Academic literature on the topic 'Infectious Disease, Host-pathogen interaction, Immunology'
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Journal articles on the topic "Infectious Disease, Host-pathogen interaction, Immunology"
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Ingrao, Fiona, Fabienne Rauw, Bénédicte Lambrecht, and Thierry van den Berg. "Infectious Bursal Disease: A complex host–pathogen interaction." Developmental & Comparative Immunology 41, no. 3 (November 2013): 429–38. http://dx.doi.org/10.1016/j.dci.2013.03.017.
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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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Thakur, Aneesh, Heidi Mikkelsen, and Gregers Jungersen. "Intracellular Pathogens: Host Immunity and Microbial Persistence Strategies." Journal of Immunology Research 2019 (April 14, 2019): 1–24. http://dx.doi.org/10.1155/2019/1356540.
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Infectious diseases caused by pathogens including viruses, bacteria, fungi, and parasites are ranked as the second leading cause of death worldwide by the World Health Organization. Despite tremendous improvements in global public health since 1950, a number of challenges remain to either prevent or eradicate infectious diseases. Many pathogens can cause acute infections that are effectively cleared by the host immunity, but a subcategory of these pathogens called “intracellular pathogens” can establish persistent and sometimes lifelong infections. Several of these intracellular pathogens manage to evade the host immune monitoring and cause disease by replicating inside the host cells. These pathogens have evolved diverse immune escape strategies and overcome immune responses by residing and multiplying inside host immune cells, primarily macrophages. While these intracellular pathogens that cause persistent infections are phylogenetically diverse and engage in diverse immune evasion and persistence strategies, they share common pathogen type-specific mechanisms during host-pathogen interaction inside host cells. Likewise, the host immune system is also equipped with a diverse range of effector functions to fight against the establishment of pathogen persistence and subsequent host damage. This article provides an overview of the immune effector functions used by the host to counter pathogens and various persistence strategies used by intracellular pathogens to counter host immunity, which enables their extended period of colonization in the host. The improved understanding of persistent intracellular pathogen-derived infections will contribute to develop improved disease diagnostics, therapeutics, and prophylactics.
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Hung, Paul. "Automatic pathogen introduction and removal for live cell imaging of host-pathogen interaction (P3237)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 192.4. http://dx.doi.org/10.4049/jimmunol.190.supp.192.4.
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Abstract Host-pathogen interactions represent a significant area of immunology, encompassing the study of how organisms cause infections and diseases. As the field advances, there is increasing interest in using in vitro cell culture models and imaging to study the interactions. However, a few barriers remain with the conventional static cell culture approach. Not only the pathogen will easily outgrow the cells over time, prohibiting further studies, but tedious liquid exchange steps are required to remove excessive pathogens or to add other reagents such as therapeutic compound. To facilitate host-pathogen interaction research with live cell imaging, a microfluidic platform which addresses the problems mentioned above was developed. The platform allows the researchers to culture the cells in a microchamber on a standard inverted microscope, as well as preload up to four different reagents which can be introduced to the cells automatically including the pathogen. The reagent switching function enable the removal of pathogens from the chamber after incision, and subsequent monitoring of host cell response over up to 3 days. The enclosed small volume microchamber also provides practical advantages for working with infectious agents during live cell imaging. An experiment using human intestinal cells infected with engineered E. coli strains was demonstrated. Both an invasive and a non-invasive bacterial strain were monitored for infection with time-lapsed imaging up to 24 hours.
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Savinelli, Stefano, Neil E. Wrigley Kelly, Eoin R. Feeney, Donal B. O'Shea, Andrew E. Hogan, Edgar T. Overton, Alan L. Landay, and Patrick W. Mallon. "Obesity in HIV infection: host-pathogen interaction." AIDS 36, no. 11 (June 21, 2022): 1477–91. http://dx.doi.org/10.1097/qad.0000000000003281.
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Castillo, Christian, and Ulrike Kemmerling. "Host–Pathogen Interaction Involved in Trypanosoma cruzi Infection." Pathogens 11, no. 5 (May 4, 2022): 540. http://dx.doi.org/10.3390/pathogens11050540.
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Henriet, Stefanie S. V., Paul E. Verweij, and Adilia Warris. "Aspergillus nidulans and Chronic Granulomatous Disease: A Unique Host–Pathogen Interaction." Journal of Infectious Diseases 206, no. 7 (July 24, 2012): 1128–37. http://dx.doi.org/10.1093/infdis/jis473.
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Hermann, Corinna. "Review: Variability of host—pathogen interaction." Journal of Endotoxin Research 13, no. 4 (August 2007): 199–218. http://dx.doi.org/10.1177/0968051907082605.
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Bandyopadhyay, Soumyendu Sekhar, Anup Kumar Halder, Sovan Saha, Piyali Chatterjee, Mita Nasipuri, and Subhadip Basu. "Assessment of GO-Based Protein Interaction Affinities in the Large-Scale Human–Coronavirus Family Interactome." Vaccines 11, no. 3 (February 25, 2023): 549. http://dx.doi.org/10.3390/vaccines11030549.
