Relevant bibliographies by topics / Immunity and Inflammation

Academic literature on the topic 'Immunity and Inflammation'

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

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Journal articles on the topic "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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Houghton, A., P. Chapman, and I. Hara. "Inflammation and immunity." Melanoma Research 3, no. 1 (March 1993): 27. http://dx.doi.org/10.1097/00008390-199303000-00091.

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Webster, NR, and HF Galley. "Inflammation and immunity." BJA CEPD Reviews 3, no. 2 (April 2003): 54–58. http://dx.doi.org/10.1093/bjacepd/mkg014.

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Li, Yao, Jiaying Yao, Chunyan Han, Jiaxin Yang, Maria Chaudhry, Shengnan Wang, Hongnan Liu, and Yulong Yin. "Quercetin, Inflammation and Immunity." Nutrients 8, no. 3 (March 15, 2016): 167. http://dx.doi.org/10.3390/nu8030167.

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Stewart, Darryl, and Alistair Nichol. "Inflammation, immunity and allergy." Anaesthesia & Intensive Care Medicine 22, no. 8 (August 2021): 488–93. http://dx.doi.org/10.1016/j.mpaic.2021.06.004.

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Singh, Rajesh, Manoj Kumar Mishra, and Himanshu Aggarwal. "Inflammation, Immunity, and Cancer." Mediators of Inflammation 2017 (2017): 1. http://dx.doi.org/10.1155/2017/6027305.

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Vincenzo, Brancaleone, Iqbal J. Asif, Paschalidis Nikolaos, and Maione Francesco. "Adaptive Immunity and Inflammation." International Journal of Inflammation 2015 (2015): 1. http://dx.doi.org/10.1155/2015/575406.

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Xiao, Tsan Sam. "Innate immunity and inflammation." Cellular & Molecular Immunology 14, no. 1 (August 22, 2016): 1–3. http://dx.doi.org/10.1038/cmi.2016.45.

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O'Connor, Cormac, and Alistair Nichol. "Inflammation, immunity and allergy." Anaesthesia & Intensive Care Medicine 16, no. 7 (July 2015): 328–33. http://dx.doi.org/10.1016/j.mpaic.2015.05.001.

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Stewart, Darryl, and Alistair Nichol. "Inflammation, immunity and allergy." Anaesthesia & Intensive Care Medicine 19, no. 10 (October 2018): 534–39. http://dx.doi.org/10.1016/j.mpaic.2018.08.011.

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Dissertations / Theses on the topic "Immunity and Inflammation"

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Wuttge, Dirk Marcus. "Cellular immunity and inflammation in atherosclerosis /." Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-7349-051-2/.

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Salzano, Sonia. "Redox regulation of inflammation and immunity." Thesis, University of Brighton, 2013. https://research.brighton.ac.uk/en/studentTheses/f28a2a37-9169-4b2a-abe8-ee83c6bfe86f.

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Inflammation is a consequence of the activation of innate immunity and represents an important component of several pathological conditions, including not only the complication of infections but also sterile and autoimmune diseases. An early event in inflammation is represented by the production of proinflammatory cytokines and both their production and action have often been associated to oxidative stress. The redox status of the cell is therefore a key regulator of inflammation and glutathionylation (formation of mixed disulphides between cysteine residues of proteins and glutathione) is considered an important mechanism of this regulation. While most of the studies in the past focused on glutathionylation of intracellular proteins and transcription factors, the main goal of this project was to verify whether glutathionylated proteins are released by inflammatory cells and if these have a biological role. Using redox proteomics, we identified several proteins in the supernatants from Raw 264.7 cells (murine macrophages) stimulated with bacterial lipopolysaccharide (LPS). Among the identified proteins, we focused our attention on Peroxiredoxin 2 (Prx2), an antioxidant enzyme involved in cells protection against oxidative stress by removing H2O2. Released Prx2 was also detected in supernatant from human peripheral blood mononuclear cells (PBMC) and human macrophages. Prx2 levels were also increased in the serum of LPS-treated mice. We could confirm that Prx2 is released in the glutathionylated form. Moreover it was observed that the intracellular level of glutathione affects Prx2 release suggesting a role for glutathionylation in the mechanism of its release. The second part of the project was to verify whether released glutathionylated proteins may act as mediators of inflammation. To this purpose, the possible inflammatory role of released Prx2 was studied. The results showed that extracellular Prx2 induced an increase of TNF-α production in Raw 264.7 cells and in human macrophages. In conclusion, Prx2 is released during inflammation in a redox-dependent manner, in addition to its well-known intracellular role as enzyme, Prx2, in its released form, can also play a role in inflammatory response.
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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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Widdrington, John David. "The role of mitochondria in innate immunity and inflammation." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3196.

