Relevant bibliographies by topics / Host-Pathogen interface

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Reports

Academic literature on the topic 'Host-Pathogen interface'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Host-Pathogen interface"

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Wilson, Van G. "Sumoylation at the Host-Pathogen Interface." Biomolecules 2, no. 2 (April 5, 2012): 203–27. http://dx.doi.org/10.3390/biom2020203.

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Kuehne, Sarah A. "Communication at the host-pathogen interface." Journal of Oral Microbiology 9, sup1 (May 30, 2017): 1325269. http://dx.doi.org/10.1080/20002297.2017.1325269.

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Liles, W. Conrad. "The dynamic pathogen–host response interface." Drug Discovery Today: Disease Mechanisms 4, no. 4 (December 2007): 205–6. http://dx.doi.org/10.1016/j.ddmec.2008.02.005.

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Kaye, Paul, and Phillip Scott. "Leishmaniasis: complexity at the host–pathogen interface." Nature Reviews Microbiology 9, no. 8 (July 11, 2011): 604–15. http://dx.doi.org/10.1038/nrmicro2608.

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Lonergan, Zachery R., and Eric P. Skaar. "Nutrient Zinc at the Host–Pathogen Interface." Trends in Biochemical Sciences 44, no. 12 (December 2019): 1041–56. http://dx.doi.org/10.1016/j.tibs.2019.06.010.

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Nosanchuk, Joshua D., and Attila Gacser. "Histoplasma capsulatum at the host–pathogen interface." Microbes and Infection 10, no. 9 (July 2008): 973–77. http://dx.doi.org/10.1016/j.micinf.2008.07.011.

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Stebbins, C. Erec. "Structural microbiology at the pathogen-host interface." Cellular Microbiology 7, no. 9 (July 5, 2005): 1227–36. http://dx.doi.org/10.1111/j.1462-5822.2005.00564.x.

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Coombes, Brian K. "Regulatory evolution at the host–pathogen interface." Canadian Journal of Microbiology 59, no. 6 (June 2013): 365–67. http://dx.doi.org/10.1139/cjm-2013-0300.

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Horizontal gene transfer plays a major role in microbial evolution by innovating the bacterial genome with new genetic blueprints to adapt to previously unexploited niches. However, to benefit from these genetic acquisitions, the bacterium must integrate the expression of these new genes into existing regulatory nodes and deploy them at the right time. There is much to gain from uncovering the genetic diversity in noncoding DNA that is selective during host infection because of the beneficial effect it has on bacterial gene expression. By identifying genes that have undergone regulatory evolution, a deeper understanding of the arms race between host and pathogen is gained.
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Colonna, Marco, Bali Pulendran, and Akiko Iwasaki. "Dendritic cells at the host-pathogen interface." Nature Immunology 7, no. 2 (February 2006): 117–20. http://dx.doi.org/10.1038/ni0206-117.

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Kelsall, Brian L., Christine A. Biron, Opendra Sharma, and Paul M. Kaye. "Dendritic cells at the host-pathogen interface." Nature Immunology 3, no. 8 (August 2002): 699–702. http://dx.doi.org/10.1038/ni0802-699.

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Dissertations / Theses on the topic "Host-Pathogen interface"

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Thomas, Graham. "The host-pathogen interface : characterising putative secreted proteins of the honeybee pathogen Nosema ceranae (Microsporidia )." Thesis, University of Exeter, 2015. http://hdl.handle.net/10871/21445.

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Microsporidia are obligate intracellular eukaryotic parasites related to fungi, possessing greatly reduced genomic and cellular components. The microsporidian Nosema ceranae threatens honeybee (Apis mellifera) populations. Nosemosis has a complex epidemiology affected by host, pathogen and environmental factors. Although a draft of the N. ceranae genome has been published, the molecular basis underpinning pathogenicity is not known. The lack of established culturing techniques and a tractable genetic system necessitates use of model systems for both host and parasite such as Saccharomyces cerevisiae. I hypothesise effectors essential to disease progression exist amongst N. ceranae secretome genes. In this study I have started characterising these genes using a combination of established and novel techniques for studying microsporidia proteins including bioinformatics, heterologous expression in S. cerevisiae, and the genome-wide analysis platform of Synthetic Genetic Arrays. This effort has yielded new insights into N. ceranae secreted proteins which lack similarity to known sequences. I identified N. ceranae protein NcS77 as a candidate effector implicated in targeting host nuclear pores. NcS50 and NcS85 co-localise with ERG6 a marker for lipid droplets (an organelle known to be targeted by another obligate intracellular pathogen Chlamydia trachomatis) when expressed in S. cerevisiae. N. ceranae polar tube proteins (PTP) induce filament formation when expressed in S. cerevisiae and PTP2 co-localises with the cell wall. Interestingly this phenotype is replicated by another secreted protein which may infer a common function. Together these data contribute to knowledge on N. ceranae pathology bringing us closer to understanding the disease and ultimately lead the way to mitigation.
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Capewell, Samantha Jessica. "Structural and functional studies of protein targets at the host-pathogen interface." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9636.

