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Relevant bibliographies by topics / Interleukin-1 receptor antagonist

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Academic literature on the topic 'Interleukin-1 receptor antagonist'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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Journal articles on the topic "Interleukin-1 receptor antagonist"

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Dinarello, Charles A. "Interleukin-1, Interleukin-1 Receptors and Interleukin-1 Receptor Antagonist." International Reviews of Immunology 16, no. 5-6 (January 1998): 457–99. http://dx.doi.org/10.3109/08830189809043005.

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Espat, N. Joseph, Michael A. Rogy, Edward M. Copeland, and Lyle L. Moldawer. "Interleukin-1, interleukin-1 receptor, and interleukin-1 receptor antagonist." Proceedings of the Nutrition Society 53, no. 2 (July 1994): 393–400. http://dx.doi.org/10.1079/pns19940044.

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Bresnihan, Barry, and Gaye Cunnane. "INTERLEUKIN-1 RECEPTOR ANTAGONIST." Rheumatic Disease Clinics of North America 24, no. 3 (August 1998): 615–28. http://dx.doi.org/10.1016/s0889-857x(05)70029-6.

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Ducharme-Crevier, Laurence, and Jacques Lacroix. "Interleukin-1 Receptor Antagonist and Interleukin-1β." Pediatric Critical Care Medicine 19, no. 10 (October 2018): 993–95. http://dx.doi.org/10.1097/pcc.0000000000001713.

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Coceani, Flavio, Jodi Lees, Jane Redford, and Isis Bishai. "Interleukin-1 receptor antagonist: effectiveness against interleokin-1 fever." Canadian Journal of Physiology and Pharmacology 70, no. 12 (December 1, 1992): 1590–96. http://dx.doi.org/10.1139/y92-228.

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Conscious cats were used to examine the effectiveness of the interleukin-1 receptor antagonist against the fever induced by interleukin-1 and endotoxin. Although inactive by itself, the antagonist (three 1-μg bolus injections at 10-min intervals), injected into the third ventricle, attenuated the febrile response to a subsequent intracerebroventricular bolus of interleukin-1. The rise in prostaglandin E2 levels in cerebrospinal fluid, which is a characteristic feature of fever, was curtailed as well. The interleukin-1 antagonist had little or no inhibitory effect on the response to an intracerebroventricular bolus of endotoxin, even though a higher dose was employed (2-μg bolus injections given three times at 10-min intervals and six times at 30-min intervals, respectively, before and after endotoxin administration). At either dosage, the intracerebroventricular antagonist was completely ineffective against an intravenous bolus injection of interleukin-1 or endotoxin and both fever and prostaglandin E2 elevation developed unabated. We conclude that brain receptors mediating the pyrogenic action of centrally injected interleukin-1 are susceptible to the antagonist. The same receptors, however, are seemingly not activated by systemic pyrogens. Our findings are consistent with the concept of circulating interleukin-1 acting outside the blood–brain barrier in the normal sequence of fever.Key words: interleukin-1, interleukin-1 receptor antagonist, endotoxin, prostaglandin E2, fever mechanism.

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Donati, D., D. Degiannis, E. Mazzola, L. Gastaldi, J. Raskova, K. Raska, and G. Camussi. "Interleukin-1 receptors and receptor antagonist in haemodialysis." Nephrology Dialysis Transplantation 12, no. 1 (January 1, 1997): 111–18. http://dx.doi.org/10.1093/ndt/12.1.111.

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Bjrök, P., and K. Ohlsson. "The interleukin-1 receptor antagonist influences interleukin-1 effects in rat and mouse." Mediators of Inflammation 1, no. 1 (1992): 27–31. http://dx.doi.org/10.1155/s0962935192000061.

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In this work we have focused on the ability of interleukin-1 to induce an acute phase protein response and a degranulation of polymorphonuclear leukocytes in vivo. The capacity of the interleukin-1 receptor antagonist to influence these events was also investigated. It was shown that interleukin-1 induced an acute phase protein response in rats and mice. In rats α2-macroglubolin levels were increased in plasma after an interleukin-1 injection whereas α1-inhibitor-3 decreased in plasma. In the mice plasma amyloidPwas increased. The interleukin-1 receptor antagonist blocked the increase of α2-macroglobulin and plasma amyloidPin a dose dependent way while the effect on the α1-inhibitor-3 decrease was less pronounced. Interleukin-1 led to polymorphonuclear leukocyte degranulation in vivo as measured by increased cathepsinGplasma levels. The interleukin-1 receptor antagonist could influence the early phase of this degranulation.