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Deactivation of blood monocytes during sepsis is associated with increased mortality and susceptibility to secondary infections. Septic monocytes may also have mitochondrial DNA (mtDNA) depletion and mitochondrial respiratory dysfunction. Two principal approaches explored the link between these phenomena in THP-1 cells, a human leukaemia cell line resembling monocytes, to test the hypothesis that mtDNA depletion is important in the pathophysiology of monocytic cell immune deactivation. Firstly, the consequences of immune deactivation for mitochondria was assessed using an endotoxin tolerance model in which repeated exposures to lipopolysaccharide (LPS) trigger diminishing inflammatory responses. In parallel with the induction of endotoxin tolerance, LPS treatment lead to increased mitochondrial respiration due to the activation of mitochondrial biogenesis. These results could not be confirmed in healthy volunteers following inhalation of LPS as this model failed to induce endotoxin tolerance in blood monocytes. Secondly, the effects of depleting mtDNA, by treatment with ethidium bromide or transfection with short-interfering RNA targeted against mitochondrial transcription factor A, on immunity were measured. THP-1 cells with mtDNA depletion displayed the key phenotypic feature of deactivated septic monocytes, a decreased LPS-induced release of the pro-inflammatory cytokine tumour necrosis factor-α. Furthermore, there were significant alterations in the nuclear transcriptome of mtDNA-depleted THP-1 cells, with a particular inhibition of key innate immune signalling pathways and a marked blunting of the transcriptomic response to LPS. These investigations confirm that there are complex but vital links between mitochondria and innate immunity. Compensatory responses following an inflammatory insult include the simultaneous induction of mitochondrial biogenesis and shift to an anti-inflammatory phenotype. Moreover, when sepsis disrupts mitochondrial homeostasis the negative effects of mtDNA depletion on innate immunity may exacerbate monocyte immune deactivation. Further investigations should focus on exploring the fundamental processes coupling mitochondria with immunity and confirming these findings in blood monocytes during sepsis.
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Blohmke, Christoph Johannes. "Innate immunity and inflammation in cystic fibrosis lung disease." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/34559.

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Inflammatory lung disease is the major life-limiting factor of cystic fibrosis (CF) and occurs through a self-sustaining cycle of airway obstruction, infection and inflammation. Although there is no consensus regarding the pathways responsible for the excessive inflammation, reducing lung-damaging pro-inflammatory responses are likely to be beneficial for CF patients. Using CF (IB3-1) and non-CF control (C38) respiratory cells, the host-pathogen interaction between the airway epithelium and the common CF pathogens P. aeruginosa and B. cepacia was investigated. Using purified Toll-like receptor (TLR) ligands and different knock-out strains of P. aeruginosa, TLR5 was identified as the receptor mediating much of the increased inflammatory response to CF pathogens. To validate TLR5 as an anti-inflammatory target, the disease modifying effects of the functionally relevant TLR5 c.1174C>T single nucleotide polymorphism (rs5744168) was analysed in approximately 80% of Canada’s CF population. rs5744168 encodes a premature stop codon and the T allele is associated with 45.5 – 76.3% reduction in flagellin responsiveness. CF patients carrying rs5744168 (CT or TT) had a significantly higher body mass index than CF patients homozygous for the common allele (CC) (p=0.044); however, similar improvements in lung function associated with the T allele were not statistically significant. Since TLR5 mediates much of the excessive inflammation to P. aeruginosa, it is of interest to understand the mechanisms underlying this dysregulated immune response. By combining gene expression arrays with network analyses and biochemical assays, ER stress was identified as a potential mechanism dysregulating p38 MAP kinase activity and leading to potentiated immune responses. Together, this thesis provides data underscoring the importance of TLR5-mediated excessive pro-inflammatory immune response by CF airway cells to P. aeruginosa. The association of the TLR5392STOP SNP with higher BMI in adult CF patients indicates an important role for TLR5 in CF disease severity. Finally, ER stress may potentiate the immune response to flagellin by signalling through p38 MAP kinase, supporting an emerging paradigm in which the imbalance of protein homeostasis can lead to altered signalling events. Strategies to inhibit either TLR5 signalling, ER stress signalling or to improve the cellular protein homeostasis may prove useful in treating life limiting inflammation in CF.
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Mazdai, Goudarz. "The influence of mineral nutrients on immunity and inflammation." Thesis, University of Ulster, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281215.