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Ferric ABC Transporters. Pathogenic bacteria have evolved specialised iron acquisition systems that allow them to effectively colonise a host. One of these systems is the ferric binding protein (Fbp) complex that is a member of the ATP-Binding Cassette (ABC) superfamily of small molecule transporters. The Fbp complex is made up of three-components (FbpABC) that transports ferric iron from the periplasm to the cytoplasm of many Gram negative bacteria. FbpA binds iron in the periplasm and transports it to the FbpB transporter complex that permeates the cytoplasmic membrane. Here the iron is actively transported by FbpB through the membrane that is powered by ATP hydrolysis catalysed by FbpC, the cytoplasmic ATPase. Burkholderia cenocepacia is an opportunist pathogen that colonises the lungs of cystic fibrosis patients and is particularly resistant to antibiotic treatment. In this study the iron uptake system of B. cenocepacia strain J2315 is investigated. A putative FbpA from B. cenocepacia J2315 was expressed in the periplasm of Escherichia coli cells and the recombinant FbpA B. cenocepacia protein purified. The structural and electrochemical properties of native FbpA B. cenocepacia were investigated using UV Visible spectroscopy, spectro-electrochemistry, mass spectrometry and crystallographic techniques. It appears that FbpA B. cenocepacia is a novel member of the FbpA superfamily that selectively utilises citrate as an exogenous anion in ferric iron co-ordination. This is the first instance that a recombinant ferric binding protein has been documented as preferentially utilising citrate in this manner. The putative ATPase from B. cenocepacia (FbpC B. cenocepacia) was also expressed in E. coli but it was found to be insoluble. A number of expression systems were tested but none were found to be successful in generating sufficient quantities of FbpC B. cenocepacia for structural studies. Human β-defensin 2. Despite daily contact with a range of microorganisms, mammals do not regularly succumb to pathogenic invasion. One reason is the presence of an important defence mechanism uses a reservoir of antimicrobial peptides (AMPs) that are expressed in eukaryotes as a means of innate immunity. The AMP superfamily is composed of over 900 members, displays broad structural and sequence diversity and is active against a wide range of bacteria, fungi and viruses. β-defensins are small (3-5 kDa), cationic peptides that display antimicrobial activity against a range of microbes and have also been shown to act as chemo-attractants (chemokines) within the adaptive immune system. In this study we obtained milligram amounts of pure human β-defensin 2 (HBD2) for functional studies by the development of a method for the rapid expression and purification of the recombinant peptide. A clone encoding a thioredoxin-HBD2 fusion protein was designed for the expression of soluble peptide in E. coli cells that was purified by simple affinity chromatography. The HBD2 peptide was cleaved from the fusion by an efficient protease step and further purified to yield pure HBD2. This recombinant HBD2 defensin was shown to be active against a Mycobacterium tuberculosis mutant strain.
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Caron, Alexandre. "Describing and understanding host-pathogen community interaction at the wildlife/domestic interface." Thesis, University of Pretoria, 2011. http://hdl.handle.net/2263/24464.

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In this thesis, I investigated the relationship between host and pathogen in multi-host and multi-pathogen systems at the interface between wildlife and domestic species. The term “epidemiological interaction” was central to my thesis, and was defined as “any ecological interaction between two host populations resulting in the transmission of one or more pathogen”. Epidemiological interactions are related to the processes of transmission between hosts and I investigated how these epidemiological interactions between different host populations could be investigated in a given ecosystem. I developed two research frameworks to estimate these epidemiological interactions: 1) an a priori approach based on the host data and assuming that the mobility of hosts and the resulting contacts between host populations would be crucial factors influencing the epidemiological interactions; 2) an a posteriori approach based on the pathogen data, assuming that epidemiological pathways previously used by some pathogen species can be used in the future by other pathogens. The animalpathogen model used to test the first approach was the bird-avian influenza viruses’ model. Longitudinal counting and sampling protocols of domestic and wild birds over two years were used to analyse community composition and abundance of hosts to compare with the prevalence of avian influenza viruses. I could, for the first time, show a persistence of low pathogenic avian influenza strains in an African ecosystem, and investigate the relationships with both the potential maintenance hosts (Afro-tropical ducks and resident species) and hosts that introduced the virus into the system from Europe or Asia (paleartic migrants). With the estimation of epidemiological interaction using host community data, I estimated the contact rate between wild and domestic avian compartments (intensive poultry, backyard and farmed ostrich compartments) and assigned a risk to this interaction based on dynamic and non dynamic factors for each bird species. This approach highlights the species or seasons at risk for the domestic compartments (or for the wild bird compartments depending on the perspective) in order to orientate surveillance or control options. This type of data and framework can also be used in mechanistic modelling to predict the spread of a pathogen after its introduction in one compartment. I tested the host approach in a broader dataset at the Southern African region level with similar counting and sampling database in multiple study sites, showing that the variability of host communities across the region could explain the variability of pathogen detection (however, finding a causal relationship was impossible). Finally, I theoretically developed the pathogen approach by combining tools used in parasite community ecology, molecular epidemiology and social network analysis and gave a theoretical example using a rodent and human macro and microparasite dataset. This thesis has explored the field of transmission ecology and offered ways to quantify the processes of transmission between host populations. Theoretically, I have developed a fundamental reflexion around epidemiological interactions and formulated hypotheses on their potential for being independent of the parasite species. Practically, I have developed tools to provide information for decision-making in order to improve efficiency of surveillance and control programmes at the wildlife/domestic interface particularly adapted to detect emerging infectious disease spill-over process.
Thesis (PhD)--University of Pretoria, 2011.
Zoology and Entomology
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Walch, Philipp Darius Konstantin [Verfasser], and Athanasios [Akademischer Betreuer] Typas. "Dissecting the host-pathogen interface during Salmonella infection / Philipp Darius Konstantin Walch ; Betreuer: Athanasios Typas." Heidelberg : Universitätsbibliothek Heidelberg, 2021. http://d-nb.info/1234987864/34.

