Relevant bibliographies by topics / Invading pathogens

Contents

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

Academic literature on the topic 'Invading pathogens'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Invading pathogens"

1

Witzell, Johanna, and Juan A. Martín. "Phenolic metabolites in the resistance of northern forest trees to pathogens — past experiences and future prospects." Canadian Journal of Forest Research 38, no. 11 (November 2008): 2711–27. http://dx.doi.org/10.1139/x08-112.

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Phenolic metabolites are frequently implicated in chemical defense mechanisms against pathogens in woody plants. However, tree breeding programmes for resistance to pathogens and practical tree-protection applications based on these compounds seem to be scarce. To identify gaps in our current knowledge of this subject, we explored some of the recent literature on the involvement of phenolic metabolites in the resistance of northern forest trees (Pinus, Picea, Betula, Populus, and Salix spp.) to pathogens. Although it is evident that the phenolic metabolism of trees is often activated by pathogen attacks, few studies have convincingly established that this induction is due to a specific defense response that is capable of stopping the invading pathogen. The role of constitutive phenolics in the resistance of trees to pathogens has also remained unclear. In future studies, the importance of phenolics in oxidative stress, cell homeostasis and tolerance, and the spatial and temporal localization of phenolics in relation to invading pathogens should be more carefully acknowledged. Possibilities for future studies using advanced methods (e.g., metabolic profiling, confocal laser scanning microscopy, and use of modified tree genotypes) are discussed.
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Mastellos, Dimitrios, and John D. Lambris. "Complement: more than a ‘guard’ against invading pathogens?" Trends in Immunology 23, no. 10 (October 2002): 485–91. http://dx.doi.org/10.1016/s1471-4906(02)02287-1.

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Islam, Waqar, Muhammad Qasim, Ali Noman, Muhammad Adnan, Muhammad Tayyab, Taimoor Hassan Farooq, Huang Wei, and Liande Wang. "Plant microRNAs: Front line players against invading pathogens." Microbial Pathogenesis 118 (May 2018): 9–17. http://dx.doi.org/10.1016/j.micpath.2018.03.008.

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Akira, Shizuo. "Innate immunity and adjuvants." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1579 (October 12, 2011): 2748–55. http://dx.doi.org/10.1098/rstb.2011.0106.

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Innate immunity was for a long time considered to be non-specific because the major function of this system is to digest pathogens and present antigens to the cells involved in acquired immunity. However, recent studies have shown that innate immunity is not non-specific, but is instead sufficiently specific to discriminate self from pathogens through evolutionarily conserved receptors, designated Toll-like receptors (TLRs). Indeed, innate immunity has a crucial role in early host defence against invading pathogens. Furthermore, TLRs were found to act as adjuvant receptors that create a bridge between innate and adaptive immunity, and to have important roles in the induction of adaptive immunity. This paradigm shift is now changing our thinking on the pathogenesis and treatment of infectious, immune and allergic diseases, as well as cancers. Besides TLRs, recent findings have revealed the presence of a cytosolic detector system for invading pathogens. I will review the mechanisms of pathogen recognition by TLRs and cytoplasmic receptors, and then discuss the roles of these receptors in the development of adaptive immunity in response to viral infection.
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DUCROT, ARNAUD, and MICHEL LANGLAIS. "TRAVELLING WAVES IN INVASION PROCESSES WITH PATHOGENS." Mathematical Models and Methods in Applied Sciences 18, no. 03 (March 2008): 325–49. http://dx.doi.org/10.1142/s021820250800270x.

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This work is devoted to the study of a singular reaction–diffusion system arising in modelling the introduction of a lethal pathogen within an invading host population. In the absence of the pathogen, the host population exhibits a bistable dynamics (or Allee effect). Earlier numerical simulations of the singular SI model under consideration have exhibited stable travelling waves and also, under some circumstances, a reversal of the wave front speed due to the introduction of the pathogen. Here we prove the existence of such travelling wave solutions, study their linear stability and give analytical conditions yielding a reversal of the wave front speed, i.e. the invading host population may eventually retreat following the introduction of the lethal pathogen.
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Qiao, Yongli, Rui Xia, Jixian Zhai, Yingnan Hou, Li Feng, Yi Zhai, and Wenbo Ma. "Small RNAs in Plant Immunity and Virulence of Filamentous Pathogens." Annual Review of Phytopathology 59, no. 1 (August 25, 2021): 265–88. http://dx.doi.org/10.1146/annurev-phyto-121520-023514.