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Croft, Nicholas Michael. "Investigation of gastrointestinal mucosal immunity and inflammation in children." Thesis, University of Edinburgh, 1996. http://hdl.handle.net/1842/21172.

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In this thesis I have introduced a new technique, whole gut lavage (WGL), for the study of gastrointestinal secretory immunity in children. Initially I arranged to collect specimens from control children, undergoing whole gut lavage prior to colonoscopy or surgery, at the Royal Hospital for Sick Children, Edinburgh. Whole gut lavage has been used to treat severe constipation and so I organised a study to look at the effectiveness of this, intending both these groups of children as immunologically normal controls. Analysis of specimens from the first five severely constipated children showed that the total IgA levels in all were very low. I went on to examine reasons for these low IgA levels including mucosal IgA deficiency, degradation and interference by other factors in the bowel lumen. Having collected specimens from control children I then arranged a study of intestinal secretory immunity in children with cystic fibrosis (CF). This was stimulated by a paper in the Lancet suggesting that CF children, taking high dose pancreatic enzyme supplements, had developed strictures of the ascending colon possibly due to direct toxic effects of these medications. As CF children have chronic lung infections I then studied the possible influence of respiratory secretions on assays of whole gut lavage fluid by measuring concentrations of immune factors in sputum. With the data from these patient groups I was able to analyse, in some detail, the clinical aspects of whole gut lavage in children. Although I had established that WGL could be an ethical and useful method for research in children it was clear, for clinical reasons, this could not be used for the study of acute diarrhoeal illness, one of the most common paediatric problems involving the gastrointestinal mucosal immune system. With the help of adult patients, I directly compared outputs of immune factors in faeces and whole gut lavage.
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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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Ellouze, Mehdi. "Identification des mécanismes anti-inflammatoires de GILZ dans les monocytes/macrophages et de son potentiel thérapeutique dans le choc septique." Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS239/document.