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&NA;. "Interleukin 1 receptor antagonist ineffective in sepsis." Inpharma Weekly &NA;, no. 948 (July 1994): 22. http://dx.doi.org/10.2165/00128413-199409480-00058.

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Kondo, Seiji, Saveria Pastore, Hiroshi Fujisawa, Gulnar M. Shivji, Roderick C. McKenzie, Charles A. Dinarello, and Daniel N. Sauder. "Interleukin-1 Receptor Antagonist Suppresses Contact Hypersensitivity." Journal of Investigative Dermatology 105, no. 3 (September 1995): 334–38. http://dx.doi.org/10.1111/1523-1747.ep12320329.

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Barriere, Steven L., and John P. Pribble. "Effects of recombinant interleukin-1-receptor antagonist." American Journal of Health-System Pharmacy 51, no. 9 (May 1, 1994): 1253–57. http://dx.doi.org/10.1093/ajhp/51.9.1253a.

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Dissertations / Theses on the topic "Interleukin-1 receptor antagonist"

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Shepherd, Joanna. "Inflammatory diseases in mice lacking interleukin-1 receptor antagonist." Thesis, University of Sheffield, 2003. http://etheses.whiterose.ac.uk/14727/.

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Greenhalgh, Andrew. "Actions of interleukin-1 receptor antagonist in cerebral ischaemia." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/actions-of-interleukin1-receptor-antagonist-in-cerebral-ischaemia(50aacd97-68c1-4f91-90b5-8f8deff5d21d).html.

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Cerebral ischaemia, or stroke, is a leading cause of death and disability worldwide. Ischaemic stroke, as a result of arterial occlusion, and subarachnoid haemorrhage (SAH), as a consequence of arterial rupture in the subarachnoid space, are major subtypes of stroke. Treatment options for both are limited, and many therapeutic strategies have failed. In ischaemic stroke, lack of evidence of brain penetration of treatments has been cited as a major weakness and contributing factor to failed clinical trials. In SAH, animal models do not always mimic key pathophysiological hallmarks of the disease, hindering development of new therapeutics. Inflammation is strongly associated with brain injury after cerebral ischaemia and inhibition of the pro-inflammatory cytokine interleukin-1 (IL-1) represents apossible therapeutic target. Therefore, the key objectives of this thesis were; (1) to improve preclinical data on a promising stroke treatment, interleukin-1 receptor antagonist (IL-1Ra), by investigating its pharmacokinetic profile and brain penetration in a rat model of ischaemic stroke, (2) to investigate the endovascular perforation model of SAH in rat, as a tool for the investigation of neuroprotectants, and (3) to examine the role of the inflammatory response in the SAH model and the effects of IL-1Ra. The neuroprotective effect, pharmacokinetic profile and brain penetration of IL-1Ra were assessed after a single subcutaneous (s.c.) dose (100mg/kg) in rats, after transient (90 min) middle cerebral artery occlusion (MCAo). A single s.c. dose of IL-1Ra reduced neuronal damage, resulted in sustained, high concentrations of IL-1Ra in plasma and cerebrospinal fluid and also penetrated brain tissue exclusively in areas of blood brain-barrier (BBB) breakdown. An endovascular perforation model of SAH in rat was investigated and produced widespread multifocal infarcts. In this model, administration of IL-1Ra (s.c.) reduced BBB breakdown, which correlated with injury at 48 h. IL-1_ was expressed in the brain early after SAH in areas associated with haem oxygenase-1 (HO-1) expression, indicating the presence of free haem. Stimulation of primary mouse mixed glial cells in vitro with haem induced expression and release of IL-1 alpha but not IL-1 beta. These data, after MCAo in rat, are the first to show that a single s.c. dose of IL-1Ra rapidly reaches salvageable brain tissue and is neuroprotective. This allows confidence that IL-1Ra is able to confer its protective actions both peripherally and centrally. After experimental SAH, we suggest that haem, a breakdown product of haemoglobin, released from lysed red blood cells in the subarachnoid space, acts as a danger associated molecular pattern (DAMP) driving IL-1- dependent inflammation. These data provide new insights into inflammation after SAH-induced brain injury and suggest IL-1Ra as a candidate treatment for the disease. Overall, these findings strengthen preclinical data supporting IL-1Ra as a neuroprotective therapy for ischaemic stroke, and identify SAH as a new indication for treatment with IL-1Ra.