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Gene silencing guided by small RNAs governs a broad range of cellular processes in eukaryotes. Small RNAs are important components of plant immunity because they contribute to pathogen-triggered transcription reprogramming and directly target pathogen RNAs. Recent research suggests that silencing of pathogen genes by plant small RNAs occurs not only during viral infection but also in nonviral pathogens through a process termed host-induced gene silencing, which involves trans-species small RNA trafficking. Similarly, small RNAs are also produced by eukaryotic pathogens and regulate virulence. This review summarizes the small RNA pathways in both plants and filamentous pathogens, including fungi and oomycetes, and discusses their role in host–pathogen interactions. We highlight secondarysmall interfering RNAs of plants as regulators of immune receptor gene expression and executors of host-induced gene silencing in invading pathogens. The current status and prospects of trans-species gene silencing at the host–pathogen interface are discussed.
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Cipriano, Michael J., and Stephen L. Hajduk. "Drivers of persistent infection: pathogen-induced extracellular vesicles." Essays in Biochemistry 62, no. 2 (April 17, 2018): 135–47. http://dx.doi.org/10.1042/ebc20170083.

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Extracellular vesicles (EVs) are produced by invading pathogens and also by host cells in response to infection. The origin, composition, and function of EVs made during infection are diverse and provide effective vehicles for localized and broad dissimilation of effector molecules in the infected host. Extracellular pathogens use EVs to communicate with each other by sensing the host environment contributing to social motility, tissue tropism, and persistence of infection. Pathogen-derived EVs can also interact with host cells to influence the adhesive properties of host membranes and to alter immune recognition and response. Intracellular pathogens can affect both the protein and RNA content of EVs produced by infected host cells. Release of pathogen-induced host EVs can affect host immune responses to infection. In this review, we will describe both the biogenesis and content of EVs produced by a number of diverse pathogens. In addition, we will examine the pathogen-induced changes to EVs produced by infected host cells.
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Slimmen, Lisa J. M., Hettie M. Janssens, Annemarie M. C. van Rossum, and Wendy W. J. Unger. "Antigen-Presenting Cells in the Airways: Moderating Asymptomatic Bacterial Carriage." Pathogens 10, no. 8 (July 28, 2021): 945. http://dx.doi.org/10.3390/pathogens10080945.

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Bacterial respiratory tract infections (RTIs) are a major global health burden, and the role of antigen-presenting cells (APCs) in mounting an immune response to contain and clear invading pathogens is well-described. However, most encounters between a host and a bacterial pathogen do not result in symptomatic infection, but in asymptomatic carriage instead. The fact that a pathogen will cause infection in one individual, but not in another does not appear to be directly related to bacterial density, but rather depend on qualitative differences in the host response. Understanding the interactions between respiratory pathogens and airway APCs that result in asymptomatic carriage, will provide better insight into the factors that can skew this interaction towards infection. This review will discuss the currently available knowledge on airway APCs in the context of asymptomatic bacterial carriage along the entire respiratory tract. Furthermore, in order to interpret past and futures studies into this topic, we propose a standardized nomenclature of the different stages of carriage and infection, based on the pathogen’s position with regard to the epithelium and the amount of inflammation present.
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Hendricks, Matthew R., and Jennifer M. Bomberger. "Who's really in control: microbial regulation of protein trafficking in the epithelium." American Journal of Physiology-Cell Physiology 306, no. 3 (February 1, 2014): C187—C197. http://dx.doi.org/10.1152/ajpcell.00277.2013.

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Due to evolutionary pressure, there are many complex interactions at the interface between pathogens and eukaryotic host cells wherein host cells attempt to clear invading microorganisms and pathogens counter these mechanisms to colonize and invade host tissues. One striking observation from studies focused on this interface is that pathogens have multiple mechanisms to modulate and disrupt normal cellular physiology to establish replication niches and avoid clearance. The precision by which pathogens exert their effects on host cells makes them excellent tools to answer questions about cell physiology of eukaryotic cells. Furthermore, an understanding of these mechanisms at the host-pathogen interface will benefit our understanding of how pathogens cause disease. In this review, we describe a few examples of how pathogens disrupt normal cellular physiology and protein trafficking at epithelial cell barriers to underscore how pathogens modulate cellular processes to cause disease and how this knowledge has been utilized to learn about cellular physiology.
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Perry, William J., Jeffrey M. Spraggins, Jessica R. Sheldon, Caroline M. Grunenwald, David E. Heinrichs, James E. Cassat, Eric P. Skaar, and Richard M. Caprioli. "Staphylococcus aureus exhibits heterogeneous siderophore production within the vertebrate host." Proceedings of the National Academy of Sciences 116, no. 44 (October 14, 2019): 21980–82. http://dx.doi.org/10.1073/pnas.1913991116.

