pro), Vibrio vulnificus produced metabolite, suppresses innate immune response (INM3P.418)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 127.23. http://dx.doi.org/10.4049/jimmunol.194.supp.127.23.
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Abstract Cyclo(Phe-Pro)(cFP), known as a secondary metabolite of some bacteria and fungi, is also produced by Vibrio vulnificus. It has been suggested that cFP has a role in bacterial cell-to-cell communication. However, the role of cFP in host immune response has not been reported yet. In this study, we investigated whether cFP modulates host innate immune responses. cFP suppressed production of pro-inflammatory cytokines, TNFa and IL6, nitric oxide, and reactive oxygen species in LPS-induced macrophages and bone marrow-derived macrophages. cFP also inhibited IKK phosphorylation, IkBa degradation, and NF-kB translocation to the nucleus, indicating that cFP affects the NF-kB pathway. These results provide evidences that cFP has immune suppressive effects that enhance the pathogen’s ability to infect and survive in host environment. Moreover, it may contribute to reveal the role of cFP in host-pathogen interaction and establish potential therapeutic strategies for the diseases related to Vibrio vulnificus.
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Prakash, C. S., and B. A. Thielges. "Interaction of geographic isolates of Melampsora medusae and Populus: effect of temperature." Canadian Journal of Botany 67, no. 2 (February 1, 1989): 486–90. http://dx.doi.org/10.1139/b89-069.
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Twelve isolates of the leaf rust pathogen Melampsora medusae Thüm., collected from six locations across the eastern U.S.A., were tested for their reaction on 18 poplar genotypes at two temperatures of incubation (16 and 26 °C). All isolates were recognized as distinct physiologic races, based on the qualitative and quantitative reaction of the isolates on the cultivars. Temperature was an important factor in determining the level and type of disease expression in most cultivar – isolate combinations. The results support the hypothesis that the physical environment may have an important role in the regulation of this "wild" pathosystem. The high degree of race specificity observed in the Populus genotypes and the polymorphism for virulence in the M. medusae population emphasize the importance of maintaining host diversity to manage this disease.
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Washington Philipson, Casandra, Josep Bassaganya-Riera, Monica Viladomiu, Barbara Kronsteiner-Dobramysl, Pawel Michalak, and Raquel Hontecillas. "Modulation of immune responses toward Helicobacter pylori infection by NLRs (INM6P.339)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 193.13. http://dx.doi.org/10.4049/jimmunol.194.supp.193.13.
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Abstract Helicobacter pylori (HP) colonizes 50% of the world’s population resulting in a decades-long gastric infection. Bacterial interaction with host intracellular environment occurs via injection of bacterial components through a TIVSS or intracellular replication. HP has been recognized for its ability to modulate intracellular NOD-like receptors (NLR). Host responses toward the bacterium can result in asymptomatic, pathogenic or even favorable immunity. Mechanisms underlying the dual role of HP as a commensal versus pathogen are not completely understood. We combined computational modeling, bioinformatics and experimental validation to investigate intracellular host-HP interactions. Global transcriptomic analysis on bone marrow-derived macrophages (BMDM) in a gentamycin protection assay unveiled that intracellular colonization of HP upregulated NOD1, NOD2, NLRP3, NLRC5 and inflammasome components (Caspase-1 and -11) but suppressed regulatory NLRX1 which was inversely correlated to TRAF6, NF-B, proinflammatory cytokines and reactive oxygen species. Loss of NLRX1 facilitates bacterial clearance in BMDM and infected mice. Lastly, we constructed a computational model to shed light on complex immune responses and pathway crosstalk regulated by NLRX1 during infection. In conclusion, NLRX1 is associated with chronic bacterial persistence during H. pylori infection and it may represent an immune evasion mechanism employed by the bacterium to facilitate long-term host colonization.
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Mi, Siyuan, Yongjie Tang, Liangyu Shi, Xueqin Liu, Jingfang Si, Yuelin Yao, Serafino M. A. Augustino, Lingzhao Fang, and Ying Yu. "Protective Roles of Folic Acid in the Responses of Bovine Mammary Epithelial Cells to Different Virulent Staphylococcus aureus Strains." Biology 10, no. 11 (November 12, 2021): 1164. http://dx.doi.org/10.3390/biology10111164.