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SARS-CoV-2 is a novel coronavirus that replicates itself via interacting with the host proteins. As a result, identifying virus and host protein-protein interactions could help researchers better understand the virus disease transmission behavior and identify possible COVID-19 drugs. The International Committee on Virus Taxonomy has determined that nCoV is genetically 89% compared to the SARS-CoV epidemic in 2003. This paper focuses on assessing the host–pathogen protein interaction affinity of the coronavirus family, having 44 different variants. In light of these considerations, a GO-semantic scoring function is provided based on Gene Ontology (GO) graphs for determining the binding affinity of any two proteins at the organism level. Based on the availability of the GO annotation of the proteins, 11 viral variants, viz., SARS-CoV-2, SARS, MERS, Bat coronavirus HKU3, Bat coronavirus Rp3/2004, Bat coronavirus HKU5, Murine coronavirus, Bovine coronavirus, Rat coronavirus, Bat coronavirus HKU4, Bat coronavirus 133/2005, are considered from 44 viral variants. The fuzzy scoring function of the entire host–pathogen network has been processed with ~180 million potential interactions generated from 19,281 host proteins and around 242 viral proteins. ~4.5 million potential level one host–pathogen interactions are computed based on the estimated interaction affinity threshold. The resulting host–pathogen interactome is also validated with state-of-the-art experimental networks. The study has also been extended further toward the drug-repurposing study by analyzing the FDA-listed COVID drugs.
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Bogaert, Debby, Paul van der Valk, Reshmi Ramdin, Marcel Sluijter, Evelyn Monninkhof, Ron Hendrix, Ronald de Groot, and Peter W. M. Hermans. "Host-Pathogen Interaction during Pneumococcal Infection in Patients with Chronic Obstructive Pulmonary Disease." Infection and Immunity 72, no. 2 (February 2004): 818–23. http://dx.doi.org/10.1128/iai.72.2.818-823.2004.
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ABSTRACT Acute exacerbation is a frequent complication of chronic obstructive pulmonary disease (COPD). Recent studies suggested a role for bacteria such as Streptococcus pneumoniae in the development of acute exacerbation. For this study, we investigated the following in COPD patients: (i) the epidemiology of pneumococcal colonization and infection, (ii) the effect of pneumococcal colonization on the development of exacerbation, and (iii) the immunological response against S. pneumoniae. We cultured sputa of 269 COPD patients during a stable state and during exacerbation of COPD and characterized 115 pneumococcal isolates by use of serotyping. Moreover, we studied serum immunoglobulin G (IgG) antibody titers, antibody avidities, and functional antibody titers against the seven conjugate vaccine serotypes in these patients. Colonization with only pneumococci (monocultures) increased the risk of exacerbation, with a hazard ratio of 2.93 (95% confidence interval, 1.41 to 6.07). The most prevalent pneumococcal serotypes found were serotypes 19F, 3, 14, 9L/N/V, 23A/B, and 11. We calculated the theoretical coverage for the 7- and 11-valent pneumococcal vaccines to be 60 and 73%, respectively. All patients had detectable IgG levels against the seven conjugate vaccine serotypes. These antibody titers were significantly lower than those in vaccinated healthy adults. Finally, on average, a 2.5-fold rise in serotype-specific and functional antibodies in S. pneumoniae-positive sputum cultures was observed during exacerbation. Our data indicate that pneumococcal colonization in COPD patients is frequently caused by vaccine serotype strains. Moreover, pneumococcal colonization is a risk factor for exacerbation of COPD. Finally, our findings demonstrate that COPD patients are able to mount a significant immune response to pneumococcal infection. COPD patients may therefore benefit from pneumococcal vaccination.
Dissertations / Theses on the topic "Infectious Disease, Host-pathogen interaction, Immunology"
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Mustafi, Sushmita. "Regulation of Rab5 GTPase activity during Pseudomonas aeruginosa-macrophage interaction." FIU Digital Commons, 2013. http://digitalcommons.fiu.edu/etd/1016.
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Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen. Several antibiotic resistant strains of P. aeruginosa are commonly found as secondary infection in immune-compromised patients leaving significant mortality and healthcare cost. Pseudomonas aeruginosa successfully avoids the process of phagocytosis, the first line of host defense, by secreting several toxic effectors. Effectors produced from P. aeruginosa Type III secretion system are critical molecules required to disrupt mammalian cell signaling and holds particular interest to the scientists studying host-pathogen interaction. Exoenzyme S (ExoS) is a bi-functional Type III effector that ADP-ribosylates several intracellular Ras (Rat sarcoma) and Rab (Response to abscisic acid) small GTPases in targeted host cells. The Rab5 protein acts as a rate limiting protein during phagocytosis by switching from a GDP- bound inactive form to a GTP-bound active form. Activation and inactivation of Rab5 protein is regulated by several Rab5-GAPs (GTPase Activating Proteins) and Rab5-GEFs (Rab5-Guanine nucleotide Exchange Factors). Some pathogenic bacteria have shown affinity for Rab proteins during infection and make their way inside the cell. This dissertation demonstrated that Rab5 plays a critical role during early steps of P. aeruginosa invasion in J774-Eclone macrophages. It was found that live, but not heat inactivated, P. aeruginosa inhibited phagocytosis that occurred in conjunction with down-regulation of Rab5 activity. Inactivation of Rab5 was dependent on ExoS ADP-ribosyltransferase activity, and more than one arginine sites in Rab5 are possible targets for ADP-ribosylation modification. However, the expression of Rin1, but not other Rab5GEFs (Rabex-5 and Rap6) reversed this down-regulation of Rab5 in vivo. Further studies revealed that the C-terminus of Rin1 carrying Rin1:Vps9 and Rin1:RA domains are required for optimal Rab5 activation in conjunction with active Ras. These observations demonstrate a novel mechanism of Rab5 targeting to phagosome via Rin1 during the phagocytosis of P. aeruginosa. The second part of this dissertation investigated antimicrobial activities of Dehydroleucodine (DhL), a secondary metabolite from Artemisia douglasiana, against P. aeruginosa growth and virulence. Populations of several P. aeruginosa strains were completely susceptible to DhL at a concentration between 0.48~0.96 mg/ml and treatment at a threshold concentration (0.12 mg/ml) inhibited growth and many virulent activities without damaging the integrity of the cell suggesting anti-Pseudomonas activity of DhL.
