Relevant bibliographies by topics / Infection, Immunity and Inflammation

Academic literature on the topic 'Infection, Immunity and Inflammation'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Infection, Immunity and Inflammation"

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Kumar, Rajiv. "Routes of Infections, Inflammation, Immunity, Immunity Response and Inflammatory Injury: Elucidation of a Biological Fight." Immunology and Inflammation Diseases Therapy 5, no. 1 (January 13, 2022): 01–04. http://dx.doi.org/10.31579/2637-8876/028.

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Infections, inflammation, immunity, and inflammatory injury are different segments of biological events and link up altogether. Route of infection has no similarity with the cellular signaling pathway of inflammation, even though when inflammation is induced by infection. The organism responds toward infection that is initiated by the pathogen via inflammation, which is a natural way of defense initiated by innate immunity as a safeguard
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Cherneva, R., and Z. Cherneva. "Infection, Inflammation and Immunity in Covid-19 Infection." Acta Medica Bulgarica 48, no. 3 (October 1, 2021): 77–82. http://dx.doi.org/10.2478/amb-2021-0040.

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Abstract The COVID-19 pandemic caused by the SARS-CoV-2 has increased the burden on healthcare system. Despite some progress in its diagnostics has been made, effective prevention and treatment are still insufficient. Since SARS-CoV-2 infections often cause systemic inflammation and multiple organ failure, the therapeutic options aimed at modulating the host immune responses to prevent subsequent systemic complications are demanding. The review provides a summary of the SARS-CoV-2 virus infection and underlines the current perception of pulmonary host’s immune response and its contributions to disease severity and systemic inflammation. Signaling pathways which have the potential to manipulate host immunity and improve clinical outcomes are also presented.
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Chmiela, Magdalena, and Pierre Michetti. "Inflammation, Immunity, Vaccines for Helicobacter Infection." Helicobacter 11, s1 (October 2006): 21–26. http://dx.doi.org/10.1111/j.1478-405x.2006.00422.x.

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Pachner, Andrew R., and Israel Steiner. "Lyme neuroborreliosis: infection, immunity, and inflammation." Lancet Neurology 6, no. 6 (June 2007): 544–52. http://dx.doi.org/10.1016/s1474-4422(07)70128-x.

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Libby, Peter, Joseph Loscalzo, Paul M. Ridker, Michael E. Farkouh, Priscilla Y. Hsue, Valentin Fuster, Ahmed A. Hasan, and Salomon Amar. "Inflammation, Immunity, and Infection in Atherothrombosis." Journal of the American College of Cardiology 72, no. 17 (October 2018): 2071–81. http://dx.doi.org/10.1016/j.jacc.2018.08.1043.

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Deretic, Vojo, Tatsuya Saitoh, and Shizuo Akira. "Autophagy in infection, inflammation and immunity." Nature Reviews Immunology 13, no. 10 (September 25, 2013): 722–37. http://dx.doi.org/10.1038/nri3532.

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Permin, Henrik, and Leif P. Andersen. "Inflammation, Immunity, and Vaccines for Helicobacter Infection." Helicobacter 10, s1 (September 2005): 21–25. http://dx.doi.org/10.1111/j.1523-5378.2005.00337.x.

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Meiers, Joscha, Eike Siebs, Eva Zahorska, and Alexander Titz. "Lectin antagonists in infection, immunity, and inflammation." Current Opinion in Chemical Biology 53 (December 2019): 51–67. http://dx.doi.org/10.1016/j.cbpa.2019.07.005.

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Raffler, Nikolai A., Jesús Rivera-Nieves, and Klaus Ley. "L-selectin in inflammation, infection and immunity." Drug Discovery Today: Therapeutic Strategies 2, no. 3 (September 2005): 213–20. http://dx.doi.org/10.1016/j.ddstr.2005.08.012.

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Huang, Y., C. Zhao, and X. Su. "Neuroimmune regulation of lung infection and inflammation." QJM: An International Journal of Medicine 112, no. 7 (July 16, 2018): 483–87. http://dx.doi.org/10.1093/qjmed/hcy154.

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Abstract The distal airway of the lung is innervated by vagus nerve. Upon stimulation, vagus nerve endings release acetylcholine or neuropeptides via C-fiber afferents to regulate lung infection and immunity. Vagal sensory nerve endings, brain integration center, acetylcholine and α7 nicotinic acetylcholine receptor (nAChR) expressing cells are key components of pulmonary parasympathetic inflammatory reflex. Meanwhile, this local machinery synergizes with spleen (as a functional hub of cholinergic anti-inflammatory pathway) to finely tune recruitment of the splenic α7 nAChR+CD11b+ cells into the inflamed lungs during lung infection. Recent studies have showed that lung group 2 innate lymphoid cells (ILC2) express both α7 nAChR and neuropeptide receptors. Acetylcholine and neuropeptides can regulate ILC2 and reshape pulmonary infection and immunity. Among the airway epithelial cells, pulmonary neuroendocrine cells are rare cell population; however, these cells are innervated by sensory nerve endings and they could secrete neuropeptides that influence lung infection and immunity.
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Dissertations / Theses on the topic "Infection, Immunity and Inflammation"

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Phan, Quang Tien. "Innate immune response to tissue-specific infection : notochord infection in the zebrafish embryo." Thesis, Montpellier, 2016. http://www.theses.fr/2016MONTT082/document.