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Siderophores, iron-scavenging small molecules, are fundamental to bacterial nutrient metal acquisition and enable pathogens to overcome challenges imposed by nutritional immunity. Multimodal imaging mass spectrometry allows visualization of host−pathogen iron competition, by mapping siderophores within infected tissue. We have observed heterogeneous distributions of Staphylococcus aureus siderophores across infectious foci, challenging the paradigm that the vertebrate host is a uniformly iron-depleted environment to invading microbes.
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Dissertations / Theses on the topic "Invading pathogens"

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Toms, Christy L. V. "The use of embryonic stem cell technology to investigate the role of transcription factors in the differentiation of CD4⁺T cell subsets." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275203.

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Kaczowka, Angela M., and Angela M. Kaczowka. "Variation in Immune Response Among Native and Invading Genotypes of Yellow Starthistle (Centaurea solstitialis)." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/624147.

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Invasive plants may leave enemies behind when they colonize a new habitat, allowing selection to favor increased investment in growth and/or reproduction over defensive traits. Previous studies have identified reduced diversity of potential bacterial pathogens and evolutionary increases in growth and reproduction in invading populations of yellow starthistle (Centaurea solstitialis). This study leverages a recently developed high-throughput assay of immune function to test for evidence of a trade-off between increased growth and defense against bacterial pathogens in yellow starthistle's invasion of California (USA). Seven bacterial strains were cultured from infected leaf tissue in the native range. Healthy leaf tissue from five native European collections and six invading collections were exposed to these native bacterial strains. A standardized assay of peroxidase activity was used measure the oxidative burst immune response to pathogen recognition by the leaf. Immune responses were compared to plant growth within and between ranges to assess evidence for a trade-off. Plant genotypes from the native range demonstrated a higher immune response to bacterial strains than did invading genotypes, consistent with a trade-off with plant growth across regions. The same trade-off was also apparent across genotypes from the native range, but not across genotypes from the invaded range. Our results provide evidence that increased growth in a highly invasive plant species may come at a cost to immune function, consistent with the hypothesis that escape from enemies can provide opportunities for shifts in resource allocation that favor the proliferation of non-native species.
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Fernandez, Garcia Elena. "Use of the fungal pathogen Hirsutella cryptosclerotium sp. nov. for the biocontrol of Rastrococcus invadens (Pseudococcidae)." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46295.

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Books on the topic "Invading pathogens"

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Gow, Neil A. R., and Alistair J. P. Brown. Physiology and metabolism of fungal pathogens. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0003.

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The metabolism and physiology of an invading fungal pathogen determine the outcome of its interaction with the host. The pathogen must be able to assimilate nutrients to grow and colonize diverse host niches. Meanwhile, the host attempts to restrict this growth by withholding some essential nutrients, by imposing stresses, and by inducing innate immune defences. These interactions involve complex regulatory networks that ultimately dictate the equilibrium between pathogen killing and the establishment of commensal or pathogenic associations.
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Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.

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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
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Galley, Helen F., and Heather M. Wilson. Immune system physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0010.

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The immune system provides protection against invading pathogens, foreign cells including tumour cells, and macromolecules. It comprises an early, non-specific, innate immune response and a later, specific, adaptive immune response that helps prevent disease or recurrence of disease. Innate and adaptive immune systems work together with mutual interactivity distinguishing ‘self’ from ‘non-self components’ to provide effective immune responses and prevent infection. This chapter describes the basic processes involved in immune responses and illustrates the particular relevance for some disease processes as well as highlighting stresses associated with anaesthesia and surgery that can modulate responses.
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Lalvani, Ajit, and Katrina Pollock. Defences against infection. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0303.