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Earnhart, Christopher G. "Dynamics of the host-parasite interaction: in vitro correlates of Crassostrea-induced modulation of Perkinsus marinus function." W&M ScholarWorks, 2004. https://scholarworks.wm.edu/etd/1539616637.
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Perkinsus marinus is an alveolate protozoan parasite of the eastern oyster (Crassostrea virginica) which is responsible for much of the decline in United States oyster populations. Perkinsus marinus can be cultured in vitro, but is rapidly attenuated in the process. Supplementation of a protein-free medium with oyster products altered proliferation, changed protease expression in the parasite extracellular products (ECP), induced morphological forms typically seen in vivo, and partially reversed parasite attenuation. Supplements derived from dissected oyster tissues were used to determine if these changes could be differentially elicited. These supplements, with the exception of adductor muscle, reduced proliferation. Whole oyster and digestive gland/gonad supplements favored palintomic, rather than binary, fission. The total ECP protease activity was generally decreased in supplemented cultures, though gill/mantle supplements may have induced proteases. A low molecular weight subset of proteases was upregulated most effectively by heart- and adductor muscle-derived supplements. Serine proteases and other ECP proteins may be virulence factors. Attempts to create antibodies to study P. marinus cells and ECP have been largely unsuccessful due to poor immune responses and crossreactivity. Ultrafiltration-concentrated P. marinus ECP were poorly immunogenic and toxic to experimental animals. Immunogenicity was not substantially affected by heat denaturation or proteolytic inhibition. Co-administration of ECP with oyster plasma caused a suppression in the anti-plasma antibody response with restriction of epitope recognition. Analysis of medium constituents revealed that a surfactant, Pluronic F-68 (PF68), was immunosuppressive. Although isolated protein antigens from the ECP remained immunosuppressive, separation of the antigens from PF68 enabled antibody production. Five monoclonal antibodies were created against ECP from unsupplemented medium and were used to study ECP function, regulation, and mechanism of storage and release. ECP are secreted by release from the cell wall and from two morphologically distinct intracellular compartments. A sandwich ELISA allowed quantification of an ECP protein with significantly reduced expression in supplemented cultures. Another antibody, which specifically bound to trophozoite and tomont walls, was used to investigate morphological and antigenic changes during thioglycollate-induced formation of prezoosporangia, and confirm supplement-induced formation of prezoosporangia. This antibody labeled P. marinus cells in fixed oyster tissue in a species-specific manner.
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Anderson, Sarah M. "The Fatty Acid Oleate in the C. elegans Innate Immune Response." eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1133.
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Host metabolism is profoundly altered during bacterial infection, both as a consequence of immune activation and secondary to virulence strategies of invading pathogens. As a result, the metabolic pathways that regulate nutrient acquisition, energy storage, and resource allocation in host cells must adapt to pathogen stress in order to meet the physiological demands of the host during infection. In this work, we uncover that the synthesis of the monounsaturated fatty acid (MUFA) oleate is necessary for the pathogen-mediated induction of immune defense genes. Accordingly, C. elegans deficient in oleate production are hypersusceptible to infection with diverse human pathogens, which can be rescued by the addition of exogenous oleate. However, oleate is not sufficient to drive protective immune activation.
Oleate is also important for proper lipid storage and abundance. We found that exposure to pathogenic bacteria drives rapid somatic depletion of lipid stores in C. elegans. Activating the p38/MAPK immune signaling pathway in the absence of pathogens was also sufficient to drive loss of somatic fat. In addition, we found that transcriptional suppression of MUFA synthesis occurs during P. aeruginosa infection, in a manner dependent on pathogen virulence. Finally, we showed that the host compensates for the pathogen-induced depletion of fatty acids by promoting the redistribution of oleate from non-intestinal tissues to support immune function in the intestine. Together, these data add to the known health-promoting effects of MUFAs, and suggest an ancient link between nutrient stores, metabolism, and host responses to bacterial infection.
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Ghosh, Sreya. "Different Journeys, Same Destination: Exploring the Role of a PYHIN Protein and Involvement of Caspase-8 in the Regulation and Activation of Inflammasomes." eScholarship@UMMS, 2009. http://escholarship.umassmed.edu/gsbs_diss/928.