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Milhano, Natacha Alexandra Korni da Fonseca. "Insight into the underlying immune interaction of Rickettsia infection in the vector-pathogen-host interface." Doctoral thesis, Universidade de Évora, 2014. http://hdl.handle.net/10174/17802.

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Ixodid ticks are second only to mosquitos in their notorious role as vectors of pathogens to both animals and humans. Rickettsioses are among the most important tick-borne diseases in Europe, Mediterranean spotted fever in particular. To date, many studies have been performed in order to uncover the underlying mechanisms of this disease, in terms of the interactions among its constituents, i.e., the pathogen, Rickettsia conorii, its vector, Rhipicephalus sanguineus tick, and a vertebrate host. However, important gaps remain in this knowledge, among them studies of the relationship of its vector and pathogen, and also the role of tick saliva in vector-host interactions. Thus, in order to approach these limitations, in the first part of this dissertation three studies were performed in order to analyze the vector-pathogen-host interface in natural settings (chapter 2). As a result of the first of these studies, co-infections of Borrelia lusitaniae with R. helvetica and R. slovaca were found in ticks collected from a natural safari park in the south of Portugal; new host-pathogen associations were found in the second study described, performed in Madeira Island, namely lizards infected with R. monacensis, as well as detection of R. helvetica in ticks, which was a first occurrence in this island; and in the last study a new species of Rickettsia was isolated from soft ticks collected from pig pens from Alentejo, Portugal. In chapter 3 experimental studies on the vector were performed through analysis of R. massiliae in Rh. sanguineus tick organs. We performed a quantitative analysis of R. massiliae in the salivary glands of feeding Rh. sanguineus ticks, and observed a statistically significant increase in bacterial load during the first two days, followed by a plateau up to day 6 of feeding. An ultrastructural study was also performed on the salivary glands, ovaries and midgut of R. massiliae infected-Rh. sanguineus, where we observed the reactivation phenomenon of Rickettsia in the salivary glands of fed ticks as a result of tick feeding. In the final part of this dissertation the role of tick saliva was ascertained in terms of bacterial burden and immune responses in a murine susceptible host, using uninfected Rh. sanguineus ticks and C3H/HeJ mice. No statistically significant differences in bacterial load were observed between the two groups of R. conorii-infected animals, one of which infested with ticks. However, host cytokine analysis of both groups of animals revealed statistically significant differences, suggesting an inhibitory effect of tick saliva on host pro-inflammatory responses (chapter 4); RESUMO: Estudo das interacções imunes do hospedeiro e vector resultantes da infecção por Rickettsia spp. Os ixodídeos desempenham um papel fundamental como vectores de agentes patogénicos tanto em animais como em humanos. As rickettsioses, com destaque para a febre escaronodular, encontram-se entre as doenças transmitidas por carraças mais importantes na Europa. Até à data muitos estudos foram efectuados de modo a descortinar os mecanismos subjacentes a esta doença, em termos das interacções entre os seus constituintes, i.e., agente patogénico, Rickettsia conorii , o seu vector, o ixodídeo Rhipicephalus sanguineus, e um hospedeiro vertebrado. Todavia, existem ainda lacunas neste conhecimento a nível da relação vector-agente patogénico, para além do papel da saliva do vector nas interacções agente patogénico-hospedeiro. Assim, numa tentativa de colmatar estas limitações, na primeira parte desta dissertação foram realizados três estudos para análise dos fenómenos que ocorrem naturalmente na interface vector-agente patogénico-hospedeiro ocorrentes na natureza (capítulo 2). Como resultado do primeiro destes estudos, foram encontradas co-infecções de Borrelia lusitaniae com R. helvetica e R. slovaca em ixodídeos capturados num parque safari no sul de Portugal. No segundo estudo descrito, efectuado na ilha da Madeira, foram encontradas novas associações hospedeiro-agente patogénico, nomeadamente lagartixas infectadas com R. monacensis, detectou-se R. helvetica em carraças, pela primeira vez nesta ilha, e foi possível isolar uma nova espécie de Rickettsia a partir de carraças de corpo mole capturados em pocilgas no Alentejo, Portugal. O capítulo 3 aborda os resultados de estudos experimentais efetuados no vector, através da análise de R. massiliae em orgãos de Rh. sanguineus. Realizámos uma análise quantitativa da R. massiliae em glândulas salivares de Rh. sanguineus durante a sua refeição sanguínea, tendo-se observado um aumento estatisticamente significativo da carga bacteriana nos dois primeiros dias de alimentação, seguido de um patamar até ao dia 6 da alimentação sanguínea. Foi também efectuado um estudo ultraestrutural nas glândulas salivares, ovários e intestino médio de Rh. sanguineus infectados com R. massiliae, onde observámos o fenómeno de reactivação da Rickettsia nas glândulas salivares dos ixodídeos alimentados, resultante do processo de alimentação. Na parte final desta dissertação analisámos o papel da saliva de ixodídeos em termos da carga bacteriana e respostas imunes num hospedeiro murino susceptível, usando Rh. sanguineus não infectados e ratinhos C3H/HeJ. Não verificámos diferenças estatisticamente significativas entre as cargas bacterianas de dois grupos de animais infectados com R. conorii, em que apenas um dos grupos estava infestado com carraças. Todavia, a análise de citoquinas no hospedeiro em ambos os grupos experimentais revelou diferenças estatisticamente significativas, sugerindo um efeito inibitório da saliva dos ixodídeos nas respostas pro-inflamatórias do hospedeiro (capítulo 4).
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Fulcher, Jennifer Ann. "Novel galectin-1 functions at the host-pathogen interface interactions with Nipah virus envelope glycoproteins and multifunctional roles in dendritic cell activation and development /." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1680017811&sid=14&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Montefusco, Pereira Carlos Victor [Verfasser]. "3D air-liquid interface culture of Cystic Fibrosis bronchial epithelia, macrophages and P. aeruginosa to assess host-pathogen interaction and drug efficacy / Carlos Victor Montefusco-Pereira." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1216503478/34.