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Tarlow, Joanna Karen. "Interleukin-1 receptor antagonist gene polymorphism in chronic inflammatory diseases." Thesis, University of Sheffield, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296761.

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Galea, James. "Pharmacokinetics of intravenous interleukin-1 receptor antagonist in subarachnoid haemorrhage." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509780.

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Khan, Shamila. "Therapeutic effect of Interleukin-4 and Interleukin-1 Receptor Antagonist in Actinobacillus pleuropneumoniae challenged pigs." Thesis, The University of Sydney, 2005. http://hdl.handle.net/2123/625.

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Immunological stressors, in the form of clinical and sub-clinical disease are currently controlled using both prophylactic antibiotics in-feed, and therapeutic antibiotic treatment. Respiratory disease, primarily Actinobacillus pleuropneumoniae (App) infection, is recognised as a major factor causing reduced productivity in pigs. This thesis reports investigations into the use of novel immunomodulators in particular Interleukin 4 (IL-4) and Interleukin 1 receptor antagonist (IL-1ra) as alternatives to antibiotics to treat App infection. Immunological and molecular biological assays were used to investigate and accumulate data. An in vitro study undertaken to find potential anti-inflammatory substances, revealed that Interleukin 8 (IL-8) mRNA production stimulated by PMA or LPS in whole pigs' blood was suppressed by IL-4. IL-1ra also suppressed stimulated IL-8 mRNA production by heat killed App bacteria (KB) in vitro. An acute LPS challenge in pigs in vivo however, showed no variation in illness or weight loss between pigs treated prophylactically with anti-inflammatory substance (IL-4 and IL-1ra) and saline treated pigs. The use of plasmids as a delivery system for anti-inflammatory substance did not show promise since it did not enhance growth or prolong the expression of the substances in the pigs. However, in the chronic App challenge model IL-4 and IL-1ra administered prophylactically in vivo showed an ability to improve growth. The therapeutic administration of IL-4 and IL-1ra to App challenged pigs showed no difference in pigs' growth, regardless of the treatment or control administered. To conclude, IL-4 and IL-1ra showed promise when administered prophylactically and improved growth and abrogated disease under conditions of App challenge. However when IL-4 and IL-1ra where administered therapeutically they did not perform as well. Moreover these compounds have potential as a commercial application to reduce the growth reduction caused by disease such as App.

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La, Eunhye. "The regulation of the interleukin 1 receptor antagonist in mouse skin carcinogenesis /." Digital version accessible at:, 1999. http://wwwlib.umi.com/cr/utexas/main.

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Cantrill, Carina. "Interactions of interleukin-1 receptor antagonist with primary porcine brain endothelial cells." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509889.

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Khan, Shamila. "Therapeutic effect of Interlenkin-4 and Interleukin-1 receptor antagonist in Actinobacillus pleuropneumoniae challenged pigs." University of Sydney. Anatomy and Pathology, 2005. http://hdl.handle.net/2123/625.