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Interferon-inducible PYHIN protein family includes the DNA-binding proteins, AIM2 and IFI16, which form ASC-caspase 1 dependent inflammasomes, important in immunity against cytosolic bacteria, DNA viruses and HIV. The role of other members of this family in the recognition of DNA and/or regulation of immune responses is unclear. We identified an immune regulatory function of p205, another member of the PYHIN family, in the transcriptional control of immune genes. Knockdown of p205 in macrophages revealed that inflammasome activation due to dsDNA and ligands that engage the NLRP3 inflammasome were severely compromised. Detailed mechanistic analysis showed that loss of p205 was associated with a decrease in Asc mRNA and protein levels. p205 knockdown resulted in reduced RNA Polymerase II-mediated endogenous Asc gene transcription and mRNA processing, suggesting a co-transcriptional control of Asc gene expression. Ectopically expressed p205 induced expression of an Asc gene-luciferase reporter and collaborated with other transcription factors, such as c/EBPβ, p65/RelA, to further enhance expression. p205 knockdown also affected the expression of the immune genes Cd86, Cox2, Cxcl2, Il1α, Il10, Il12α, Il6 and Ifnα in LPS-stimulated macrophages. Together these findings suggest that p205 regulates inflammation through control of Asc gene expression, and other immune genes.
Fungal infections activate both caspase 1-dependent and -independent inflammasomes. In an independent study, we show that Paracoccidioides brasiliensis fungal infection also induces caspase 8-dependent non-canonical inflammasome. Caspase 8-dependent IL-1β processing required dectin-1, Syk and Asc. Rip3-/- Casp8-/- mice infected with P. brasiliensis displayed increased fungal load and showed worse disease progression compared to wild type and Rip3-/- mice. These results revealed the importance of caspase 8 in activating and regulating inflammasome responses during fungal infection in vivo.
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Ghosh, Sreya. "Different Journeys, Same Destination: Exploring the Role of a PYHIN Protein and Involvement of Caspase-8 in the Regulation and Activation of Inflammasomes." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/928.
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Interferon-inducible PYHIN protein family includes the DNA-binding proteins, AIM2 and IFI16, which form ASC-caspase 1 dependent inflammasomes, important in immunity against cytosolic bacteria, DNA viruses and HIV. The role of other members of this family in the recognition of DNA and/or regulation of immune responses is unclear. We identified an immune regulatory function of p205, another member of the PYHIN family, in the transcriptional control of immune genes. Knockdown of p205 in macrophages revealed that inflammasome activation due to dsDNA and ligands that engage the NLRP3 inflammasome were severely compromised. Detailed mechanistic analysis showed that loss of p205 was associated with a decrease in Asc mRNA and protein levels. p205 knockdown resulted in reduced RNA Polymerase II-mediated endogenous Asc gene transcription and mRNA processing, suggesting a co-transcriptional control of Asc gene expression. Ectopically expressed p205 induced expression of an Asc gene-luciferase reporter and collaborated with other transcription factors, such as c/EBPβ, p65/RelA, to further enhance expression. p205 knockdown also affected the expression of the immune genes Cd86, Cox2, Cxcl2, Il1α, Il10, Il12α, Il6 and Ifnα in LPS-stimulated macrophages. Together these findings suggest that p205 regulates inflammation through control of Asc gene expression, and other immune genes.
Fungal infections activate both caspase 1-dependent and -independent inflammasomes. In an independent study, we show that Paracoccidioides brasiliensis fungal infection also induces caspase 8-dependent non-canonical inflammasome. Caspase 8-dependent IL-1β processing required dectin-1, Syk and Asc. Rip3-/- Casp8-/- mice infected with P. brasiliensis displayed increased fungal load and showed worse disease progression compared to wild type and Rip3-/- mice. These results revealed the importance of caspase 8 in activating and regulating inflammasome responses during fungal infection in vivo.
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Weng, Dan. "Caspase-8 and RIP Kinases Regulate Bacteria-Induced Innate Immune Responses and Cell Death: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/727.
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Yersinia pestis (Y. pestis), as the causative agent of plague, has caused deaths estimated to more than 200 million people in three historical plague pandemics, including the infamous Black Death in medieval Europe. Although infection with Yersinia pestis can mostly be limited by antibiotics and only 2000-5000 cases are observed worldwide each year, this bacterium is still a concern for bioterrorism and recognized as a category A select agent by the Centers for Disease Control and Prevention (CDC). The investigation into the host-pathogen interactions during Y. pestis infection is important to advance and broaden our knowledge about plague pathogenesis for the development of better vaccines and treatments.
Y. pestis is an expert at evading innate immune surveillance through multiple strategies, several mediated by its type three secretion system (T3SS). It is known that the bacterium induces rapid and robust cell death in host macrophages and dendritic cells. Although the T3SS effector YopJ has been determined to be the factor inducing cytotoxicity, the specific host cellular pathways which are targeted by YopJ and responsible for cell death remain poorly defined. This thesis research has established the critical roles of caspase-8 and RIP kinases in Y. pestis-induced macrophage cell death. Y. pestis-induced cytotoxicity is completely inhibited in RIP1-/- or RIP3-/-caspase-8-/- macrophages or by specific chemical inhibitors. Strikingly, this work also indicates that macrophages deficient in either RIP1, or caspase-8 and RIP3, have significantly reduced infection-induced production of IL-1β, IL-18, TNFα and IL-6 cytokines; impaired activation of NF-κB signaling pathway and greatly compromised caspase-1 processing; all of which are critical for innate immune responses and contribute to fight against pathogen infection. Y. pestis infection causes severe and often rapid fatal disease before the development of adaptive immunity to the V bacterium, thus the innate immune responses are critical to control Y. pestis infection. Our group has previously established the important roles of key molecules of the innate immune system: TLR4, MyD88, NLRP12, NLRP3, IL-18 and IL-1β, in host responses against Y. pestis and attenuated strains. Yersinia has proven to be a good model for evaluating the innate immune responses during bacterial infection. Using this model, the role of caspase-8 and RIP3 in counteracting bacterial infection has been determined in this thesis work. Mice deficient in caspase-8 and RIP3 are very susceptible to Y. pestis infection and display reduced levels of pro-inflammatory cytokines in spleen and serum, and decreased myeloid cell death. Thus, both in vitro and in vivo results indicate that caspase-8 and RIP kinases are key regulators of macrophage cell death, NF-κB and caspase-1 activation in Yersinia infection. This thesis work defines novel roles for caspase-8 and RIP kinases as the central components in innate immune responses against Y. pestis infection, and provides further insights to the host-pathogen interaction during bacterial challenge.