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Montefusco-Pereira, Carlos Victor [Verfasser]. "3D air-liquid interface culture of Cystic Fibrosis bronchial epithelia, macrophages and P. aeruginosa to assess host-pathogen interaction and drug efficacy / Carlos Victor Montefusco-Pereira." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1216503478/34.

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Edward, Grahame. "Development and use of an in vitro air-liquid interface model of the bovine respiratory tract and multifaceted proteomic approaches to investigate host-pathogen interactions of Mannheimia haemolytica." Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7777/.

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In the present study, an air-liquid interface culture system was optimised for the use of bovine airway epithelial cells. This culture system has been adopted for other species, where a pseudostratified epithelium comprising multiple cell types and resembling the in vivo environment is produced. Several aspects of the epithelial culture process were optimised, including (i) the cell harvesting process and the expansion of cells in submerged culture, (ii) the substrate material used for air-liquid interface culture, the effects of collagen-coating of the substrate, and the substrate porosity, (iii) the oxygen tension (iv) growth factor (retinoic acid and epidermal growth factor) concentration used during culture and (v) the anatomical region of the respiratory tract from which the epithelial cells were harvested. The optimisation of the aforementioned conditions resulted in the production of an in vitro respiratory tract model that was more than 40% ciliated, pseudostratified with a layer of P63-expressing basal cells and capable of mucus and CC10 (Clara cell secretory protein) production. Thus, an in vitro model of the bovine respiratory tract was established to determine the host-pathogen interactions of M. haemolytica with the respiratory epithelium. A rigorous proteomic characterisation was carried out on the outer membrane of M. haemolytica. The Sarkosyl insoluble fractions of seven M. haemolytica and one M. glucosida isolates, representing a range of serotypes and host species, were prepared in triplicate. Tryptic digests of each sample were prepared using gel-based and gel-free proteomic digests before analysis by LC-MS/MS. Data was searched against the NCBI Uniprot database using MSCOT (Matrix Science). Assembly of the data revealed that a total of 83 unique outer membrane proteins were distributed amongst the eight Mannheimia spp. isolates. Fifty seven of the 83 OMPs were identified using both gel-free and gel-based methodologies with a further 18 and eight identified with a single methodology alone. Several proteins were identified in an isolate specific manner; two OMPs exhibited a strong pattern of serotype-specific identification. The YadA-like trimeric autotransporter was identified with full reproducibility in A2 serotype strains yet not in strains of different serotype. Conversely, the lipoprotein, plpD was identified in at least two replicates of all isolates except those of serotype A2 where it was not identified at all. The air-liquid interface culture system was used to study the adherence and colonisation of Mannheimia haemolytica to the bovine respiratory tract. In a pilot study, pathogenic bovine and ovine isolates M. haemolytica isolates were studied with bovine and ovine air-liquid interface airway epithelial cells. Bovine and ovine M. haemolytica isolates were found to adhere to the epithelial cells, six hours post-infection in the case of an ovine isolate and 24 hours in the case of a bovine isolate. Bovine isolates of M. haemolytica were predominantly found to invade and adhere to the sub-apical regions of the epithelium with relatively few bacteria found on the apical face. Adherence to the sub-apical epithelium represents the first description of M. haemoyltica causing invasive disease. Microscopic evidence of outer membrane vesicle production and exopolymeric material were also noted for one of the ovine isolates during infection. Following optimisation of the bovine air-liquid interface culture system, an experiment was conducted that examined the ability of M. haemolytica to adhere and colonise air-liquid interface cultures with epithelial cells derived from different anatomical regions of the respiratory tract. Cells derived from the nasopharynx, the mid-trachea and the secondary/tertiary bronchi were differentiated at ALI and infected with pathogenic and non-pathogenic bovine isolates of M. haemolytica. The non-pathogenic M. haemolytica isolate was found to adhere and colonise the nasopharyngeal derived cells better than either the bronchial or tracheal derived cells. Conversely, the pathogenic M. haemolytica isolate was found to have significantly greater adherence to the bronchial derived epithelial cultures and significantly higher adherence (P > 0.0001) than the non-pathogenic isolate. The pathogenic M. haemolytica isolate was also found to colonise the nasopharyngeal-derived epithelial culture albeit with lower frequency than was observed for the bronchial-derived epithelial cells. The results presented herein demonstrate the development of a novel in vitro tool for studying the infection process of respiratory pathogens. The use of this tool to study the infection properties of M. haemolytica in combination with characterisation of the outer membrane proteome provides new insight into the process of colonisation and highlights the protein machinery that likely contributes to the process.
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O'Meara, Teresa Rodgers. "Cryptococcus neoformans transcriptional regulation of the host-pathogen interface." Diss., 2013. http://hdl.handle.net/10161/7237.

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Cryptococcus neoformans is a human fungal pathogen that is also ubiquitous in the environment. To cause disease inside a human host, C. neoformans must be able to sense and respond to a multitude of stresses. One of the major responses to the host is the induction of a polysaccharide capsule, which allows the fungus to resist damage and evade the host immune response. This capsule is regulated by a number of signal transduction cascades, but a major contributor is the conserved cAMP/PKA pathway.