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Mastitis caused by Staphylococcus aureus (S. aureus) infection is one of the most difficult diseases to treat in dairy cattle. Exploring the biological progression of S. aureus mastitis via the interaction between host, pathogen, and environment is the key to an effective and sustainable improvement of animal health. Here, two strains of S. aureus and a strain of MRSA (Methicillin-resistant Staphylococcus aureus) isolated from cows with different inflammation phenotypes were used to challenge Mac-T cells and to investigate their effects on the global transcriptome of the cells, then to explore the potential regulatory mechanisms of folic acid on S. aureus mastitis prevention. Differential gene expression or splicing analysis showed that different strains of S. aureus led to distinct transcriptional responses from the host immune system. Folic acid could protect host defense against the challenge of S. aureus and MRSA partially through activating cytoplasmic DNA sensing and tight junction pathway. ZBP1 at the upstream of cytoplasmic DNA sensing pathway was verified and related to anti-pathogen through RNA interference. Further enrichment analysis using these transcriptome data with cattle large-scale genome-wide association study (GWAS) data confirmed that ZBP1 gene is highly associated with bovine somatic cell score (SCS) trait. Our data shed light on the potential effect of FA through regulating key gene and then protect host cells’ defense against S. aureus and MRSA.
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Oberstein, Adam, and Thomas Shenk. "Cellular responses to human cytomegalovirus infection: Induction of a mesenchymal-to-epithelial transition (MET) phenotype." Proceedings of the National Academy of Sciences 114, no. 39 (September 5, 2017): E8244—E8253. http://dx.doi.org/10.1073/pnas.1710799114.
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Human cytomegalovirus (HCMV) is the prototypical human β-herpes virus. Here we perform a systems analysis of the HCMV host-cell transcriptome, using gene set enrichment analysis (GSEA) as an engine to globally map the host–pathogen interaction across two cell types. Our analysis identified several previously unknown signatures of infection, such as induction of potassium channels and amino acid transporters, derepression of genes marked with histone H3 lysine 27 trimethylation (H3K27me3), and inhibition of genes related to epithelial-to-mesenchymal transition (EMT). The repression of EMT genes was dependent on early viral gene expression and correlated with induction E-cadherin (CDH1) and mesenchymal-to-epithelial transition (MET) genes. Infection of transformed breast carcinoma and glioma stem cells similarly inhibited EMT and induced MET, arguing that HCMV induces an epithelium-like cellular environment during infection.
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Mannaa, Mohamed, and Young-Su Seo. "Plants under the Attack of Allies: Moving towards the Plant Pathobiome Paradigm." Plants 10, no. 1 (January 9, 2021): 125. http://dx.doi.org/10.3390/plants10010125.
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Plants are functional macrobes living in a close association with diverse communities of microbes and viruses as complex systems that continuously interact with the surrounding environment. The microbiota within the plant holobiont serves various essential and beneficial roles, such as in plant growth at different stages, starting from seed germination. Meanwhile, pathogenic microbes—differentiated from the rest of the plant microbiome based on their ability to damage the plant tissues through transient blooming under specific conditions—are also a part of the plant microbiome. Recent advances in multi-omics have furthered our understanding of the structure and functions of plant-associated microbes, and a pathobiome paradigm has emerged as a set of organisms (i.e., complex eukaryotic, microbial, and viral communities) within the plant’s biotic environment which interact with the host to deteriorate its health status. Recent studies have demonstrated that the one pathogen–one disease hypothesis is insufficient to describe the disease process in many cases, particularly when complex organismic communities are involved. The present review discusses the plant holobiont and covers the steady transition of plant pathology from the one pathogen–one disease hypothesis to the pathobiome paradigm. Moreover, previous reports on model plant diseases, in which more than one pathogen or co-operative interaction amongst pathogenic microbes is implicated, are reviewed and discussed.