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Lors des infections bactériennes, selon les tissus infectés, et selon la nature des pathogènes, l’organisme répond en mobilisant différents acteurs. Nous avons décidé d’utiliser le modèle du zebrafish ou Danio rério pour étudier la réponse immunitaire innée dans les situations d’infection bactérienne où les phagocytes professionnels ne peuvent pas venir au contact direct des bactéries. Pour cela, j’ai développé un modèle d’infection de la notochorde del’embryon de zebrafish. Lors de l’injection des bactéries dans ce compartiment, les bactéries se retrouvent protégées par une épaisse gaine de collagènes que les phagocytes ne peuvent pas pénétrer. Alors que les mycobactéries,protégées par la gaine de collagène ne sont pas détectées par les phagocytes, les bactéries E. coli sont immédiatement détectées ce qui déclenche une importante inflammation locale autour de la notochorde. Alors que les bactéries E. coli, bien qu’inaccessibles à la phagocytose sont éliminées dans les première 24 heures qui suivent l’injection, l’inflammation dure plusieurs jours.J’ai étudié les mécanismes qui conduisent à cette inflammation persistante et ses conséquences à long terme sur le développement du poisson. J’ai montré le rôle central de la cytokine IL1b dans ce processus, et j’ai développé une lignée transgénique qui permet d’étudier l’induction de cette cytokine in vivo chez le poisson.J’ai ensuite étudié le rôle des deux principales populations de phagocytes dans l’élimination des bactéries E coli. J’ai montré que les macrophages ne sont pas impliqués dans la disparition des bactéries alors que les neutrophiles, bien qu’incapable de pénétrer à l’intérieur de la gaine de collagène sont nécessaires à l’élimination des bactéries.J’ai ensuite montré que la myelopéroxidase et le monoxyde d’azote ne sont pas impliqués dans l’élimination des bactéries alors que les espèces réactives de l’oxygène produites par les neutrophiles sont nécessaires pour éradiquer l’infection
In bacterial infections, according to the infected tissue and the nature of pathogens, the body responds by mobilizing various actors. I decided to use zebrafish or Danio rerio model to study the innate immune response to bacterial infection in the situations that professional phagocytes cannot come in direct contact with the bacteria. For this, I developed a model of infection in the notochord of zebrafish embryo. Upon injection of bacteria in this compartment, the microbes find themselves protected by the thick collagensheath where the phagocytes cannot penetrate. While mycobacteria are not detected by phagocytes; E. coli bacteria are sensed and a significant local inflammation around the notochord is mounted. The E. coli, although inaccessible to phagocytosis are eliminated within the first 24 hours after injection, the inflammation lasts several days.I studied the mechanisms that lead to this persistent inflammation and its long term consequences on the development of the fish. I showed the central role of the cytokine IL1B in this process, and I developed a transgenic line that allows studying in vivo the induction of this cytokine in fish.I then studied the roles of the two main populations of phagocytes in the elimination of E. coli. I revealed that macrophages are not involved in the removal of bacteria but neutrophils, although unable to penetrate inside the collagen casing, are necessary for the bacterial elimination. I also confirmed that myeloperoxidase and nitrogen monoxide are not involved in the removal of bacteria, rather the reactive oxygen species produced by neutrophils are needed to eradicate the infection
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Ragheb, Ramy. "Etude de l'intéraction entre inflammation et infection chez la drosophile." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4104.

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In mammals, both sterile wounding and infection induce inflammation and activate the innate immune system, and combining both challenges can lead to severe health defects, revealing that the balance between the intensity and resolution of the inflammatory response is central for the organism's fitness. The underlying mechanisms remain however elusive. Using Drosophila as a model, we show that a sterile wounding induces a reduced resistance to a bacterial challenge and is accompanied by an increased host mortality upon infection. We further investigate the underlying molecular mechanisms of flies susceptibility to bacterial infection by comparing the transcriptome landscape of SH flies (Simple Hit: infection only), DH flies (Double Hit: trauma + infection) and control flies (sterile trauma alone) during the early steps. We observed that genes with increased expression in DH flies compared to SH ones are significantly enriched for stress related annotations, including members of the JNK pathway and demonstrate that the JNK pathway plays a central role in the DH phenotype. In addition, the CrebA/Creb3-like transcription factor and its targets are up regulated in SH flies and we show that CrebA is required for mounting the innate immune response. We also investigated the potential role of the TNF receptor grnd in SH and DH flies. Our results reveal its function in innate immune response since flies with reduced grnd function display reduced viability upon infection. Drosophila thus appears as a relevant model to investigate the complex interactions between inflammation and infection and allows to unravel key pathways involved in the acquisition of a hyper-inflammatory state
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Lajunen, T. (Taina). "Persistent Chlamydia pneumoniae infection, inflammation and innate immunity." Doctoral thesis, University of Oulu, 2008. http://urn.fi/urn:isbn:9789514289965.

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Abstract Chlamydia pneumoniae is an obligatory intracellular pathogen that causes upper and lower respiratory tract infections. Like other Chlamydial species, also C. pneumoniae has a tendency to cause persistent infections, which have been associated with different cardiovascular, neurological, and respiratory diseases. In addition, a few studies have reported an association between C. pneumoniae seropositivity and an elevated body mass index (BMI), and it has been shown that C. pneumoniae is capable of infecting preadipocytes and adipocytes. The main aims of this study were to study if certain gene polymorphisms regulate the serum levels of innate immunity and inflammation proteins, and if the polymorphisms are associated with markers of C. pneumoniae infection; to compare different methods in detection of C pneumoniae in atherosclerotic tissue; and to study if serum levels of chlamydial LPS (cLPS) are associated with BMI. The serum levels of inflammatory and innate immunity markers, namely interleukin 6 (IL-6), C-reactive protein (CRP), LPS-binding protein (LBP), and soluble CD14, in apparently healthy individuals were found to correlate with each other and possibly be regulated by the polymorphisms of genes important in inflammation and innate immunity. Especially the serum LBP levels may be regulated by the LBP (rs2232618) and toll-like receptor 4 (rs4986790) polymorphisms. The IL-6 (rs1800795) polymorphism was found to be associated with C. pneumoniae antibody positivity. C. pneumoniae DNA and cLPS could be found from atherosclerotic tissue. A new, cLPS enzyme immunoassay method was developed in this study, and it might provide a standardized, commercial method for the detection of chlamydia in tissue samples, if the sensitivity of the method could be increased e.g. by testing multiple pieces of tissue. In situ hybridization method was found to be complicated by technical problems and the repeatability of polymerase chain reaction was poor. C. pneumoniae IgG positivity and elevated serum cLPS and CRP levels were associated with an elevated BMI. There was also a strong association between cLPS levels and inflammation as measured by CRP levels. The lack of association between serum total endotoxin activity and BMI implies that the association between infection and an elevated BMI may be specific to certain pathogens.
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Thursfield, Rebecca Marie. "Infection, inflammation & innate immunity in the paediatric CF airway." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/43757.