Using genetic and molecular biology techniques, I identified Gcn5 and Rim101 as key transcriptional regulators of capsule within the host. I determined that C. neoformans Rim101 is activated by a combination of the canonical pH sensing pathway and the cAMP/PKA pathway. This novel connection potentially gives the pathogen greater flexibility in responding to environmental stimuli, thus allowing for a greater capacity for disease.

I determined that the Rim101 transcription factor regulates cell wall remodeling in the context of the host by deep mRNA sequencing, electron microscopy, and biochemical assays. Using chromatin immunoprecipitation, I confirmed that these cell wall changes are under direct control of Rim101. I then confirmed the importance of cell wall changes in the host by nanoString profiling of fungal RNA in the context of a murine lung infection. I also examined the lungs of infected mice for cytokine and immune cell infiltrate and determined that C. neoformans cell wall changes are important in avoiding triggering an aberrant host response. I hypothesize that this cell wall remodeling via Rim101 activation is required for full capsule attachment and for masking immunogenic molecules from the host immune system.


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Books on the topic "Host-Pathogen interface"

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Vogt, Peter K., and Michael J. Mahan, eds. Bacterial Infection: Close Encounters at the Host Pathogen Interface. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80451-9.

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Vogt, Peter K., and Michael J. Mahan. Bacterial Infection: Close Encounters at the Host Pathogen Interface. Springer London, Limited, 2011.

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Vogt, Peter K., and Michael J. Mahan. Bacterial Infection: Close Encounters at the Host Pathogen Interface. Springer London, Limited, 2012.

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Simões, Isaura, Daniel E. Voth, and Luís Jaime Mota, eds. Obligate Intracellular Bacteria: Evasion and Adaptative Tactics Shaping the Host-Pathogen Interface. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-753-3.

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Bacterial Infection: CLOSE ENCOUNTERS AT THE HOST PATHOGEN INTERFACE (Current Topics in Microbiology & Immunology). SPRINGER-VERLAG, 1998.

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Book chapters on the topic "Host-Pathogen interface"

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Chang, Yung-Chi, and Victor Nizet. "Siglecs at the Host–Pathogen Interface." In Advances in Experimental Medicine and Biology, 197–214. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1580-4_8.

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Burchmore, Richard. "Proteomics at the host: pathogen interface." In Farm animal proteomics 2013, 37. Wageningen: Wageningen Academic Publishers, 2013. http://dx.doi.org/10.3920/978-90-8686-776-9_11.

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Passalacqua, Karla D., Marie-Eve Charbonneau, and Mary X. D. O'riordan. "Bacterial Metabolism Shapes the Host-Pathogen Interface." In Virulence Mechanisms of Bacterial Pathogens, 15–41. Washington, DC, USA: ASM Press, 2016. http://dx.doi.org/10.1128/9781555819286.ch2.

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Guven-Maiorov, Emine, Chung-Jung Tsai, Buyong Ma, and Ruth Nussinov. "Interface-Based Structural Prediction of Novel Host-Pathogen Interactions." In Methods in Molecular Biology, 317–35. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8736-8_18.

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Kovalyova, Yekaterina, and Stavroula K. Hatzios. "Activity-Based Protein Profiling at the Host–Pathogen Interface." In Current Topics in Microbiology and Immunology, 73–91. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/82_2018_129.

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Comer, Jason E., Ellen A. Lorange, and B. Joseph Hinnebusch. "Examining the Vector–Host–Pathogen Interface With Quantitative Molecular Tools." In Bacterial Pathogenesis, 123–31. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-032-8_10.

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Naseem, Muhammad, Shabana Shams, and Thomas Roitsch. "Modulating the Levels of Plant Hormone Cytokinins at the Host-Pathogen Interface." In Methods in Molecular Biology, 141–50. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6831-2_11.

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Burchmore, Richard. "Proteomics at the host: pathogen interface." In Farm animal proteomics 2013, 37. Brill | Wageningen Academic, 2013. http://dx.doi.org/10.3920/9789086867769_013.

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Anand, Kushi, and Varadharajan Sundaramurthy. "Mycobacterial lipids in the host–pathogen interface." In Biology of Mycobacterial Lipids, 51–82. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-91948-7.00005-1.

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Kelliher, J. L., and T. E. Kehl-Fie. "Competition for Manganese at the Host–Pathogen Interface." In Progress in Molecular Biology and Translational Science, 1–25. Elsevier, 2016. http://dx.doi.org/10.1016/bs.pmbts.2016.05.002.

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Reports on the topic "Host-Pathogen interface"

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Horwitz, Benjamin A., and Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7709885.bard.