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Weng, Dan. "Caspase-8 and RIP Kinases Regulate Bacteria-Induced Innate Immune Responses and Cell Death: A Dissertation." eScholarship@UMMS, 2007. http://escholarship.umassmed.edu/gsbs_diss/727.
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Yersinia pestis (Y. pestis), as the causative agent of plague, has caused deaths estimated to more than 200 million people in three historical plague pandemics, including the infamous Black Death in medieval Europe. Although infection with Yersinia pestis can mostly be limited by antibiotics and only 2000-5000 cases are observed worldwide each year, this bacterium is still a concern for bioterrorism and recognized as a category A select agent by the Centers for Disease Control and Prevention (CDC). The investigation into the host-pathogen interactions during Y. pestis infection is important to advance and broaden our knowledge about plague pathogenesis for the development of better vaccines and treatments.
Y. pestis is an expert at evading innate immune surveillance through multiple strategies, several mediated by its type three secretion system (T3SS). It is known that the bacterium induces rapid and robust cell death in host macrophages and dendritic cells. Although the T3SS effector YopJ has been determined to be the factor inducing cytotoxicity, the specific host cellular pathways which are targeted by YopJ and responsible for cell death remain poorly defined. This thesis research has established the critical roles of caspase-8 and RIP kinases in Y. pestis-induced macrophage cell death. Y. pestis-induced cytotoxicity is completely inhibited in RIP1-/- or RIP3-/-caspase-8-/- macrophages or by specific chemical inhibitors. Strikingly, this work also indicates that macrophages deficient in either RIP1, or caspase-8 and RIP3, have significantly reduced infection-induced production of IL-1β, IL-18, TNFα and IL-6 cytokines; impaired activation of NF-κB signaling pathway and greatly compromised caspase-1 processing; all of which are critical for innate immune responses and contribute to fight against pathogen infection. Y. pestis infection causes severe and often rapid fatal disease before the development of adaptive immunity to the V bacterium, thus the innate immune responses are critical to control Y. pestis infection. Our group has previously established the important roles of key molecules of the innate immune system: TLR4, MyD88, NLRP12, NLRP3, IL-18 and IL-1β, in host responses against Y. pestis and attenuated strains. Yersinia has proven to be a good model for evaluating the innate immune responses during bacterial infection. Using this model, the role of caspase-8 and RIP3 in counteracting bacterial infection has been determined in this thesis work. Mice deficient in caspase-8 and RIP3 are very susceptible to Y. pestis infection and display reduced levels of pro-inflammatory cytokines in spleen and serum, and decreased myeloid cell death. Thus, both in vitro and in vivo results indicate that caspase-8 and RIP kinases are key regulators of macrophage cell death, NF-κB and caspase-1 activation in Yersinia infection. This thesis work defines novel roles for caspase-8 and RIP kinases as the central components in innate immune responses against Y. pestis infection, and provides further insights to the host-pathogen interaction during bacterial challenge.
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Dai, Weiwei. "SERINC5: Its Sensitivity to Nef and Restriction of HIV-1." eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/984.
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The accessory protein Nef of human immunodeficiency virus type 1 (HIV-1) has long been known to enhance the infectivity of HIV-1 progeny virions. The multipass transmembrane proteins serine incorporator 3 (SERINC3) and SERINC5 were recently identified as novel antiviral proteins that restrict HIV-1 infectivity. Nef enhances HIV-1 infectivity by removing SERINCs from the plasma membrane, which prevents their incorporation into progeny HIV-1 virions. To exploit this potent intrinsic antiretroviral factor for potential therapy development, it is critical to explore the determinants in SERINC5 that govern its downregulation by Nef and its restriction on HIV-1 infectivity. Here I report that the ability to inhibit HIV-1 infectivity is conserved among vertebrate SERINC5 proteins, whereas the sensitivity to downregulation by Nef is not. However, a Nef-resistant SERINC5 became Nef-sensitive when its intracellular loop 4 (ICL4) was replaced by that of Nef-sensitive human SERINC5. Conversely, human SERINC5 became resistant to Nef when its ICL4 was replaced by that of a Nef-resistant SERINC5. In general, ICL4 regions from SERINCs that exhibited resistance to a given Nef conferred resistance to the same Nef when transferred to a sensitive SERINC, and vice versa. I demonstrate that human SERINC5 can be modified to restrict HIV-1 infectivity even in the presence of Nef. Moreover, by generating chimeras between SERINC5 and SERINC2, which does not exhibit antiretroviral activity, I demonstrate that SERINC5’s inhibitory function, unlike the sensitivity to Nef, requires the participation of more than one region. Helix 4 and extracellular loop 5 (ECL5) of SERINC5 are both required for the potent restriction of HIV-1 infectivity. In contrast, a large amino-terminal portion of SERINC5 is not required for its antiretroviral activity of SERINC5. The determinants in ECL5 disperse throughout the loop. Furthermore, the ECL5 of SERINC5 is a hotspot region that determines the Env-dependent antiretroviral activity of SERINC5.