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This thesis focuses on infection and immunity within the airways in cystic fibrosis (CF), particularly the role of the antimicrobial peptides (part of the innate immune system) and their relationship to vitamin D status. Vitamin D response elements have been identified in the genes encoding the antimicrobial peptides cathelicidin (LL37) and human β defensins (HBD-2) and in-vitro vitamin D significantly induces expression of these peptides in both CF and non-CF bronchial epithelial cells. As innate defence is pivotal to airway health and is one of the proposed ways that vitamin D deficiency contributes to worsening respiratory health, this thesis will consider first immunity of the normal airway and the interactions with vitamin D and then discuss the pathophysiology of CF and the role of vitamin D on the innate immune system within CF. The role of vitamin D on infection and inflammation in the airways of infants with CF is explored and the impact of Vitamin D levels seen immunologically and functionally over the first year of life is described. Finally the role of vitamin D as an immunomodulatory molecule is explored in a greater range of CF disease severity and age. Through the various parameters explored, in different CF patient populations, the conclusion remains the same; vitamin D deficiency is not associated with increased infection, greater inflammation nor a worse clinical outcome. The possible reasons for the lack of any relationship are discussed in the final chapter; either a missed signal because the levels studied were on the low or high flat parts of a 2 sigmoid relationship thus effects seen only in really severe deficiency or because supra-high levels are needed to see any effect, the effect being lost in the inflammation seen within the CF airway or a true lack of relationship.
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Blackshaw, Sasha. "The manipulation of inflammation, immunity and infection by novel derivatives of halichlorine." Thesis, Manchester Metropolitan University, 2017. http://e-space.mmu.ac.uk/618825/.

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Halichlorine 1 is a marine spirocyclic alkaloid, which has shown to exhibit anti-inflammatory properties.1 Due to the complexity of this structure, and the low abundance in nature, the development of total and partial syntheses of this compound have become of interest to the organic chemist. This project aimed to evaluate the therapeutic potential of this class of compounds by producing a library of simplified halichlorine derivatives by addition of Grignard reagents onto a key spironitrone that maps onto the core structure of halichlorine and thence to monitor potential bioactivity by conducting a series of biological assays to determine what effects these compounds have on human U937 cells. Addition of a wide range of Grignard reagents to spironitrone 128 was successful and generally proceed with high diastereoselectivity. In addition, reductive cleavage of the resulting N-hydroxyspirocycles with Zn/AcOH provided a host of N-acetyl-C7-substiuted spirocyclic derivatives 167-172. Reduction with indium provided free amines 173-181. As additions to spironitrone 128 proceeded with undesired stereoselectivity attempts were made to access O-protected spironitrone 204 by oxidation of spiroamines such as 199. This strategy was unsuccessful. In order to explore alternative spirocyclic derivatives, synthetic studies were also directed in attempts to access un-substituted derivatives by ring closing metathesis (RCM) of diene precursors 222-224. While RCM substrates were accessed cyclisation of these did not proceed. It was discovered that heating 6,5-spiroisoxazolidine 102 under pressure in a microwave reactor provided access to the corresponding 6,6-isomer 164 which maps onto the core structure of the amphibian toxin histrionicotoxin (HTX). Oxidation to 6,6-spironitrone 192, as followed by conversion to cycloadducts 193-195, which represent new analogues of the HTX family of alkaloids. Grignard additions to this nitrone, did not proceed in general. Biological screenings using undifferentiated and LPS activated U937 cells helped to identify a number of biologically active derivatives, when tested in the NO and growth and viability assays. The NO assay using LPS activated cells, identified that the adducts containing larger alkyl or aryl chains, particularly the pentyl, hexyl and benzyl adducts, expressed significant differences in NO inhibition at both 10-4 M and 10-5 M concentrations tested, compared to the untreated cells.
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Maurer, Kirk J. "A systematic evaluation of the role of infection, immunity and inflammation in cholesterol gallstone pathogenesis." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/39917.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Biological Engineering Division, 2007.
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Cholesterol gallstones are exceptionally common and cost nearly 10 billion U.S. dollars annually. Despite a half-century of basic and clinical research questions still remain about cholesterol gallstone pathogenesis. The purpose of the study presented herein is to analyze the roles of infection, and immunity in cholelithogenesis. The first two aims of this work were to analyze the role of enterohepatic Helicobacter spp. and the human gastric pathogen H. pylori in cholesterol gallstone formation. To test this, we prospectively infected C57UJ mice with a variety of Helicobacter spp. and fed infected and uninfected mice a lithogenic diet for eight weeks and analyzed biliary phenotype. Mice infected with H. bilis or coinfected with H. hepaticus and H. rodentium and fed a lithogenic diet developed cholesterol gallstones at 80% prevalence compared with approximately 10% in uninfected controls (P<0.05). Monoinfections with H. hepaticus, H. cinaedi, H. rodentium, and H. pylori gave a cholesterol gallstone prevalence of 40% (P<0.05), 30%, 20% and 20%, respectively; with the exception of H. hepaticus, cholesterol gallstone formation in these groups did not differ significantly from uninfected animals.
(cont.) These findings suggest that some Helicobacter spp. play a role in the cholesterol gallstone formation in mice and perhaps humans. We further hypothesized that inflammation and immunity were important in cholesterol gallstone formation and that cholelithogenic bacteria were promoting gallstones through immune stimulation. To test this we utilized BALB/c and isogenic Rag2-/- mice. When fed a lithogenic diet for eight-weeks, wild-type mice developed cholesterol gallstones (27-80% prevalence) significantly more than Rag2-/- mice (~5%, P<0.05). Transfer of functional splenocytes, or T-lymphocytes to Rag2-/- mice markedly increased cholesterol gallstone formation (26% and 40% respectively, P<0.05) whereas transfer of B-cells did not (13%). The presence of T-cells and solid cholesterol monohydrate crystals induced proinflammatory cytokine expression in the gallbladder. These studies indicate that T-cells are critical in murine cholelithogenesis and function by promoting gallbladder inflammation. In summary, these results illustrate that microbial pathogens can influence cholesterol gallstone formation; this most likely occurs by modulating the immune response with T-cells being a critical component in this immunomodulation.
by Kirk J. Maurer.
Ph.D.
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Wachholz, Kristina Lora Catherine. "Placental Infection by Salmonella Typhimurium in a Murine Model: The Role of Innate Immune Mediators in Cell Death at the Fetal-Maternal Interface." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34190.