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Our project focused on genes for high affinity iron acquisition in Cochliobolus heterostrophus, a necrotrophic pathogen of maize, and their intertwined relationship to oxidative stress status and virulence of the fungus on the host. An intriguing question was why mutants lacking the nonribosomal peptide synthetase (NRPS) gene (NPS6) responsible for synthesis of the extracellular siderophore, coprogen, are sensitive to oxidative stress. Our overall objective was to understand the mechanistic connection between iron stress and oxidative stress as related to virulence of a plant pathogen to its host. The first objective was to examine the interface where small molecule peptide and reactive oxygen species (ROS) mechanisms overlap. The second objective was to determine if the molecular explanation for common function is common signal transduction pathways. These pathways, built around sensor kinases, response regulators, and transcription factors may link sequestering of iron, production of antioxidants, resistance to oxidative stress, and virulence. We tested these hypotheses by genetic manipulation of the pathogen, virulence assays on the host plant, and by following the expression of key fungal genes. An addition to the original program, made in the first year, was to develop, for fungi, a genetically encoded indicator of redox state based on the commercially available Gfp-based probe pHyper, designed for animal cell biology. We implemented several tools including a genetically encoded indicator of redox state, a procedure to grow iron-depleted plants, and constructed a number of new mutants in regulatory genes. Lack of the major Fe acquisition pathways results in an almost completely avirulent phenotype, showing how critical Fe acquisition is for the pathogen to cause disease. Mutants in conserved signaling pathways have normal ability to regulate NPS6 in response to Fe levels, as do mutants in Lae1 and Vel1, two master regulators of gene expression. Vel1 mutants are sensitive to oxidative stress, and the reason may be underexpression of a catalase gene. In nps6 mutants, CAT3 is also underexpressed, perhaps explaining the sensitivity to oxidative stress. We constructed a deletion mutant for the Fe sensor-regulator SreA and found that it is required for down regulation of NPS6 under Fe-replete conditions. Lack of SreA, though, did not make the fungus over-sensitive to ROS, though the mutant had a slow growth rate. This suggests that overproduction of siderophore under Fe-replete conditions is not very damaging. On the other hand, increasing Fe levels protected nps6 mutants from inhibition by ROS, implying that Fe-catalyzed Fenton reactions are not the main factor in its sensitivity to ROS. We have made some progress in understanding why siderophore mutants are sensitive to oxidative stress, and in doing so, defined some novel regulatory relationships. Catalase genes, which are not directly related to siderophore biosynthesis, are underexpressed in nps6 mutants, suggesting that the siderophore product (with or without bound Fe) may act as a signal. Siderophores, therefore, could be a target for intervention in the field, either by supplying an incorrect signal or blocking a signal normally provided during infection. We already know that nps6 mutants cause smaller lesions and have difficulty establishing invasive growth in the host. Lae1 and Vel1 are the first factors shown to regulate both super virulence conferred by T-toxin, and basic pathogenicity, due to unknown factors. The mutants are also altered in oxidative stress responses, key to success in the infection court, asexual and sexual development, essential for fungal dissemination in the field, aerial hyphal growth, and pigment biosynthesis, essential for survival in the field. Mutants in genes encoding NADPH oxidase (Nox) are compromised in development and virulence. Indeed the triple mutant, which should lack all Nox activity, was nearly avirulent. Again, gene expression experiments provided us with initial evidence that superoxide produced by the fungus may be most important as a signal. Blocking oxidant production by the pathogen may be a way to protect the plant host, in interactions with necrotrophs such as C. heterostrophus which seem to thrive in an oxidant environment.
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Dickman, Martin B., and Oded Yarden. Characterization of the chorismate mutase effector (SsCm1) from Sclerotinia sclerotiorum. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600027.bard.

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Sclerotinia sclerotiorum is a filamentous fungus (mold) that causes plant disease. It has an extremely wide range of hosts (>400 species) and causes considerable damage (annual multimillion dollar losses) in economically important crops. It has proven difficult to control (culturally or chemically) and host resistance to this fungus has generally been inadequate. It is believed that this fungus occurs in almost every country. Virulence of this aggressive pathogen is bolstered by a wide array of plant cell wall degrading enzymes and various compounds (secondary metabolites) produced by the fungus. It is well established that plant pathogenic fungi secrete proteins and small molecules that interact with host cells and play a critical role in disease development. Such secreted proteins have been collectively designated as “effectors”. Plant resistance against some pathogens can be mediated by recognition of such effectors. Alternatively, effectors can interfere with plant defense. Some such effectors are recognized by the host plant and can culminate in a programmed cell death (PCD) resistant response. During the course of this study, we analyzed an effector in Sclerotiniasclerotiorum. This specific effector, SsCM1 is the protein chorismatemutase, which is an enzyme involved in a pathway which is important in the production of important amino acids, such a Tryptophan. We have characterized the Sclerotiniaeffector, SsCM1, and have shown that inactivation of Sscm1 does not affect fungal vegetative growth, development or production of oxalic acid (one of this fungus’ secondary metabolites associated with disease) production. However, yhis does result in reduced fungal virulence. We show that, unexpectedly, the SsCM1 protein translocates to the host chloroplast, and demonstrated that this process is required for full fungal virulence. We have also determined that the fungal SsCM1 protein can interact with similar proteins produced by the host. In addition, we have shown that the fungal SsCM1 is able to suppress at least some of the effects imposed by reactive oxygen species which are produced as a defense mechanism by the host. Last, but not least, the results of our studies have provided evidence contradicting the current dogma on at least some of the mechanist aspects of how this pathogen infects the host. Contrary to previousons, indicating that this pathogen kills its host by use of metabolites and enzymes that degrade the host tissue (a process called necrotrophy), we now know that at least in the early phases of infection, the fungus interacts with live host tissue (a phenomenon known as biotrophy). Taken together, the results of our studies provide novel insights concerning the mechanistic aspects of Sclerotinia-host interactions. We hope this information will be used to interfere with the disease cycle in a manner that will protect plants from this devastating fungus.
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Coplin, David L., Shulamit Manulis, and Isaac Barash. roles Hrp-dependent effector proteins and hrp gene regulation as determinants of virulence and host-specificity in Erwinia stewartii and E. herbicola pvs. gypsophilae and betae. United States Department of Agriculture, June 2005. http://dx.doi.org/10.32747/2005.7587216.bard.