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Immunological stressors, in the form of clinical and sub-clinical disease are currently controlled using both prophylactic antibiotics in-feed, and therapeutic antibiotic treatment. Respiratory disease, primarily Actinobacillus pleuropneumoniae (App) infection, is recognised as a major factor causing reduced productivity in pigs. This thesis reports investigations into the use of novel immunomodulators in particular Interleukin 4 (IL-4) and Interleukin 1 receptor antagonist (IL-1ra) as alternatives to antibiotics to treat App infection. Immunological and molecular biological assays were used to investigate and accumulate data. An in vitro study undertaken to find potential anti-inflammatory substances, revealed that Interleukin 8 (IL-8) mRNA production stimulated by PMA or LPS in whole pigs' blood was suppressed by IL-4. IL-1ra also suppressed stimulated IL-8 mRNA production by heat killed App bacteria (KB) in vitro. An acute LPS challenge in pigs in vivo however, showed no variation in illness or weight loss between pigs treated prophylactically with anti-inflammatory substance (IL-4 and IL-1ra) and saline treated pigs. The use of plasmids as a delivery system for anti-inflammatory substance did not show promise since it did not enhance growth or prolong the expression of the substances in the pigs. However, in the chronic App challenge model IL-4 and IL-1ra administered prophylactically in vivo showed an ability to improve growth. The therapeutic administration of IL-4 and IL-1ra to App challenged pigs showed no difference in pigs' growth, regardless of the treatment or control administered. To conclude, IL-4 and IL-1ra showed promise when administered prophylactically and improved growth and abrogated disease under conditions of App challenge. However when IL-4 and IL-1ra where administered therapeutically they did not perform as well. Moreover these compounds have potential as a commercial application to reduce the growth reduction caused by disease such as App.

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Fischer, Philipp. "Inhibition of inflammatory vasculopathic processes by interleukin-1 receptor antagonist - transduced endothelial progenitor cells." kostenfrei, 2008. http://mediatum2.ub.tum.de/node?id=669329.

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Ashawesh, Mohamed. "Ultrasound enhanced gene delivery of secreted Interleukin 1 receptor antagonist in a murine vascular injury model." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/18481/.

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Ultrasound (US) mediated gene delivery (UMGD) is a non-viral technique for gene transfer that has been a developing technology over the past 18 years. Non-viral UMGD as an approach is safe, relatively cheap and can be tolerated even over multiple exposures. US exposure has previously been demonstrated to increase DNA transfer and expression in endothelial cells (EC) and vascular smooth muscle cells (VSMC) in vitro and ex vivo in a saphenous vein graft model. Interleukin-1 (IL-1) is a pro-inflammatory cytokine that plays a key role in cardiovascular diseases and vascular injury. Treatment with the endogenous inhibitor interleukin-1 receptor antagonist (IL-1Ra) is an effective treatment in animal models of vascular disease and some inflammatory clinical conditions. However, Anakinra (the clinically approved formulation of IL-1Ra) must be given as daily subcutaneous (SC) injections (due to a short t ½), which is inconvenient (high burden for compliance) and very expensive. In this project I have tested US parameters for ‘best’ gene expression in the mouse hind limb, demonstrated long-term expression utilising a repeat dosing regime and finally investigated the therapeutic efficacy of intramuscular (IM) UMGD of pCMV6-SIL1Ra in a rodent arterial injury model compared with continuous delivery of Anakinra via osmotic mini-pump. Following experiments to determine the US dose, duration of expression and therefore treatment schedule, I have demonstrated that this new UMGD technique of pCMV6-SIL1Ra, every 4 days over a period of 28 days significantly decreased neointima/media (N/M) ratio in a murine vascular injury model. Furthermore, there was no significant difference between mice treated with pCMV6-SIL1Ra-UMGD and those receiving continuous Anakinra infusion by osmotic mini-pump (25 mg/kg/), suggesting that UMGD was at least as efficacious as drug treatment in reducing neointima formation. The role of IL-1 in neointima formation following vascular injury is not new but these novel data demonstrate the potential for UMGD to achieve therapeutic levels of gene/protein expression in an animal model and highlight the potential for further development. This technique of UMGD utilising a secreted protein and easily accessible muscle tissue from which to express it warrants further investigation as a possible treatment for other cardiovascular and systemic/peripheral diseases where a secreted protein is an attractive drug treatment.

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Book chapters on the topic "Interleukin-1 receptor antagonist"

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Smith, Michael F. "Interleukin-1 receptor antagonist." In Novel Cytokine Inhibitors, 177–99. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8450-1_9.

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Batu, Ezgi D., Roberta Audrey Berard, and Erkan Demirkaya. "Deficiency of Interleukin 1 Receptor Antagonist (DIRA)." In Genetic Syndromes, 1–4. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-66816-1_651-1.