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Rahmani, Alexandra. "Identification des facteurs de pathogénicité de la bactérie Vibrio tapetis, responsable de la maladie de l'anneau brun chez la palourde japonaise Ruditapes philippinarum et de mortalités chez les poissons marins Transcriptomic analysis of clam extrapallial fluids reveals immunity and cytoskeleton alterations in the first week of Brown Ring Disease development, in Fish & Shellfish Immunology 93, October 2019." Thesis, Brest, 2019. http://www.theses.fr/2019BRES0059.
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L’objectif principal de cette thèse est d’étudier les mécanismes liés au pouvoir pathogène de V. tapetis.Pour cela, nous avons développé 2 axes de recherche. Le premier axe vise à étudier la virulence de V. tapetis en répondant aux 2 problématiques suivantes : Quels sont les gènes impliqués dans la virulence de V. tapetis ? et Existe-t-il des marqueurs hôtes-spécifiques de la virulence de V. tapetis ? Le second axe de recherche concerne l’interaction hôte pathogène et répond aux 2 problématiques suivantes : Quels sont les gènes exprimés lors de l’infection chez l’hôte ? et Quelles sont les modulations au sein de l’animal associées au pH et à la température lors de l’infection ?Les principales découvertes de cette thèse sont : (i) La bactérie V. tapetis, dans le cadre de la MAB, induit une sous expression des gènes impliqués dans la réponseimmunitaire et une dérégulation des gènes impliqués dans la stabilisation et la synthèse des filaments d’actine (ii) Ce pathogène induit également une diminution de l’activité lysosomale sur les hémocytes exposés (iii) L’effet de V. tapetis sur le cytosquelette d’actine et sur la diminution de l’activité lysosomale est indépendante du système de sécrétion de type IV (T4SS) (iv) Le système de sécrétion de type IV (T4SS) est impliqué dans le développement de la MAB mais n’est pas essentiel pour induire cette affection(v) Dans le cadre de la MAB et de la perte des adhérences des hémocytes in vitro, V. tapetis est capable de moduler le pH des fluides extra-palléaux, respectivement dans les premiers jours et premières heures de l’infection (vi) Enfin, l’approche de « strains typing » basée sur la technique MALDI-TOF permet de discriminer les souches de V. tapetis en fonction de leur pouvoir pathogène vis à vis de la palourde japonaiseThe main objective of this thesis is to study the mechanisms related to the pathogenicity of V. tapetis. For this purpose, we developed 2 research axes. The first one aimed at studying the virulence of V. tapetis by answering the following 2 issues: What are the genes involved in the virulence of V. tapetis? and Are there host-specific markers of the virulence of V. tapetis? The second research axis concerned pathogen-host interactions and addressed the following 2 issues: What are the genes expressed during infection in the host? and What are the modulations in the animal associated with pH and temperature during infection? The main findings of this thesis are: (i) V. tapetis, in the context of BRD, induces a down expression of genes involved in the immune response anda deregulation of genes involved in the stabilization and synthesis of actin filaments (ii) This pathogen also induces a decrease in lysosomal activity on exposed hemocytes (iii) The effect of V. tapetis on the actin cytoskeleton and on the decrease in lysosomal activity is independent of the type IV secretion system (T4SS) (iv) The type IV secretion system (T4SS) is involved in the development of BRD but is not essential to induce this disease (v) In the context of BRD and of the loss of hemocyte adhesions properties in vitro, V. tapetis is able to modulate the pH of extrapallial fluids, respectively in the first days and hours of infection (vi) Finally, the "strains typing" approach based on MALDITOF makes it possible to discriminate between V. tapetis strains according to their pathogenicity with regard to Manila clam
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Borbora, Salik Miskat. "Immunological consequences of host signaling-regulated epigenetic modification(s) during mycobacterial pathogenesis." Thesis, 2020. https://etd.iisc.ac.in/handle/2005/5753.
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Introduction: Mycobacterium tuberculosis (Mtb), the principal etiological agent of pulmonary tuberculosis (TB), continues to co-evolve with the human population making itself one of the most potent infectious killer in the modern-day world. The primary site of TB infection is the lung, wherein the tubercle bacillus is taken up by phagocytic cells such as macrophages, dendritic cells as well as neutrophils. Emerging studies have also indicated that Mtb immigrates into non-myelocytic cells to ensure itself a safe niche from the concerted immune onslaught of the host. In course of infecting the host, the bacterium attunes distinct cellular processes that would otherwise contribute to bacterial clearance viz. apoptosis, autophagy, antigen presentation, cytokine responses and lipid accumulation. Interestingly, Mtb, has been shown to initiate ectopic expression of a gamut of cellular signaling pathways, by virtue of which the immune activities of the host are tempered. The current work brings to light critical signaling nodes that are deregulated upon mycobacterial infection and demonstrates key epigenetic molecules that act downstream to these signaling intermediates to aid Mtb pathogenesis. Importantly, the study builds upon the critical role(s) of NOTCH and WNT signaling pathways during Mtb infection as well as reports the significance of SLIT-ROBO pathway that was hitherto unexplored in the context of mycobacterial pathogenesis.
