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Books on the topic 'Inflammasones'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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1

Couillin, Isabelle, Virginie Pétrilli, and Fabio Martinon, eds. The Inflammasomes. Basel: Springer Basel, 2011. http://dx.doi.org/10.1007/978-3-0348-0148-5.

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Couillin, Isabelle. The Inflammasomes. Basel: Springer Basel AG, 2011.

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3

De Nardo, Christine M., and Eicke Latz, eds. The Inflammasome. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-523-1.

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4

Cordero, Mario D., and Elísabet Alcocer-Gómez, eds. Inflammasomes: Clinical and Therapeutic Implications. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89390-7.

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5

Nardo, Christine De, and Eicke Latz. The inflammasome: Methods and protocols. New York: Humana Press, 2013.

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6

Backert, Steffen, ed. Inflammasome Signaling and Bacterial Infections. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41171-2.

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7

Couillin, Isabelle, Virginie Pétrilli, and Fabio Martinon. The Inflammasomes. Springer, 2013.

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8

DNA Sensors and Inflammasomes. Elsevier, 2019. http://dx.doi.org/10.1016/s0076-6879(19)x0011-7.

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9

Inflammasomes: Clinical and Therapeutic Implications. Springer, 2019.

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10

Cordero, Mario D., and Elísabet Alcocer-Gómez. Inflammasomes: Clinical and Therapeutic Implications. Springer, 2018.

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11

Backert, Steffen. Inflammasome Signaling and Bacterial Infections. Springer, 2018.

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12

Mason, Angie. Inflammasomes: Mechanism of Action, Regulation and Role in Disease. Nova Science Publishers, Incorporated, 2016.

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13

Frenkel, Joost, and Hans R. Waterham. Mevalonate Kinase Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0039.

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Mevalonate kinase deficiency (MKD) is an autosomal recessive inborn error of isoprenoid biosynthesis, a pathway yielding sterols and nonsterol isoprenoids.In patients, the enzyme activity of mevalonate kinase is severely reduced due to mutations in the encoding gene, MVK. The substrate, mevalonate, accumulates and is elevated in blood and urine. Shortage of certain downstream products of the pathway, nonsterol isoprenoids, leads to dysregulation of the innate immune system, activation of inflammasomes, and interleukin (IL)-1 mediated inflammation.Symptoms start in early childhood with recurrent attacks of fever, vomiting, diarrhea, headache, sore throat, abdominal pain, arthralgias, painful lymphadenopathy, hepatosplenomegaly, skin rash, and mucosal ulcers. Severely affected patients have additional symptoms, such as intellectual impairment, progressive cerebellar ataxia, and tapetoretinal degeneration. Complications include intestinal obstruction, AA-amyloidosis, hemophagocytosis, and severe infection.Management of MKD is directed at controlling inflammation.

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14

Wiersinga, W. Joost, and Tom van der Poll. The host response to infection in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0303.

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Infection continues to be a leading cause of intensive care unit death. The host response to infection can be seen as a pattern recognition receptor (PRR)-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. A measured and rapid response to microbial invasion is essential to health. The same immunological and coagulation systems that protect against localized infection can act to our disadvantage when these systems are activated systemically during generalized microbial infection. Toll-like receptors (TLR), the inflammasomes and other PRRs initiate the host response after recognition of pathogen-associated-molecular-patterns (PAMPs) or endogenous danger-associated-molecular-patterns (DAMPs). The systemic host response to infection will result in activation of coagulation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Further dissection of the role of host–pathogen interactions, the cytokine response, the coagulation cascade and their multidirectional interactions in sepsis should lead towards the development of new therapeutic approaches in the critically ill who are faced with infection.

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15

Dalbeth, Nicola. Epidemiology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198748311.003.0003.

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The aetiopathogenesis of gout is initiated by urate overproduction and uric acid under-excretion, leading to hyperuricaemia. Foods such as seafood, red meat, beer, and sugar-sweetened beverages contribute to overproduction. Under-excretion is mediated by renal and gut uric acid transporters such as SLC2A9, ABCG2, and URAT1. In hyperurcaemia, there is formation of monosodium urate (MSU) crystals in joints, with acute gouty arthritis mediated by the innate immune system occurring in response to these crystals. Factors such as urate concentration, proteins present in synovial fluid, temperature, and pH control crystal nucleation and growth. Activation of the inflammasome by MSU crystals and production of interleukin-1ß‎ is central to acute gouty arthritis. Advanced gout occurs when there is persistent gouty arthritis and tophus with the tophus being an organized immune tissue response to MSU crystals that involves both innate and adaptive immune cells. Progression through the gout checkpoints (hyperuricaemia, MSU crystal formation, and immune response) is governed by inherited genetic variants, lifetime environmental exposures, and their interaction.

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16

Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.

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

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17

Abhishek, Abhishek, and Michael Doherty. Pathophysiology of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0049.

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Calcium pyrophosphate (CPP) dihydrate crystals form extracellularly. Their formation requires sufficient extracellular inorganic pyrophosphate (ePPi), calcium, and pro-nucleating factors. As inorganic pyrophosphate (PPi) cannot cross cell membranes passively due to its large size, ePPi results either from hydrolysis of extracellular ATP by the enzyme ectonucleotide pyrophosphatase/phosphodiesterase 1 (also known as plasma cell membrane glycoprotein 1) or from the transcellular transport of PPi by ANKH. ePPi is hydrolyzed to phosphate (Pi) by tissue non-specific alkaline phosphatase. The level of extracellular PPi and Pi is tightly regulated by several interlinked feedback mechanisms and growth factors. The relative concentration of Pi and PPi determines whether CPP or hydroxyapatite crystal is formed, with low Pi/PPi ratio resulting in CPP crystal formation, while a high Pi/PPi ratio promotes basic calcium phosphate crystal formation. CPP crystals are deposited in the cartilage matrix (preferentially in the middle layer) or in areas of chondroid metaplasia. Hypertrophic chondrocytes and specific cartilage matrix changes (e.g. high levels of dermatan sulfate and S-100 protein) are related to CPP crystal deposition and growth. CPP crystals cause inflammation by engaging with the NALP3 inflammasome, and with other components of the innate immune system, and is marked with a prolonged neutrophilic inflitrate. The pathogenesis of resolution of CPP crystal-induced inflammation is not well understood.

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