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Le Sepsis et le choc septique, associés à une inflammation systémique sévère et incontrôlée, sont les principales causes de mortalité dans les unités de soins intensifs. Les macrophages jouent un rôle central dans ces pathologies. Ils participent à l'initiation et à la régulation de l'inflammation. Lors d'une infection bactérienne, ils reconnaissent le LPS de la paroi bactérienne par l’intermédiaire du TLR4 ce qui déclenche l’activation des MAPK, des facteurs de transcription NF-kB et AP1 et, in fine, la production des cytokines pro-inflammatoires dont le TNF et l'IL6. L’expression de la protéine GILZ dans les macrophages limite, in vitro, la production d'IL6 et de TNF en réponse au LPS. Cet effet est attribué à une inactivation de NF-kB. D’autre part, l'expression de GILZ décroît dans les macrophages humains et murins après une stimulation par du LPS.Compte tenu des effets régulateurs de GILZ dans les macrophages, les objectifs de notre étude sont 1) de déterminer si l’expression de GILZ est altérée dans les monocytes/macrophages (M/M) au cours du Sepsis, 2) de déterminer si une modulation de l’expression de GILZ dans les M/M est suffisante pour influencer l’inflammation systémique, et 3) d’identifier le mécanisme d'action de GILZ dans les M/M humains.Nous avons mesuré l’expression de GILZ dans les M/M de patients atteints de choc septique ou de syndrome de détresse respiratoire aiguë, et dans un modèle murin d’endotoxémie. Nous avons observé une diminution significative de GILZ dans ces contextes pathologiques chez l’homme et la souris. L'impact de cette altération a été exploré dans des souris transgéniques uniques dont les macrophages surexpriment GILZ de façon non régulable. Nous avons confirmé que la surexpression de GILZ limite la production de TNF et favorise celle de l'IL-10 dans les macrophages stimulés in vitro par du LPS. Nous avons ensuite étudié la réponse inflammatoire et la survie de ces souris dans un modèle d’endotoxémie et de choc septique, et montré que cette surexpression de GILZ restreinte aux macrophages limite la production sérique de cytokines pro-inflammatoires et, par conséquent, l'inflammation systémique en améliorant significativement la survie des souris. Ces résultats mettent en évidence les conséquences, au niveau systémique, de la régulation des macrophages par GILZ.Dans l’optique d’élucider les mécanismes impliqués dans la régulation des macrophages par GILZ, nous avons confirmé que GILZ inhibe NF-kB dans les macrophages humains sans toutefois retrouver l’interaction directe décrite entre GILZ murin et la sous-unité p65 de NF-kB.Ce résultat nous a conforté dans la nécessité de caractériser l’interactome de GILZ dans les macrophages humains. Deux approches complémentaires ont été utilisées. La première est un criblage pan-génomique des interactants de GILZ humain par la technique du double-hybride. La seconde méthode consiste en une purification d'affinité en tandem (TAP-TAG) de la protéine GILZ et de ses interactants, suivie d'une identification de ces protéines par spectrométrie de masse. Ce complexe a été isolé à partir d'extraits nucléaires ou cytoplasmiques de cellules humaines différenciées en macrophages et génétiquement modifiées afin d’exprimer la protéine GILZ flanquée des deux étiquettes nécessaires à sa purification. Ces deux approches ont mis en évidence des interactions nouvelles entre GILZ et des protéines clés de la signalisation du TLR4 dans les macrophages humains ainsi qu'un rôle probable de GILZ comme facteur régulateur de la transcription.Ces résultats montrent que la régulation de la réponse anti-inflammatoire des macrophages par GILZ a un impact sur l’inflammation systémique in vivo et améliore la survie dans un modèle de choc septique sévère. De plus, ces travaux identifient pour la première fois les partenaires cytoplasmiques et nucléaires de GILZ dans les macrophages humains et devraient permettre dans le futur, une meilleure compréhension de cette protéine
Sepsis and septic shock, associated with a severe and uncontrolled systemic inflammation, are the main causes of death in intensive care units. Macrophages play a central role in these pathologies. They are involved in the initiation and regulation of inflammation. They recognize LPS from the bacterial cell wall via TLR4, which triggers the activation of MAPK signaling pathway and transcription factors such as NF-KB and AP1 and ultimately, the production of pro-inflammatory cytokines including TNF and IL6. The expression of the protein GILZ in macrophages limits in vitro the production of IL6 and TNF in response to LPS. This effect is attributed to inactivation of NF-kB. Moreover, GILZ expression decreases in human and mouse macrophages exposed to LPS.Given the regulatory effects of GILZ in macrophages, the objectives of our study were 1) to determine whether GILZ expression is down-regulated in monocytes / macrophages (M/M) in the sepsis, 2) to determine whether the modulation of GILZ expression in M/M is sufficient to influence systemic inflammation, and 3) to identify GILZ mechanism of action in human M/M.GILZ expression was measured in the M/M of patients with septic shock or acute respiratory distress syndrome, and in a murine model of endotoxemia. We observed a significant reduced expression of GILZ in these pathological contexts in human and mice. The impact of this alteration was explored in unique transgenic mouse model in which macrophages stably overexpress GILZ (CD68-GILZ).We confirmed that GILZ overexpression limits TNF production and promotes IL-10 production in in vitro LPS-stimulated macrophages. We further studied the inflammatory response and survival of these mice in models of endotoxemia and septic shock. We showed that GILZ overexpression restricted to macrophages, limits serum pro-inflammatory cytokines production, therefore decreases systemic inflammation and significantly improves mice survival. These results highlight the effects of macrophage polarization by GILZ at a systemic level.This result confirmed the need to characterize GILZ interactome in human macrophages. Two complementary approaches have been used. The first one consists of a pan-genomic double hybrid screening of human GILZ partners. The second method consists of a tandem affinity purification (TAP-TAG) of GILZ protein and its associated partners, followed by the identification of these partners by mass spectrometry. Analyses have been performed independently on nuclear and cytoplasmic extracts from human macrophage cells, genetically engineered to express GILZ protein with the two tags required for purification. This dual approach led us to identify new direct and indirect interactions between GILZ and other key proteins of TLR4 signaling pathway in human macrophages and highlight a likely role of GILZ as a transcription regulatory factor.These results confirm the anti-inflammatory role of GILZ on systemic inflammation and enhancement of lifetime in murine models of endotoxemia and septic shock. Furthermore, this work identifies for the first time the cytoplasmic and nuclear GILZ partners in human macrophages and would allow in the future, a better understanding of GILZ mechanism of action
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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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Books on the topic "Immunity and Inflammation"

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Seya, Tsukasa, Misako Matsumoto, Keiko Udaka, and Noriyuki Sato, eds. Inflammation and Immunity in Cancer. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55327-4.

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Alper, Scott, and William J. Janssen, eds. Lung Innate Immunity and Inflammation. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8570-8.