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Gram-negative plant pathogenic bacteria employ specialized type-III secretion systems (TTSS) to deliver an arsenal of pathogenicity proteins directly into host cells. These secretion systems are encoded by hrp genes (for hypersensitive response and pathogenicity) and the effector proteins by so-called dsp or avr genes. The functions of effectors are to enable bacterial multiplication by damaging host cells and/or by blocking host defenses. We characterized essential hrp gene clusters in the Stewart's Wilt of maize pathogen, Pantoea stewartii subsp. stewartii (Pnss; formerly Erwinia stewartii) and the gall-forming bacterium, Pantoea agglomerans (formerly Erwinia herbicola) pvs. gypsophilae (Pag) and betae (Pab). We proposed that the virulence and host specificity of these pathogens is a function of a) the perception of specific host signals resulting in bacterial hrp gene expression and b) the action of specialized signal proteins (i.e. Hrp effectors) delivered into the plant cell. The specific objectives of the proposal were: 1) How is the expression of the hrp and effector genes regulated in response to host cell contact and the apoplastic environment? 2) What additional effector proteins are involved in pathogenicity? 3) Do the presently known Pantoea effector proteins enter host cells? 4) What host proteins interact with these effectors? We characterized the components of the hrp regulatory cascade (HrpXY ->7 HrpS ->7 HrpL ->7 hrp promoters), showed that they are conserved in both Pnss and Fag, and discovered that the regulation of the hrpS promoter (hrpSp) may be a key point in integrating apoplastic signals. We also analyzed the promoters recognized by HrpL and demonstrated the relationship between their composition and efficiency. Moreover, we showed that promoter strength can influence disease expression. In Pnss, we found that the HrpXY two-component signal system may sense the metabolic status of the bacterium and is required for full hrp gene expression in planta. In both species, acyl-homoserine lactone-mediated quorum sensing may also regulate epiphytic fitness and/or pathogenicity. A common Hrp effector protein, DspE/WtsE, is conserved and required for virulence of both species. When introduced into corn cells, Pnss WtsE protein caused water-soaked lesions. In other plants, it either caused cell death or acted as an Avr determinant. Using a yeast- two-hybrid system, WtsE was shown to interact with a number of maize signal transduction proteins that are likely to have roles in either programmed cell death or disease resistance. In Pag and Pab, we have characterized the effector proteins HsvG, HsvB and PthG. HsvG and HsvB are homologous proteins that determine host specificity of Pag and Pab on gypsophila and beet, respectively. Both possess a transcriptional activation domain that functions in yeast. PthG was found to act as an Avr determinant on multiple beet species, but was required for virulence on gypsophila. In addition, we demonstrated that PthG acts within the host cell. Additional effector genes have been characterized on the pathogenicity plasmid, pPATHₚₐg, in Pag. A screen for HrpL- regulated genes in Pnsspointed up 18 candidate effector proteins and four of these were required for full virulence. It is now well established that the virulence of Gram-negative plant pathogenic bacteria is governed by Hrp-dependent effector proteins. However; the mode of action of many effectors is still unresolved. This BARD supported research will significantly contribute to the understanding of how Hrp effectors operate in Pantoea spp. and how they control host specificity and affect symptom production. This may lead to novel approaches for genetically engineering plants resistant to a wide range of bacterial pathogens by inactivating the Hrp effectors with "plantabodies" or modifying their receptors, thereby blocking the induction of the susceptible response. Alternatively, innovative technologies could be used to interfere with the Hrp regulatory cascade by blocking a critical step or mimicking plant or quorum sensing signals.
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Coplin, David, Isaac Barash, and Shulamit Manulis. Role of Proteins Secreted by the Hrp-Pathways of Erwinia stewartii and E. herbicola pv. gypsophilae in Eliciting Water-Soaking Symptoms and Initiating Galls. United States Department of Agriculture, June 2001. http://dx.doi.org/10.32747/2001.7580675.bard.

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Many bacterial pathogens of plants can inject pathogenicity proteins into host cells using a specialized type III secretion system encoded by hrpgenes. This system deliver effector proteins, into plant cells that function in both susceptible and resistant interactions. We have found that the virulence of Erwinia stewartii(Es; syn. Pantoea stewartii) and Erwinia herbicola pv. gypsophilae (Ehg, syn. Pantoea agglomerans), which cause Stewart's wilt of corn and galls on Gypsophila, respectively, depends on hrpgenes. The major objectives of this project were: To increase expression of hrpgenes in order to identify secreted proteins; to identify genes for proteins secreted by the type-III systems and determine if they are required for pathogenicity; and to determine if the secreted proteins can function within eukaryotic cells. We found that transcription of the hrp and effector genes in Es and Ehg is controlled by at least four genes that constitute a regulatory cascade. Environmental and/or physiological signaling appears to be mediated by the HrpX/HrpY two component system, with HrpX functioning as a sensor-kinase and HrpY as a response regulator. HrpYupregulateshrpS, which encodes a transcriptional enhancer. HrpS then activates hrpL, which encodes an alternate sigma factor that recognizes "hrp boxes". All of the regulatory genes are essential for pathogenicity, except HrpX, which appears only to be required for induction of the HR in tobacco by Es. In elucidating this regulatory pathway in both species, we made a number of significant new discoveries. HrpX is unusual for a sensor-kinase because it is cytoplasmic and contains PAS domains, which may sense the redox state of the bacterium. In Es, a novel methyl-accepting protein may function upstream of hrpY and repress hrp gene expression in planta. The esaIR quorum sensing system in Es represses hrp gene expression in Es in response to cell-density. We have discovered six new type III effector proteins in these species, one of which (DspE in Ehg and WtsE in Es) is common to both pathogens. In addition, Es wtsG, which is a homolog of an avrPpiB from P. syringae pv. pisi, and an Ehg ORF, which is a homolog of P. syringae pv. phaseolicola AvrPphD, were both demonstrated to encode virulence proteins. Two plasmidborne, Ehg Hop proteins, HsvG and PthG, are required for infection of gypsophilia, but interestingly, PthG also acts as an Avr elicitor in beets. Using a calmodulin-dependent adenylate cyclase (cyaA) reporter gene, we were successful in demonstrating that an HsvG-CyaA fusion protein can be transferred into human HeLa cells by the type-III system of enteropathogenic E. coli. This is a highly significant accomplishment because it is the first direct demonstration that an effector protein from a plant pathogenic bacterium is capable of being translocated into a eukaryotic cell by a type-III secretion system. Ehg is considered a limiting factor in Gypsophila production in Israel and Stewart’s Wilt is a serious disease in the Eastern and North Central USA, especially on sweet corn in epidemic years. We believe that our basic research on the characterization of type III virulence effectors should enable future identification of their receptors in plant cells. This may lead to novel approaches for genetically engineering resistant plants by modifying their receptors or inactivating effectors and thus blocking the induction of the susceptible response. Alternatively, hrp gene regulation might also provide a target for plant produced compounds that interfere with recognition of the host by the pathogen. Such strategies would be broadly applicable to a wide range of serious bacterial diseases on many crops throughout the USA and Israel.
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5