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The immune system is classified into a series of component parts, each specialized to defend the host against infection. Cells of the innate immune system are distributed throughout the body, in the tissues, and in the circulation, to defend against the first signs of danger, combining the acute inflammatory response with the ability to kill and remove invading pathogens. Monocytes, macrophages, and neutrophils phagocytose and kill exogenous and endogenous targets, using both oxygen-dependent and oxygen-independent mechanisms. The adaptive immune system creates a structurally specific and prolonged response, mediated by lymphocytes to clear infection and generate immunological memory. In this chapter, the functions of the innate and adaptive immune system are reviewed, together with the clinical features and investigation of acquired and inherited immune deficiencies.
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Eljaafari, Assia, and Pierre Miossec. Cellular side of acquired immunity (T cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0049.

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The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites, and Th17 cells act against extracellular bacteria and fungi that are not cleared by Th1 and Th2 cells. Among the new subsets, Th22 cells protect against disruption of epithelial layers secondary to invading pathogens. Finally these effector subsets are regulated by regulatory T cells. These T helper subsets counteract each other to maintain the homeostasis of the immune system, but this balance can be easily disrupted, leading to chronic inflammation or autoimmune diseases. The challenge is to detect early changes in this balance, prior to its clinical expression. New molecular tools such as microarrays could be used to determine the predominant profile of the immune effector cells involved in a disease process. Such understanding should provide better therapeutic tools to counteract deregulated effector cells.
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Ali, Ased. Pathogenesis of urinary tract infection. Edited by Rob Pickard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0001.

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The realization of the harms resulting from indiscriminate use of antibiotics for minor infection has added impetus to the need to understand better the interaction between urogenital tract epithelium and invading bacteria during the initial stages of urinary tract infection (UTI). It is thought that uropathogenic Escherichia coli clones develop in the gut and migrate across the perineum to the urethra and up into the bladder. The response of the epithelium to bacterial adherence and the evolution of the invading bacteria will then govern the clinical consequences. These can vary between rapid invasion and further migration to produce systemic sepsis to tolerance of the bacteria in a planktonic state in asymptomatic bacteriuria. The key to these differences is the activation of epithelial pathogen-associated molecular pattern receptors by expressed proteins on the bacterial cell wall. Increased understanding of these interactions will lead to non-antibiotic-based strategies for clinical management of urinary infection.
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Book chapters on the topic "Invading pathogens"

1

Voll, Reinhard E., and Barbara M. Bröker. "Innate vs acquired immunity." In Oxford Textbook of Rheumatology, 356–64. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048_update_001.

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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens’ life cycles. Hence, escape mutants strongly reduce the pathogen’s fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
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2

Kaur, Sandeep, Mandeep Kaur Panaich, Simrat Kaur Virk, Mahima Choudhary, Chandni Sharma, Sunita Chauhan, Parul Chadha, and Vandana Sharma. "Prophylactic and Therapeutic Role of Human Breast Milk Proteins and Bioactive Peptides against Neonatal Bacterial Infections." In Infant Feeding - Breast versus Formula. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.91865.

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Breast milk represents nature’s best mechanism to provide complete nourishment and protection to the newborn. Human breast milk acts as a store house of an array of bioactive factors, which includes antimicrobial proteins and antimicrobial peptides that confer early protection while lowering the incidence of developing various infections and exhibiting immune modulation property to activate the immune cells to fight against the invading pathogens. Among the bioactive peptides, endogenous peptides present in breast milk have opened a new window of research on studying their unique mechanisms of action. This will help in incorporating these peptides in formula milk for meeting special needs where breastfeeding is not possible. The present chapter aims to give a deep insight into the various antimicrobial peptides and the newly reported endogenous peptides in human breast milk with emphasis on their levels and activity in preterm milk as data related to this is lacking and preterm newborns are highly vulnerable to acquire infections. Further, the chapter focuses on highlighting the antibacterial mechanisms adopted by the bioactive peptides for protection against the neonatal bacterial pathogens with special emphasis on the infections caused by resistant bacterial strains in hospital settings (neonatal wards) and their future implications.
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Eljaafari, Assia, and Pierre Miossec. "Cellular side of acquired immunity (T cells)." In Oxford Textbook of Rheumatology, 365–70. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0049_update_001.