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Maternal tolerance during pregnancy increases the risk of infection with certain intracellular pathogens such as Salmonella enterica serovar Typhimurium (S.Tm). Systemic S.Tm infection during pregnancy in normally resistant 129X1/SvJ mice, with a functional natural resistance-associated macrophage protein-1 (Nramp1), leads to severe placental infection followed by fetal and maternal death. We hypothesized infection-induced inflammatory trophoblast cell death contributes to adverse pregnancy outcomes. We therefore investigated the kinetics of systemic and oral S.Tm infection in wild-type and gene deficient mice with defects in specific inflammatory pathways. Systemic infection with S.Tm resulted in preferential placental replication compared to other tissues in Nramp1+/+ mice. At 24 hours, <25% of individual placentas per mouse were infected, progressively increasing to >75% by 72 hours which correlated with a steady increase in resorption rates. Moreover, placental infection was associated with increased neutrophils, macrophages and natural killer cells whereas neutrophil numbers in the spleen remained unchanged, suggesting dichotomous modulation of inflammation in the systemic compartment compared to the feto-maternal interface. Oral infection resulted in systemic dissemination of the bacteria, substantial placental colonization and fetal loss five days post-infection in C57BL/6J mice. Systemic infection in pregnant cell death deficient Rip3-/-Nramp1+/+ mice (with defective necroptosis) resulted in decreased fetal demise relative to Nramp1+/+ and Caspase-1,11-/-Nramp1+/+ mice (with defective pyroptosis) suggesting a role for necroptotic inflammation. This study provides insight into the kinetics and mechanism of inflammation and cell death during placental S.Tm infection. Such studies may assist in the rational management of foodborne pathogens contracted during pregnancy.
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Lemaitre, Julien. "Heterogeneity of polymorphonuclear neutrophils in HIV-1 infection. Study of SIV-infected cynomolgus macaque model." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS267.

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La persistance du VIH-1 est associée au maintien de l’inflammation chronique chez les patients infectés, malgré la mise en place de combinaison de traitements antirétroviraux. L’inflammation chronique est associée à un risque augmenté de développer des comorbidités, non associées au SIDA. Les polynucléaires neutrophiles (PNN) sont des cellules myéloïdes qui ont été impliqués dans de multiples maladies inflammatoires chroniques. Néanmoins, leur rôle dans l’infection par le VIH-1 est moins bien connue. Afin de pallier ce manque de connaissances, nous avons évalué l’hétérogénéité des PNNs dans le modèle macaque cynomolgus infecté par le SIVmac251. L’analyse phénotypique par cytométrie de masse a révélé la circulation de PNNs immatures en phase chronique de l’infection. En caractérisant l’hétérogénéité des PNNs au cours de l’infection par le SIV, nous avons observé une augmentation des fréquences des neutrophiles immatures et activés dans le sang dès la primo-infection. En phase chronique, les PNNs immatures et activés étaient toujours significativement augmentés dans le sang et la moelle osseuse. Au cours de l’infection, les PNNs avaient une fonction immunostimulatrice envers la prolifération et la sécrétion cytokinique des lymphocytaire T. L’initiation d’un traitement antirétroviral précoce a permis de restaurer le phénotype des PNNs. Les PNNs sont des cellules à fort potentiel pro-inflammatoire abondantes qui devraient être ainsi considérés comme de nouveaux effecteurs de l’inflammation chronique associée au VIH-1
Even under combinational antiretroviral treatments (cART), HIV-1 persistence is associated with chronic inflammation in infected patients, leading to an increased risk of non-AIDS-related comorbidities. Polymorphonuclear neutrophils (PMN), have been less studied in HIV infection whereas they were associated with chronic inflammation diseases. To evaluate PMN heterogeneity in SIVmac251 nonhuman primate infection model, we first performed multiparameter single-cell phenotyping by mass cytometry giving a global vision of the immune system. This analysis demonstrated circulation of immature PMN with impaired during chronic infection. Then, we characterized neutrophils heterogeneity in the course of SIV infection. In primary infection, there was an increased frequency of CD10- immature and CD62L-low primed PMNs in peripheral blood. In chronic phase, CD10- immature PMNs were significantly higher in bone marrow and blood, maintaining a primed profile. During SIV infection, PMNs demonstrated variable immunomodulatory function against T cells proliferation and cytokine production. Early cART allowed to restore PMN phenotype. In this study, we provide unprecedented insight into PMN heterogeneity in the course of SIV infection. Since PMN represent 40-70% of circulating leukocytes and primed PMN are more potent to release pro-inflammatory cytokines and to transmigrate, they should be considered as a new player in HIV-1 chronic inflammation
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Sävykoski, née Huittinen T. (Tiina). "Chlamydia pneumoniae infection, inflammation and heat shock protein 60 immunity in asthma and coronary heart disease." Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:9514269853.