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Maria, De Sousa, and Brock Jeremy H, eds. Iron in immunity, cancer, and inflammation. Chichester: Wiley, 1989.

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D'Ambrosio, Daniele, and Francesco Sinigaglia. Cell Migration in Inflammation and Immunity. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592594352.

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Mazdai, Goudarz. The influence of mineral nutrients on immunity and inflammation. [s.l: The Author], 1990.

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missing], [name. Cell migration in inflammation and immunity: Methods and protocols. Totowa, NJ: Humana Press, 2003.

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Asea, Alexzander A. A., and Antonio De Maio, eds. Heat Shock Proteins: Potent Mediators of Inflammation and Immunity. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-5585-0.

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Antonio, De Maio, and SpringerLink (Online service), eds. Heat Shock Proteins: Potent Mediators of Inflammation and Immunity. Dordrecht: Springer, 2007.

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Zachariae, Bobby. Mind and immunity: Psychological modulation of immunological and inflammatory parameters. Munksgaard: Rosinante, 1996.

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Belotsky, Sandro. Vospalenie: Mobilizat͡sii͡a kletok i klinicheskie ėffekty. Moskva: Binom, 2008.

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Book chapters on the topic "Immunity and Inflammation"

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Boin, Francesco, and Carlo Chizzolini. "Inflammation and Immunity." In Scleroderma, 161–95. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31407-5_13.

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Perera, Liyanage P. "Interleukin 15: Its Role in Inflammation and Immunity." In Inflammation, 35–49. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9702-9_4.

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Ronchetti, Simona, and Carlo Riccardi. "Glucocorticoids: Immunity and Inflammation." In Immunopharmacology and Inflammation, 267–81. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77658-3_12.

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Cignarella, Andrea, and Chiara Bolego. "Innate Immunity in Inflammation." In Immunopharmacology and Inflammation, 179–90. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77658-3_7.

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Lahoute, Charlotte, Alain Tedgui, and Ziad Mallat. "Adaptive T Cell Immunity." In Inflammation and Atherosclerosis, 397–421. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0338-8_20.

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Frantz, Stefan. "Inflammation and Innate Immunity." In Heart Failure, 57–59. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98184-0_3.

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Carlberg, Carsten, and Eunike Velleuer. "Innate Immunity and Inflammation." In Molecular Immunology, 19–40. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04025-2_2.

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Petrillo, Maria G., Carl D. Bortner, and John A. Cidlowski. "Glucocorticoids: Inflammation and Immunity." In The Hypothalamic-Pituitary-Adrenal Axis in Health and Disease, 43–63. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45950-9_3.

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Hansson, Göran K. "Immunity to Low-Density Lipoprotein." In Inflammation and Atherosclerosis, 423–34. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0338-8_21.

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Shichita, Takashi, Minako Ito, Rimpei Morita, and Akihiko Yoshimura. "The Role of Innate Immunity in Ischemic Stroke." In Chronic Inflammation, 649–60. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56068-5_49.

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Conference papers on the topic "Immunity and Inflammation"

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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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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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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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Zhu, Feng, Zhisong Chen, Jami Willette-Brown, Dakshayani Lomada, Sean R. Davis, Timothy Back, Teizo Yoshimura, et al. "Abstract 4873: IKKα bridges central tolerance to innate immunity and inflammation." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4873.

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O'Donnell, Valerie. "The biosynthesis and action of enzymatically-oxidized lipids during innate immunity and inflammation." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/emxs7632.

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In this presentation, I will review our knowledge about the generation and biological action of enzymatically-oxidized phospholipids (eoxPL) formed by circulating blood cells during inflammation and clotting. While the existence of nonenzymatically-oxidized PL has been known about since the 1990's, the fact that similar lipids are generated endogenously by enzymes, and that they act as part of innate immunity, has only been known for about the last 15 years. In our laboratory, using precursor scanning tandem mass spectrometry, in collaboration with Robert Murphy in Denver, we identified related families of lipids that are formed by the action of lipoxygenases/cyclooxygenases, and the Lands pathway acting in series. EoxPL comprise primarily mono-oxygenated arachidonate esterified to phosphatidylcholine and phosphatidylethanolamine, termed HETE-PC or HETE-PE, although there are also lower abundance forms derived from docosahexaenoic and eicosapentaenoic acids formed in human platelets. HETE-PL are mainly generated on acute activation of cells (platelets, neutrophils) or are present basally in eosinophils and some monocyte populations. They are not secreted, and instead stay in the membrane compartment and to some extent are present on the outer leaflet of cells. When externalised by platelets, they can enhance blood clotting through changing membrane biophysics. We also found they can activate PPARγ and regulate neutrophil antibacterial activities. All these are events of importance for innate immunity. In collaboration with clinical colleagues, we are looking at their generation in atherosclerosis, rheumatoid arthritis and venous thrombosis. We found that they are elevated in antiphospholipid syndrome, along with higher levels of autoantibodies that recognise them being present in the plasma of patients. Mice lacking eoxPL are protected against lesion development in a model of abdominal aortic aneurysm (AAA), and eoxPL are detected in human AAA lesions. Last, the Lands cycle esterification of oxylipins may represent a mechanism for reducing their bioactivity during inflammation.
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Landa, Karenia, Eda Holl, Michael Brown, James Herndon, Lars Grimm, Jeremy Force, Darell Bigner, Shelley Hwang, Matthias Gromeier, and Smita Nair. "Abstract LB-302: Oncolytic poliovirus-mediated inflammation and immunity in breast cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-lb-302.