PART I: Elucidation of the regulation of an E3 ubiquitin ligase by Mtb-elicited epigenetic modifier.
Mtb adopts diverse strategies to impede the host-mediated immunological offenses. As one of its many shrewd strategies, Mtb generates lipid-laden cells (foamy macrophages-FMs) that offer a favorable shelter for its persistence. FMs are formed by the complex regulation of influx, metabolism, storage, and mobilization of lipid molecules. The excess accumulation of lipids is often attributed to the surge in the expression of lipid influx genes with a concomitant decrease in the lipid efflux genes. In this part, we delineated a post-translational regulation of proteins involved in lipid accrual during Mtb infection. Notably, we observed significant reduction in the expression of a specific E3 ubiquitin ligase ITCH, that allowed the sustenance of key lipid accretion molecules (ADRP and CD36), by curbing their proteasomal turnover. Further, we found the repression of ITCH to be dependent on the concerted action of the bifunctional transcription factor YY1 and an arginine methyl transferase PRMT5. NOTCH signaling pathway was identified as a master-regulator of YY1 expression, and in vitro Mtb CFU analysis using small molecule inhibitors against NOTCH and PRMT5 revealed critical roles for these molecules in regulating innate responses during mycobacterial infection.
PART II: Molecular insights into the regulation of lipid peroxidation in macrophages upon mycobacterial infection.
During infection, Mtb mediates reactive oxygen species (ROS) generation within the host cellular milieu as an auxiliary manifestation of the host defence system. ROS accumulation can contribute to myriad events within a cell, including lipid peroxidation,
which could contribute to programmed cell necrosis. Recently, it was reported that ferroptosis, a form of cell death brought about by iron overload and lipid peroxidation, contributes to cellular necrosis in macrophages upon virulent mycobacterial infection. In line with the reported observations, we evaluated the expression of key molecules implicated during lipid peroxidation in Mtb-infected macrophages. To our interest, ACSL4 and ALOX15 displayed robust upregulation upon Mtb infection in a WNT-signaling dependent manner. As a result, enhanced lipid peroxidation leading to the accumulation of copious amount of a bioactive lipid alkenal, 4-Hydroxynonenal (4-HNE), was observed in infected macrophages. Accumulation of 4-HNE bears significance as it has been shown to modulate several processes by forming covalent adducts with the nucleophilic functional groups of proteins. Besides, Gpx4, the principal selenoprotein responsible for mitigating lipid peroxidation, was found to be downregulated, consequent upon the Mtb-mediated diminished expression of SIRT1. Thus, we uncover molecular details underlying the critical process of Mtb-induced lipid peroxidation in infected macrophages and demonstrate their impact on mycobacterial survival.
PART III: Delineation of the role for SLIT-ROBO signaling during mycobacterial infection.
Continuing with our line of investigation in implicating the role of distinct signaling pathways during mycobacterial pathogenesis, we chose to scrutinize the possible role of SLIT-ROBO pathway in Mtb-infected macrophages. It might be appreciated that a seminal report suggested the role of SLIT-ROBO signaling in LPS induced endothelial inflammation and endotoxemia. Our experiments revealed that Mtb-infection, both in vitro and in vivo, enhanced the expression of SLIT2 ligand and cognate ROBO2 receptor. The elevated levels of SLIT2 was found to be associated with an enhanced phosphorylation at the Serine 28 residue of Histone3, and a consequent reduction in the repressive histone methylation signature at the Slit2 promoter. We found that the activation of SLIT-ROBO pathway contributed to an enhanced expression of VNN1, a cellular pantetheinase involved in regulating oxidative stress, in an AHR dependent manner. in vitro CFU analysis revealed compromised mycobacterial survival upon perturbation of VNN1 or AHR, thereby, indicating the important role(s) for these mediators in contributing towards mycobacterial survival. Together, we uncover additional functions for NOTCH and WNT signaling pathways in regulating cellular processes during Mtb infection. Also, we report the intricate mechanism of the activation of SLIT-ROBO pathway during mycobacterial infection and indicate its potential role in modulating crucial inflammatory mediators during Mtb pathogenesis.University Grants Commission Fellowship
Books on the topic "Infectious Disease, Host-pathogen interaction, Immunology"
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E, Kaufmann S. H., ed. Host response to intracellular pathogens. Austin, Tex: R.G. Landes, 1996.
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1968-, Rescigno Maria, ed. Dendritic cell interactions with bacteria. Cambridge, UK: Cambridge University Press, 2007.
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PhD, Henderson Brian, ed. Cellular microbiology: Bacteria-host interactions in health and disease. Chichester: J. Wiley, 1999.
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1942-, Cabello Felipe C., Pruzzo Carla, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Bacteria, complement, and the phagocytic cell. Berlin: Springer-Verlag, 1988.
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Jean-Pierre, Gorvel, ed. Intracellular pathogens in membrane interactions and vacuole biogenesis. Georgetown, Tex: Landes Bioscience, 2004.
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Hostpathogen Interactions In Streptococcal Diseases. Springer-Verlag Berlin and Heidelberg GmbH &, 2013.