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Abstract Chlamydia pneumoniae is a common respiratory pathogen worldwide. It does not only cause acute respiratory infections, but is also associated with chronic inflammatory diseases, such as asthma and coronary heart disease (CHD). Chlamydial heat shock protein 60 (Hsp60) is associated with the development of immunopathological damage following C. trachomatis infections, but the role of Hsp60 in C. pneumoniae infections is unclear. A slightly elevated level of C-reactive protein (CRP), as a marker of systemic inflammation, predicts cardiovascular events, but its role in asthma has not been studied. The aim of this study was to develop an EIA method for the measurement of Hsp60 antibodies and for studying the host immune responses to C. pneumoniae and chlamydial and human Hsp60 proteins, CRP levels and their interactions in asthma and CHD. Elevated levels of serum IgA antibodies to the Hsp60 protein of C. pneumoniae were associated with asthma and decreased pulmonary function. CRP levels were also higher in the asthma patients than in the controls. The patients with moderate asthma had higher CRP levels than those with mild asthma. The patients with a CRP level over 2 mg/l had higher levels of serum IgA antibodies to C. pneumoniae and chlamydial Hsp60 than the patients with lower CRP levels. A prospective nested case-control study was carried out, to study the role of Hsp60 antibodies as coronary risk predictors, and their association with C. pneumoniae infection and inflammation. The participants were obtained from the Helsinki Heart Study: 241 myocardial infarctions or coronary deaths occurred during the 8.5-year period among dyslipidemic middle-aged men. An elevated level of human Hsp60 IgA antibodies in baseline serum predicted the occurrence of a coronary event several years later, especially when present simultaneously with a high C. pneumoniae IgA antibody level and an elevated CRP level. Further studies showed that only persistently, not transiently, elevated levels predicted coronary events. The risk associated with elevated antibody levels increased markedly in the presence of an elevated CRP level, and vice versa. In conclusion, these results suggest that chlamydial Hsp60 is involved in the association between C. pneumoniae infection and asthma, while autoimmunity to human Hsp60 is implicated in the association between C. pneumoniae infection and CHD. Inflammation evidently plays an important role in these associations. It can also be concluded that IgA antibodies, compared to IgG antibodies, against C. pneumoniae and Hsp60 are better markers of chronicity, especially when they are persistently elevated.
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Marshall, Benjamin Giles. "Genetically modified mycobacteria as potential anti-tuberculous vaccines : an investigation of the links between inflammation, immunity and fibrosis in mycobacterial disease." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324918.

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Books on the topic "Infection, Immunity and Inflammation"

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Playfair, J. H. L. Infection and immunity. 2nd ed. Oxford: Oxford University Press, 2004.

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Infection and immunity. Oxford: Oxford University Press, 1995.

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1959-, Davies Huw, ed. Infection and immunity. London: Taylor & Francis, 1999.

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Gupta, Noopur. Corneal Infection and Inflammation. Edited by Ritika Mukhija and Radhika Tandon. First edition. | Boca Raton, FL : CRC Press, 2021.: CRC Press, 2021. http://dx.doi.org/10.1201/9781003024897.

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Pokorski, Mieczyslaw, ed. Pulmonary Infection and Inflammation. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44485-7.

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Kreier, Julius P. Infection, resistance and immunity. 2nd ed. New York, NY: Taylor & Francis, c2002., 2002.

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Kreier, Julius P. Infection, resistance and immunity. 2nd ed. New York, NY: Taylor & Francis, c2002., 2002.

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Burt, Anderson, Friedman Herman 1931-, and Bendinelli Mauro, eds. Rickettsial infection and immunity. New York: Plenum Press, 1997.

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F, Mortensen Richard, ed. Infection, resistance, and immunity. New York: Harper & Row, 1990.

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Shetty, P., ed. Nutrition, immunity and infection. Wallingford: CABI, 2010. http://dx.doi.org/10.1079/9780851995311.0000.

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Book chapters on the topic "Infection, Immunity and Inflammation"

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Rose, Aaron H., and Peter R. Hoffmann. "Selenium as a Regulator of Inflammation and Immunity." In Nutrition, Immunity, and Infection, 231–44. Boca Raton : Taylor & Francis, 2018.: CRC Press, 2017. http://dx.doi.org/10.1201/9781315118901-14.

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Thurnham, David I., and Christine A. Northrop-Clewes. "Influence of Infection and Inflammation on Nutrient Status." In Nutrition, Immunity, and Infection, 57–82. Boca Raton : Taylor & Francis, 2018.: CRC Press, 2017. http://dx.doi.org/10.1201/9781315118901-5.

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Garlanda, Cecilia, Barbara Bottazzi, Giovanni Salvatori, Rita De Santis, Alessia Cotena, Livija Deban, Viriginia Maina, et al. "Pentraxins in Innate Immunity and Inflammation." In Innate Immunity to Pulmonary Infection, 80–91. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470035399.ch7.

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Keshav, Satish. "Paneth Cells in Innate Immunity and Intestinal Inflammation." In The Innate Immune Response to Infection, 171–96. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817671.ch9.

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Pearce, Edward J. "Th2 Cell Responses in Immunity and Inflammation Following Helminth Infection." In The Th2 Type Immune Response in Health and Disease, 53–72. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2911-5_4.

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Steinhoff, Ulrich, and Alexander Visekruna. "Mucosal Immunity and Inflammation." In Immunology of Infection, 353–67. Elsevier, 2010. http://dx.doi.org/10.1016/s0580-9517(10)37015-2.

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Burkitt, H. George, Clive R. G. Quick, and Joanna B. Reed. "Immunity, inflammation and infection." In Essential Surgery, 27–51. Elsevier, 2007. http://dx.doi.org/10.1016/b978-0-443-10345-2.50009-4.

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Solomons, N. W. "Malnutrition, immunity and infection." In Diet, Immunity and Inflammation, 686–717. Elsevier, 2013. http://dx.doi.org/10.1533/9780857095749.4.686.

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Rueda, R. "Gangliosides, immunity, infection and inflammation." In Diet, Immunity and Inflammation, 341–58. Elsevier, 2013. http://dx.doi.org/10.1533/9780857095749.3.341.

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"Infection and immunity." In Oxford Handbook of Medical Sciences, edited by Robert Wilkins, Ian Megson, and David Meredith, 853–920. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198789895.003.0012.

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‘Infection and immunity’ considers the response of the body to pathogens, such as bacteria, viruses, prions, fungi, and parasites, which are discussed in terms of their nature, life cycle, and modes of infection. The role of the immune system in defence against infection is discussed, including innate and adaptive (acquired) immunity, antigens, the major histocompatibility complex, and the different cell types involved (antigen-presenting cells, T-cells, and B-cells). The mechanisms and cellular basis of inflammation are considered, as are post-infection repair mechanisms, and pathologies of the immune system such as hypersensitivity, autoimmunity and transplantations, and immunodeficiency (both primary and secondary to other diseases).
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Conference papers on the topic "Infection, Immunity and Inflammation"

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Boszczyk, Bronek, and Marcin Czyz. "Infection, Inflammation and Metabolic Disease." In eccElearning Postgraduate Diploma in Spine Surgery. eccElearning, 2017. http://dx.doi.org/10.28962/01.2.008.