Dickman, Martin B., and Oded Yarden. Genetic and chemical intervention in ROS signaling pathways affecting development and pathogenicity of Sclerotinia sclerotiorum. United States Department of Agriculture, July 2015. http://dx.doi.org/10.32747/2015.7699866.bard.

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Abstract: The long-term goals of our research are to understand the regulation of sclerotial development and pathogenicity in S. sclerotior11111. The focus in this project was on the elucidation of the signaling events and environmental cues involved in the regulation of these processes, utilizing and continuously developing tools our research groups have established and/or adapted for analysis of S. sclerotiorum, Our stated objectives: To take advantage of the recent conceptual (ROS/PPs signaling) and technical (amenability of S. sclerotiorumto manipulations coupled with chemical genomics and next generation sequencing) developments to address and extend our fundamental and potentially applicable knowledge of the following questions concerning the involvement of REDOX signaling and protein dephosphorylation in the regulation of hyphal/sclerotial development and pathogenicity of S. sclerotiorum: (i) How do defects in genes involved in ROS signaling affect S. sclerotiorumdevelopment and pathogenicity? (ii) In what manner do phosphotyrosinephosphatases affect S. sclerotiorumdevelopment and pathogenicity and how are they linked with ROS and other signaling pathways? And (iii) What is the nature of activity of newly identified compounds that affect S. sclerotiori,111 growth? What are the fungal targets and do they interfere with ROS signaling? We have met a significant portion of the specific goals set in our research project. Much of our work has been published. Briefly. we can summarize that: (a) Silencing of SsNox1(NADPHoxidase) expression indicated a central role for this enzyme in both virulence and pathogenic development, while inactivation of the SsNox2 gene resulted in limited sclerotial development, but the organism remained fully pathogenic. (b) A catalase gene (Scatl), whose expression was highly induced during host infection is involved in hyphal growth, branching, sclerotia formation and infection. (c) Protein tyrosine phosphatase l (ptpl) is required for sclerotial development and is involved in fungal infection. (d) Deletion of a superoxidedismutase gene (Sssodl) significantly reduced in virulence on both tomato and tobacco plants yet pathogenicity was mostly restored following supplementation with oxalate. (e) We have participated in comparative genome sequence analysis of S. sclerotiorumand B. cinerea. (f) S. sclerotiorumexhibits a potential switch between biotrophic and necrotrophic lifestyles (g) During plant­ microbe interactions cell death can occur in both resistant and susceptible events. Non­ pathogenic fungal mutants S. sclerotior111n also cause a cell death but with opposing results. We investigated PCD in more detail and showed that, although PCD occurs in both circumstances they exhibit distinctly different features. The mutants trigger a restricted cell death phenotype in the host that unexpectedly exhibits markers associated with the plant hypersensitive (resistant) response. Using electron and fluorescence microscopy, chemical effectors and reverse genetics, we have established that this restricted cell death is autophagic. Inhibition of autophagy rescued the non-pathogenic mutant phenotype. These findings indicate that autophagy is a defense response in this interaction Thus the control of cell death, dictated by the plant (autophagy) סr the fungus (apoptosis), is decisive to the outcome of certain plant­ microbe interactions. In addition to the time and efforts invested towards reaching the specific goals mentioned, both Pls have initiated utilizing (as stated as an objective in our proposal) state of the art RNA-seq tools in order to harness this technology for the study of S. sclerotiorum. The Pls have met twice (in Israel and in the US), in order to discuss .נחd coordinate the research efforts. This included a working visit at the US Pls laboratory for performing RNA-seq experiments and data analysis as well as working on a joint publication (now published). The work we have performed expands our understanding of the fundamental biology (developmental and pathogenic) of S. sclerotioז111וז. Furthermore, based on our results we have now reached the conclusion that this fungus is not a bona fide necrotroph, but can also display a biotrophic lifestyle at the early phases of infection. The data obtained can eventually serve .נ basis of rational intervention with the disease cycle of this pathogen.
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