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Lax, Alistair J., Michael F. Wilson, Rod McNab, and Brian Henderson. Cellular Microbiology: Bacteria-Host Interactions in Health and Disease. Wiley, 1999.
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Lax, Alistair J., Michael F. Wilson, Rod McNab, and Brian Henderson. Cellular Microbiology: Bacteria-Host Interactions in Health and Disease. Wiley, 1999.
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Rescigno, Maria. Dendritic Cell Interactions with Bacteria (Advances in Molecular and Cellular Microbiology). Cambridge University Press, 2007.
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Natural Hosts of SIV: Implication in AIDS. Elsevier Science & Technology Books, 2014.
Find full textBook chapters on the topic "Infectious Disease, Host-pathogen interaction, Immunology"
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Rohani, Pejman, Helen J. Wearing, Daniel A. Vasco, and Yunxin Huang. "Chapter Three. Understanding Host- Multipathogen Systems: Modeling the Interaction Between Ecology and Immunology." In Infectious Disease Ecology, edited by Richard S. Ostfeld, Felicia Keesing, and Valerie T. Eviner, 48–70. Princeton: Princeton University Press, 2010. http://dx.doi.org/10.1515/9781400837885.48.
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Patgiri, Himangshu, Ankita Khataniar, Pitimoni Boro, Sushmita Baishnab, and Sanchaita Rajkhowa. "Systems Biology Approaches Towards Immunity against Plasmodium." In Mosquito Research - Recent Advances in Pathogen Interactions, Immunity, and Vector Control Strategies [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104614.
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Malaria is one of the most devastating infectious diseases known to humans. It is caused by unicellular protozoan parasites belonging to the genus Plasmodium. Till date, over 200 species of Plasmodium have been formally described, and each species infects a certain range of hosts. However, the human infection is limited to only five of the species, of which P. falciparum is the most responsible. Due to the emergence of parasite resistance to frontline chemotherapies and mosquito resistance to current insecticides which threaten the control programmes, new antimalarial therapeutics or approaches capable of predicting useful models of how different cells of the innate immune system function, is the need of the hour. Systems Immunology is a relatively recent discipline under Systems Biology to understand the structure and function of the immune system and how the components of the immune system work together as a whole. Thus, this chapter aims to give insight into the approaches of Systems Biology for investigating the immune factors that are formed during Plasmodium falciparum infection in the human body. Here, the numerous experimental and computational works with the ongoing methodologies using Systems Biology approaches along with the interactions of host and pathogen will be discussed.
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Boulaki, Vasiliki, Dimitrios Vlachakis, Smaragda Sotiraki, and Sophia Kossida. "An Up-To-Date Review of Piglet Isosporosis." In Veterinary Science, 116–31. IGI Global, 2018. http://dx.doi.org/10.4018/978-1-5225-5640-4.ch006.
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Piglet isosporosis caused by Isospora suis represents a considerable problem worldwide with great economic losses and veterinary importance in pig production. So the control of this parasite is a great need. However, little is known about porcine coccidiosis concerning dynamics, pathophysiology and immunology of this disease, as well as host-parasite interactions. In addition, only few studies deal with experimental modelling of this illness with parameters such as the excretion patterns and the age-related susceptibility. However, besides natural I. suis infections occurring in pig farms, there are some experimental infections described that allow investigating accurately the course of infection. Experimental infections could contribute to a more effective control of these infections. In addition, managerial practices of farrowing facilities and piglet manipulations can contribute to this purpose. So, the description of hygiene measures, the appropriate management of farrowing facilities and piglet manipulations, as well as appropriate farm-specific environment, comprising appropriate design and materials of the farrowing pen and enough room, could diminish the occurrence and transmission of this parasite. However, unfortunately there are only very few reports documenting all this subjects that are so important for the effective control of this disease.
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E. Olguín, Jonadab, and Luis Ignacio Terrazas. "Regulation of the Immune Response in Cysticercosis: Lessons from an Old Acquainted Infection." In Current State of the Art in Cysticercosis and Neurocysticercosis. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.100137.
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In the last decades, we have learned some critical lessons about the relationship between the human body and its interaction with many infectious diseases, where regularly, the immune system has a major role in protection. We learned to differentiate between the immune response occurring in either an intracellular or extracellular parasitic infection, between innate and adaptive immune response, between either inflammatory or anti-inflammatory responses, and finally, we learned to recognize very particular mechanisms, such as the inability of the immune system to respond during very particular scenarios, such as the inability of T cells to both proliferate and produce cytokines even after their exposure to mitogens or specific-antigens. Along with our increase in the knowledge in immunology, we figured out that immunoregulation and immunosuppression are processes used by many parasites to reduce the capacity of the immune system to eliminate them, and to persist in the host favoring their transmission and also to complete their life cycles. Immunoregulation involves several mechanisms such as anergy, apoptosis, induction of both suppressive cytokines and membrane-bound molecules, as well as specialized cell populations of the immune system like regulatory T cells, Alternative Activated Macrophages, or Myeloid-derived Suppressor Cells, that together modify the outcome of the immune response. In this chapter we will review the general differences between the different types of immunoregulation, the kind of cellular populations of the immune system used by the helminths Taenia solium and Taenia crassiceps to induce immunoregulation and immunosuppression and also, the mechanisms used by these parasites such as mimicking molecules of the immune system to replace directly these mechanisms. Understanding and deciphering all these regulatory mechanisms could be useful to develop new tools to control this infection.