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Diaz, Arturo. "Deficiency of the Interleukin-1 Receptor Antagonist (DIRA)." In Auto-Inflammatory Syndromes, 69–83. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-96929-9_6.

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Dinarello, C. A. "Interleukin-1-Induced Hypotension and the Effect of an Interleukin-1 Receptor Antagonist." In Host Defense Dysfunction in Trauma, Shock and Sepsis, 571–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77405-8_72.

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Opal, S. M., C. J. Fisher, and J. Pribble. "The Treatment of Sepsis with Interleukin-1 Receptor Antagonist." In Update in Intensive Care and Emergency Medicine, 382–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85036-3_30.

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Brown, Zarin, Lynette Fairbanks, Robert M. Strieter, Guy H. Neild, Steven L. Kunkel, and John Westwick. "Human Mesangial Cell-Derived Interleukin 8 and Interleukin 6: Modulation by an Interleukin 1 Receptor Antagonist." In Chemotactic Cytokines, 137–45. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-6009-4_16.

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Rothwell, Nancy J., and Sarah A. Loddick. "Interleukin-1 and IL-1 receptor antagonist in stroke: mechanisms and potential therapeutics." In Inflammation and Stroke, 173–80. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8297-2_14.

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van der Meer, Jos W. M., Maité Vogels, Jo H. A. J. Curfs, Bart-Jan Kuliberg, and Wynand M. C. Eling. "Interleukin-1 and its Receptor Antagonist as Candidate Therapeutic Agents for Severe Infections." In Shock, Sepsis, and Organ Failure, 332–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77420-1_14.

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Conti, P., M. R. Panara, R. C. Barbacane, F. C. Placido, S. Fridas, M. Reale, and M. Bongrazio. "Inhibition of Prostaglandin E2 (PGE2) by Human Recombinant Interleukin-1 Receptor Antagonist (hrIL-1ra)." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 517–23. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_102.

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Masasda, Tetsuya, Y. Hua, G. Xi, G. Y. Yang, J. T. Hoff, R. F. Keep, and S. Nagao. "Overexpression of interleukin-1 receptor antagonist reduces brain edema induced by intracerebral hemorrhage and thrombin." In Brain Edema XII, 463–67. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_95.

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Conference papers on the topic "Interleukin-1 receptor antagonist"

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Hernandez Parada, J., JA Ruano Ruiz, M. Sáez-Torres de Vicente, PJ Gómez Arias, F. Gómez García, and B. Isla Tejera. "4CPS-161 Scoping review on the use of canakinumab and anakinra in interleukin-1 antagonist receptor deficiency." In 24th EAHP Congress, 27th–29th March 2019, Barcelona, Spain. British Medical Journal Publishing Group, 2019. http://dx.doi.org/10.1136/ejhpharm-2019-eahpconf.310.

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Hudock, Kristin M., Yuhong Liu, and G. Scott Worthen. "Interleukin-1 Receptor Antagonist Knockout Mice Have An Increased Acute Inflammatory Response In The Lung After LPS Exposure." 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.a1089.

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Shao, Yongzhao, Mengling Liu, Linda Rogers, Qinyi Cheng, Maria Elena Fernandez-Beros, Peter Gregersen, Michael Seldin, Joel Hirschhorn, and Joan Reibman. "Replication Of An Association Of The Interleukin-1 Receptor Antagonist Gene With Asthma In An Adult Urban Admixed Population." 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.a1321.

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Martin, P., G. Palmer, E. Rodriguez, J. Palomo, and C. Gabay. "P097 Intracellular interleukin-1 receptor antagonist released upon cell death acts as an alarmin inhibitor in aldara cream-induced psoriasis-like skin inflammation." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.86.

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Reports on the topic "Interleukin-1 receptor antagonist"

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Rokita, Hanna, Ruta Neta, and Jean D. Sipe. Increased Fibrinogen Synthesis in Mice During the Acute Phase Response: Co-Operative Interaction of Interleukin 1, Interleukin 6, and Interleukin 1 Receptor Antagonist. Fort Belvoir, VA: Defense Technical Information Center, September 1993. http://dx.doi.org/10.21236/ada280464.

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