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Bartlett, Nathan W., Louise Slater, Gaetano Caramori, Simon Message, Sebastian L. Johnston, and Michael R. Edwards. "Reduced NF-ºB P65 Expression Inhibits Rhinovirus-Induced Inflammation Without Compromising Antiviral Immunity." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3875.

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Bobeck, Elizabeth. "Bioactive lipids and related nutrients in companion animal and poultry diets for reducing inflammation and improving immunity." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/vqxl3869.

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Beyond meeting nutritional requirements for growth and maintenance, select dietary ingredients can have additional effects, intended or not, on animal physiology and immune function. Diets can be enriched to benefit the animal, and a dual benefit can be achieved in the case of enriching animal products for the downstream human consumer. Many immune-altering nutrients are fat-soluble, including Vitamin E and D. Importantly, dietary lipids themselves can impact immune function; therefore, a focused and intentional selection of specific dietary fats, specifically omega-3 polyunsaturated fatty acids (PUFA), is one method to alter inflammatory cascades in animals consuming the diet. Examples of other related ingredients to which the immune system is responsive include zinc and probiotics. While work in human, livestock, and companion animal models is working to identify therapeutic inclusion rates for these nutrients and ingredients, it should be noted that physiological alterations are seen in both over and under-inclusion and are nutrient-specific. For example, inclusion above currently recommended levels may optimize immune function and reduce inflammation in the case of vitamin D or omega-3 PUFA, while for zinc, additional pharmacological supplementation above requirements may inhibit immune function. Importantly, when a diet is formulated to reduce overall systemic inflammation, it must be considered that important “background” functions of the immune system, including monitoring for and clearing pathogenic microbial populations, may be down-regulated due to a general reduction in immune reactivity. Continued work to understand how diet and nutrition impact immunity, and how to balance inflammation through nutrition, is an area of active research and will inform downstream users how to best use data to impact consumers of that feed in desirable ways.
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Mittendorf, Elizabeth A., Gheath Alatrash, Na Qiao, Haile Xiao, Pariya Sukhumalchandra, Kathryn Quintanilla, Karen Clise-Dwyer, and Jeffrey Molldrem. "Abstract 801: Uptake of exogenous neutrophil elastase by breast cancer cells: A novel link between innate immunity, inflammation and breast cancer immunity." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-801.

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Maidhof, Robert, Neena Rajan, and Nadeen O. Chahine. "Effect of Inflammation on the Osmotic Response of Nucleus Pulposus Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80358.

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Intervertebral disc (IVD) degeneration is accompanied by elevated levels of pro-inflammatory cytokines, particularly IL-1β and TNF-α [1]. Disc cells from the nucleus pulposus (NPs) respond to cytokine stimulation with increased catabolic breakdown of the tissue, resulting in a positive feedback of disc integrity loss and further inflammation [2]. Previous studies by our group have examined the response of NP cells to Toll-Like Receptor-4 (TLR-4) activation through stimulation with lipopolysaccharide (LPS). TLR-4 is a pattern recognition receptor that is activated in innate immunity and by polysaccharide fragments from degenerated proteoglycans. TLR-4 activation by LPS results in stimulation of multiple cytokines by NP cells [3]. Moreover, we have shown that in vivo LPS injection results in catabolic changes in the IVD, including matrix breakdown, decrease in biomechanical properties and loss of disc height [4]. However, the specific cellular mechanisms for these catabolic changes remain to be elucidated.
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Reports on the topic "Immunity and Inflammation"

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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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