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Krysan, Kostyantyn, Linh M. Tran, Brandon S. Grimes, and Steven M. Dubinett. "Abstract IA09: Inflammation and immunity in pulmonary premalignancy." In Abstracts: Fifth AACR-IASLC International Joint Conference: Lung Cancer Translational Science from the Bench to the Clinic; January 8-11, 2018; San Diego, CA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.aacriaslc18-ia09.

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Chronopoulos, J., E. Pernet, Y. Ishii, U. Fujii, M. Divangahi, and J. G. Martin. "Immunity to Influenza A Virus Infection During Pregnancy." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2936.

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Bonfield, Tracey L., Craig Hodges, James Chmiel, and Mitchell Drumm. "PPARGamma And Inflammation/Infection Resolution In Cystic Fibrosis." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5735.

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Wood, Will. "Blood cell migration during inflammation, wounding, and infection." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.106672.

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Padovani, Alessandro, and Barbara Borroni. "Fronto-temporal dementia: The role of inflammation and immunity." In Rijeka Forum on Neurodegenerative Diseases (2 ; 2018 ; Rijeka). Hrvatska akademija znanosti i umjetnosti, 2019. http://dx.doi.org/10.21857/ygjwrcjzxy.

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Jones, Samuel, Matt Kesic, Margaret Sanders, Ilona Jaspers, Benny Joyner, Shiara Ortiz-Pujols, Kathleen Short, et al. "Bacterial Infection And Airway Inflammation In Acute Inhalational Injury." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5834.

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Schneider, Dina, Deepti R. Nagarkar, Ying Zhao, Christina L. McHenry, Marisa J. Linn, Emily R. Bowman, Jason B. Weinberg, Nicholas W. Lukacs, and Marc B. Hershenson. "Effects Of Early Life Rhinovirus Infection On Lung Inflammation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4223.

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Li, Y., T. Vigil, S. Kuo, A. Goldsmith, J. K. Bentley, R. Mortensen, and M. B. Hershenson. "Itaconate Is Required for Anti-Inflammation During Rhinovirus Infection." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2601.

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Green, Douglas R. "Abstract IA13: LC3-associated phagocytosis in inflammation and anticancer immunity." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-ia13.

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Reports on the topic "Infection, Immunity and Inflammation"

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Mackey, Katherine, Irina Arkhipova-Jenkins, Charlotte Armstrong, Emily Gean, Johanna Anderson, Robin A. Paynter, and Mark Helfand. Antibody Response Following SARS-CoV-2 Infection and Implications for Immunity: A Rapid Living Review. Agency for Healthcare Research and Quality (AHRQ), March 2021. http://dx.doi.org/10.23970/ahrqepccovidimmunity.

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 Evidence suggests that the majority of adults develop detectable levels of immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies following infection with SARS-CoV-2 (moderate strength of evidence* [SoE]).  IgM levels peak approximately 20 days after symptom onset or RT-PCR diagnosis and subsequently decline. IgG levels peak approximately 25 days after symptom onset or RT-PCR diagnosis and may remain detectable for at least 120 days (moderate SoE*).  Almost all adults develop neutralizing antibodies in response to SARS-CoV-2 infection, and these antibodies may remain detectable for at least 152 days (low SoE*).  A small percentage of people do not develop antibodies in response to SARS-CoV-2 infection for reasons that are largely unclear but may be related to less severe disease or absence of symptoms.  Antibody prevalence does not appear to vary by age or sex, but older age may be associated with higher antibody levels (low SoE*). Non-White race may be associated with higher antibody prevalence and levels (low SoE*). COVID-19 severity and presence of symptoms may also be associated with higher antibody prevalence or levels (low SoE*). More evidence is needed to draw stronger conclusions regarding how the antibody response varies by patient characteristics and disease factors.  Studies to date have not established the relationship between the development of antibodies after RT-PCR-diagnosed SARS-CoV-2 infection and the risk of reinfection. Studies based on index serologic testing suggest that the presence of antibodies is associated with a lower risk of a subsequent positive SARS-CoV-2 RT-PCR test.
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Holmer, Haley K., Katherine Mackey, Celia V. Fiordalisi, Charlotte Armstrong, Emily Gean, Irina Arkhipova-Jenkins, and Mark Helfand. Antibody Response Following SARS-CoV-2 Infection and Implications for Immunity: Final Update of a Rapid, Living Review. Agency for Healthcare Research and Quality (AHRQ), October 2022. http://dx.doi.org/10.23970/ahrqepccovidimmunity3.

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Walger, et al. 8. Ad-hoc-Stellungnahme: Strategiewechsel notwendig. Monitor Versorgungsforschung, 2022. http://dx.doi.org/10.24945/mvf.05.22.1866-0533.2450.

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The 8th ad hoc statement of the Thesis Paper Authors‘ Group deals with the fact that in the meantime natural infection and vaccination have led to broad immunity in the population. In the future, identification of the truly vulnerable and prioritization on their protection will be essential.
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DeMartini, James C., Abraham Yaniv, Jonathan O. Carlson, Arnona Gazit, Leonard E. Pearson, Kalman Perk, J. K. Young, Noam Safran, and A. Friedman. Evaluation of Naked Proviral DNA as a Vaccine for Ovine Lentivirus Infection. United States Department of Agriculture, September 1994. http://dx.doi.org/10.32747/1994.7570553.bard.

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Ovine lentivirus (OvLV) infection is widespread in sheep of the United States and Israel and is responsible for substantial economic losses. The primary goal of this project was to evaluate naked proviral DNA as a vaccine to induce protective immunity in sheep in endemic areas. Contrary to expectations, inoculation of sheep with proviral DNA derived from the full length OvLV molecular clone pkv72 did not result in detectable OvLV infection, but infectious virus was recovered from transfected ovine cells. Kv72 virus produced by these cells infected sheep and induced antibody responses, and was used as a viral challenge in subsequent experiments. To improve in vivo transfection efficiency and compare the viral LTR with other romoters, expression of reporter genes was studied in sheep transfected in vivo by injection of cationic liposome-DNA complexes; one formulation produced gene expression in a sheep for 4 months following a single intravenous injection. Since the pol-deleted OvLV construct was not stable in vivo, twelve lambs were injected with plasmids containing the Kv72 gag region (pCMVgag) or env region (pCMVenv), or saline. Prior to challenge, no detectable anti-OvLV immune responses were detected. Following homologous challenge with OvLV. Although the naked DNA approach to vaccination holds promise for control of ovine lentivirus-induced disease, further work needs to be done to develop more effective methods of transfecting sheep with DNA.
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Helfand, Mark, Celia Fiordalisi, Jack Wiedrick, Katrina L. Ramsey, Charlotte Armstrong, Emily Gean, Kara Winchell, and Irina Arkhipova-Jenkins. Risk of Reinfection From SARS-CoV-2 – An Update of an Antibody Response Following SARS-CoV-2 Infection and Implications for Immunity: A Living Rapid Review. Agency for Healthcare Research and Quality (AHRQ), January 2022. http://dx.doi.org/10.23970/ahrqepccovidimmunity2.