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Abstract:
The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites, and Th17 cells act against extracellular bacteria and fungi that are not cleared by Th1 and Th2 cells. Among the new subsets, Th22 cells protect against disruption of epithelial layers secondary to invading pathogens. Finally these effector subsets are regulated by regulatory T cells. These T helper subsets counteract each other to maintain the homeostasis of the immune system, but this balance can be easily disrupted, leading to chronic inflammation or autoimmune diseases. The challenge is to detect early changes in this balance, prior to its clinical expression. New molecular tools such as microarrays could be used to determine the predominant profile of the immune effector cells involved in a disease process. Such understanding should provide better therapeutic tools to counteract deregulated effector cells.
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4

Ponist, Silvester, Katarina Pruzinska, and Katarina Bauerova. "Inflammation in the Pathogenesis of Rheumatoid Arthritis and in Experimental Arthritis: Evaluation of Combinations of Carnosic Acid and Extract of Rhodiola rosea L. with Methotrexate." In Inflammation [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99073.

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The host immune response generates the pro-inflammatory immune response as a protective measure against invading pathogens, allergens, and/or trauma. However, dysregulated and chronic inflammation may result in secondary damage to tissues and immune pathology to the host. Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease which primarily involves synovial inflammation, joint pain, immobility, and stiffness. Increased infiltration of inflammatory immune cells and fibroblast-like synoviocytes into joints, form pannus and small blood vessels that lead to synovium and cartilage destruction. In this chapter we will focus on the role of inflammatory cytokines (IL-1β, IL-6 and IL-17), chemokine monocyte chemotactic protein-1 and matrix metalloproteinase-9 in the pathogenesis of experimental arthritis in animals and in human RA. Further, we will be discussing about methotrexate’s (cornerstone of anti-rheumatic therapy) immune suppressing activity, anti-inflammatory properties of carnosic acid and extract of Rhodiola rosea L., and their innovative combination treatments with methotrexate in rat adjuvant arthritis.
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Lucchesi, John C. "Developmental systems and their dysfunction." In Epigenetics, Nuclear Organization & Gene Function, 254–72. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.003.0022.

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A specific function performed by the brain is learning—new information is stored as short-term memory by the activation of the transcription factor CREB, and as long-term memory by DNA methylation and demethylation of specific genes. Learning also involves a neuron-specific remodeling complex (BAF) and several micro RNAs (miRNAs) and long non-coding (lncRNAs). Rubinstein–Taybi, Rett or fragile X syndromes, as well as Alzheimer’s, Parkinson’s or Huntington’s diseases, involve epigenetic alterations. Epigenetic misregulation occurs in cardiopathies such as Wolf–Hirschhorn and Kabuki syndromes. The innate immune system consists of cells that can destroy invading bacteria and virus-infected cells, and of circulating proteins that destroy pathogens. The adaptive immune system consists of macrophages and dendritic cells, T lymphocytes and B lymphocytes. Failure to recognize antigens as one’s own leads to autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Cells from RA and SLE patients exhibit changes in histone acetyl transferases, deacetylases and methyl transferases, and in miRNAs. Arginines can be converted to citrulline, and citrullinated proteins are considered as non-self by the immune system. RA is characterized by the presence of autoantibodies against citrullinated peptides.
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Reports on the topic "Invading pathogens"

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Harms, Nathan, Judy Shearer, James Cronin, and John Gaskin. Geographic and genetic variation in susceptibility of Butomus umbellatus to foliar fungal pathogens. Engineer Research and Development Center (U.S.), August 2021. http://dx.doi.org/10.21079/11681/41662.

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Large-scale patterns of plant invasions may reflect regional heterogeneity in biotic and abiotic factors and genetic variation within and between invading populations. Having information on how effects of biotic resistance vary spatially can be especially important when implementing biological control because introduced agents may have different Impacts through interactions with host-plant genotype, local environment, or other novel enemies. We conducted a series of field surveys and laboratory studies to determine whether there was evidence of biotic resistance, as foliar fungal pathogens, in two introduced genotypes (triploid G1, diploid G4) of the Eurasian wetland weed, Butomus umbellatus L. in the USA. We tested whether genotypes differed in disease attack and whether spatial patterns in disease incidence were related to geographic location or climate for either genotype. After accounting for location (latitude, climate), G1 plants had lower disease incidence than G4 plants in the field (38% vs. 70%) but similar pathogen richness. In contrast, bioassays revealed G1 plants consistently received a higher damage score and had larger leaf lesions regardless of pathogen. These results demonstrate that two widespread B. umbellatus genotypes exhibit different susceptibility to pathogens and effectiveness of pathogen biological controls may depend on local conditions.
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