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Chejanovsky, Nor, and Bruce A. Webb. Potentiation of pest control by insect immunosuppression. United States Department of Agriculture, July 2004. http://dx.doi.org/10.32747/2004.7587236.bard.

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Our original aims were to elucidate the mechanisms through which the immunosuppressive insect virus, the Campoletis sonorensis polydnavirus (CsV) promotes replication of a well-characterized pathogenic virus, the Autographa californica multiple nucleopolyhedrovirus (AcMNPV) in hosts that are mildly or non-permissive to virus replication. According to the BARD panels criticism we modified our short-term goals (see below). Thus, in this feasibility study (one-year funding) we aimed to show that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen (a baculovirus) to infect the pest. 3. S. littoralis cells constitute an efficient tool to study some aspects of the anti- viral immune response. We achieved the above objectives by: 1. Finding melanized viral foci upon following the baculoviral infection in S . littoralis larvae infected with a polyhedra - positive AcMNPV recombinant that expressed the GFP gene under the control of the Drosophila heat shock promoter. 2. Studying the effect of AcMNPV-infection in S . littoralis immunosuppressed by parasitation with the Braconidae wasp Chelonus inanitus that bears the CiV polydna virus, that resulted in higher susceptibility of S. littoralis to AcMNPV- infection. 3. Proving that S. littoralis hemocytes resist AcMNPV -infection. 4. Defining SL2 as a granulocyte-like cell line and demonstrating that as littoralis hemocytic cell line undergoes apoptosis upon AcMNPV -infection. 5. Showing that some of the recombinant AcMNPV expressing the immuno-suppressive polydna virus CsV- vankyrin genes inhibit baculoviral-induced lysis of SL2 cells. This information paves the way to elucidate the mechanisms through which the immuno- suppressive polydna insect viruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication by: - Assessing the extent to which and the mechanisms whereby the immunosuppressive viruses, CiV and CsV or their genes enhance AcMNPV replication in polydnavirus- immunosuppressed H. zea and S. littoralis insects and S. littoralis cells. - Identifying CiV and CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). This study will provide insight to the molecular mechanisms of viral pathogenesis and improve our understanding of insect immunity. This knowledge is of fundamental importance to controlling insect vectored diseases of humans, animals and plants and essential to developing novel means for pest control (including baculoviruses) that strategically weaken insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence.
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Baszler, Timothy, Igor Savitsky, Christopher Davies, Lauren Staska, and Varda Shkap. Identification of bovine Neospora caninum cytotoxic T-lymphocyte epitopes for development of peptide-based vaccine. United States Department of Agriculture, March 2006. http://dx.doi.org/10.32747/2006.7695592.bard.

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The goal of the one-year feasibility study was to identify specific cytotoxic T-lymphocyte (CTL) epitopes to Neosporacaninum in the natural bovine host in order to make progress toward developing an effective peptide-based vaccine against bovine neosporosis. We tested the hypothesis that: N. caninum SRS2 peptides contain immunogenicCTLepitope clusters cross-presented by multiple bovine MHC-I and MHC-IIhaplotypes. The specific objectives were: (1) Map bovine CTLepitopes of N. caninum NcSRS-2 and identify consensus MHC-I and class-II binding motifs; and (2) Determine if subunit immunization with peptides containing N. caninum-specificCTLepitopes cross-reactive to multiple bovine MHChaplotypes induces a CTL response in cattle with disparate MHChaplotypes. Neosporosis is a major cause of infectious abortion and congenital disease in cattle, persisting in cattle herds via vertical transmission.5 N. caninum abortions are reported in Israel; a serological survey of 52 Israeli dairy herds with reported abortions indicated a 31% infection rate in cows and 16% infection rate in aborted fetuses.9,14 Broad economic loss due to bovine neosporosis is estimated at $35,000,000 per year in California, USA, and $100,000,000 (Australian) per year in Australia and New Zealand.13 Per herd losses in a Canadian herd of 50 cattle are estimated more conservatively at $2,305 (Canadian) annually.4 Up to date practical measures to reduce losses from neosporosis in cattle have not been achieved. There is no chemotherapy available and, although progress has been made toward understanding immunity to Neospora infections, no efficacious vaccine is available to limit outbreaks or prevent abortions. Vaccine development to prevent N. caninum abortion and congenital infection remains a high research priority. To this end, our research group has over the past decade: 1) Identified the importance of T-lymphocyte-mediated immunity, particularly IFN-γ responses, as necessary for immune protection to congenital neosporosis in mice,1,2,10,11 and 2) Identified MHC class II restricted CD4+ CTL in Neosporainfected Holstein cattle,16 and 3) Identified NcSRS2 as a highly conserved surface protein associated with immunity to Neospora infections in mice and cattle.7,8,15 In this BARD-funded 12 month feasibility study, we continued our study of Neospora immunity in cattle and successfully completed T-lymphocyte epitope mapping of NcSRS2 surface protein with peptides and bovine immune cells,15 fulfilling objective 1. We also documented the importance of immune responses NcSRS2 by showing that immunization with native NcSRS2 reduces congenital Neospora transmission in mice,7 and that antibodies to NcSRS2 specifically inhibition invasion of placental trophoblasts.8 Most importantly we showed that T-lymphocyte responses similar to parasite infection, namely induction of activated IFN-γ secreting Tlymphocytes, could be induced by subunit immunization with NcSRS2 peptides containing the Neospora-specificCTLepitopes (Baszler et al, In preparation) fulfilling objective 2. Both DNA and peptide-based subunit approaches were tested. Only lipopeptide-based NcSRS2 subunits, modified with N-terminal linked palmitic acid to enhance Toll-like receptors 2 and 1 (TLR2-TLR1), stimulated robust antigen-specific T-lymphocyte proliferation, IFN-γ secretion, and serum antibody production across different MHC-IIhaplotypes. The discovery of MHC-II cross-reactive T-cellinducing parasite peptides capable of inducing a potentially protective immune response following subunit immunization in cattle is of significant practical importance to vaccine development to bovine neosporosis. In addition, our findings are more widely applicable in future investigations of protective T-cell, subunit-based immunity against other infectious diseases in outbred cattle populations.
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Lin, Hongwei, Yanjun Gao, Kang Sun, and Faguang Jin. Association between PM2.5 pollution and outpatient visits for respiratory diseases in China: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0144.

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Review question / Objective: Previous epidemiological studies on the association between PM2.5 pollution and outpatient visits for respiratory diseases in China were mostly limited to one region， and the different papers have no coherent results. Our objective is to perform a systematic review and meta-analysis of the relevant literature in order to summarize the association between PM2.5 pollution and outpatient visits for respiratory diseases in multiple cities in China. Condition being studied: As an important component of air pollutants, particulate matter 2.5 (PM2.5) can float in the atmosphere for a long time with a small aerodynamic size (≤2.5μm) and large specific surface area which is attached to a variety of toxic and harmful substances . PM2.5 can deposite under the trachea of the respiratory tract, reaching deep into the alveolar area, damaging alveolar macrophages and type Ⅱ alveolar epithelial cells, inducing alveolar inflammation, resulting in decreased immunity of the respiratory tract and interfering with normal physiological functions of the lungs.
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Zheng, Ruo-xiang, Xun Li, Jing Li, Zhen-wei Liu, Feng Jiang, Nicola Robinson, and Jian-ping Liu. Does Chinese herbal remedy Tangcao tablet work for the treatment of HIV/AIDS：a systematic review of controlled clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0042.

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Review question / Objective: This study aims to evaluate the effectiveness and safety of Tangcao tablet (Tangcao) for treating people with HIV/AIDS. Condition being studied: Acquired immunodeficiency syndrome (AIDS) is a chronic infectious disease characterized by severe immunodeficiency caused by the human immunodeficiency virus (HIV). The infection attacks specifically the white blood cells, CD4+T (CD4) cells, weakening the immunity of individuals against infections such as tuberculosis. Without treatment, patients with AIDS may survive up to 2 years. Pneumocystis pneumonia and infections of the central nervous system are two of the most common causes of death in people with AIDS. AIDS still remains a significant global public health problem, with an estimated 37.7 million people infected with HIV at the end of 2020.
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Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann, and Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7586538.bard.

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The objectives of the BARD proposal were to determine the mechanisms of nonspecific cytotoxic cells (NCC) that are necessary to provide heightened innate resistance to infection and to identify the antigenic determinants in Streptococcus iniae that are best suited for vaccine development. Our central hypothesis was that anti-bacterial immunity in trout and tilapia can only be acquired by combining "innate" NCC responses with antibody responses to polysaccharide antigens. These Objectives were accomplished by experiments delineated by the following Specific Aims: Specific aim (SA) #1 (USA) "Clone and Identify the Apoptosis Regulatory Genes in NCC"; Specific aim #2 (USA)"Identify Regulatory Factors that Control NCC Responses to S. iniae"; Specific aim #3 (Israel) "Characterize the Biological Properties of the S. iniae Capsular Polysaccharide"; and Specific aim #4 (Israel) "Development of an Acellular Vaccine". Our model of S. iniae pathogenesis encompassed two approaches, identify apoptosis regulatory genes and proteins in tilapia that affected NCC activities (USA group) and determine the participation of S.iniae capsular polysaccharides as potential immunogens for the development of an acellular vaccine (Israel group). We previously established that it was possible to immunize tilapia and trout against experimental S. difficile/iniaeinfections. However these studies indicated that antibody responses in protected fish were short lived (3-4 months). Thus available vaccines were useful for short-term protection only. To address the issues of regulation of pathogenesis and immunogens of S. iniae, we have emphasized the role of the innate immune response regarding activation of NCC and mechanisms of invasiveness. Considerable progress was made toward accomplishing SA #1. We have cloned the cDNA of the following tilapia genes: cellular apoptosis susceptibility (CAS/AF547173»; tumor necrosis factor alpha (TNF / A Y 428948); and nascent polypeptide-associated complex alpha polypeptide (NACA/ A Y168640). Similar attempts were made to sequence the tilapia FasLgene/cDNA, however these experiments were not successful. Aim #2 was to "Identify Regulatory Factors that Control NCC Responses to S. iniae." To accomplish this, a new membrane receptor has been identified that may control innate responses (including apoptosis) of NCC to S. iniae. The receptor is a membrane protein on teleost NCC. This protein (NCC cationic antimicrobial protein-1/ncamp-1/AAQ99138) has been sequenced and the cDNA cloned (A Y324398). In recombinant form, ncamp-l kills S. iniae in vitro. Specific aim 3 ("Characterize the Biological Properties of the S.iniae Capsular Polysaccharide") utilized an in- vitro model using rainbow trout primary skin epithelial cell mono layers. These experiments demonstrated colonization into epithelial cells followed by a rapid decline of viable intracellular bacteria and translocation out of the cell. This pathogenesis model suggested that the bacterium escapes the endosome and translocates through the rainbow trout skin barrier to further invade and infect the host. Specific aim #4 ("Development of an Acellular Vaccine") was not specifically addressed. These studies demonstrated that several different apoptotic regulatory genes/proteins are expressed by tilapia NCC. These are the first studies demonstrating that such factors exist in tilapia. Because tilapia NCC bind to and are activated by S. iniae bacterial DNA, we predict that the apoptotic regulatory activity of S. iniae previously demonstrated by our group may be associated with innate antibacterial responses in tilapia.
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