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

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Published: 4 June 2021

Last updated: 21 February 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

&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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9

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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10

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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11

Arend, William P., Mark Malyak, Carla J. Guthridge, and Cem Gabay. "INTERLEUKIN-1 RECEPTOR ANTAGONIST: Role in Biology." Annual Review of Immunology 16, no. 1 (April 1998): 27–55. http://dx.doi.org/10.1146/annurev.immunol.16.1.27.

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12

Rolfe, Mark W., Theodore J. Standiford, Steven L. Kunkel, Marie D. Burdick, Andrew R. Gilbert, Joseph P. Lynch, and Robert M. Strieter. "Interleukin-1 Receptor Antagonist Expression in Sarcoidosis." American Review of Respiratory Disease 148, no. 5 (November 1993): 1378–84. http://dx.doi.org/10.1164/ajrccm/148.5.1378.

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13

Loddick, Sarah A., Ma-Li Wong, Peter B. Bongiorno, Philip W. Gold, Julio Licinio, and Nancy J. Rothwell. "Endogenous Interleukin-1 Receptor Antagonist is Neuroprotective." Biochemical and Biophysical Research Communications 234, no. 1 (May 1997): 211–15. http://dx.doi.org/10.1006/bbrc.1997.6436.

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14

Chang, D. M. "Interleukin-1 and Interleukin-1 Receptor Antagonist in Systemic Lupus Erythematosus." Immunological Investigations 26, no. 5-7 (January 1997): 649–59. http://dx.doi.org/10.3109/08820139709088547.

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15

Stevens, A. Christopher, and Mark Peppercorn. "INTERLEUKIN-1 AND INTERLEUKIN-1 RECEPTOR ANTAGONIST: FROM BENCH TO BEDSIDE." Inflammatory Bowel Diseases 2, no. 2 (1996): 157–58. http://dx.doi.org/10.1097/00054725-199606000-00015.

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16

Opp, M. R., and J. M. Krueger. "Interleukin 1-receptor antagonist blocks interleukin 1-induced sleep and fever." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 2 (February 1, 1991): R453—R457. http://dx.doi.org/10.1152/ajpregu.1991.260.2.r453.

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The recent purification and characterization of an interleukin 1-receptor antagonist (IL-1ra) has provided an additional means of elucidating the mechanisms involved in the responses initiated by IL-1. Central administration of IL-1 to rabbits results in a characteristic febrile response and in increased non-rapid-eye-movement sleep (NREMS). In this study, rabbits received various doses of IL-1ra (10-1,000 micrograms) or pyrogen-free saline intracerebroventricularly, and sleep-wake activity and brain temperature (Tbr) were determined for the next 24 h. All doses of IL-1ra tested tended to reduce NREMS in the first postinjection hour with little effect on Tbr. When rabbits were pretreated with 100 micrograms IL-1ra and then injected with 10 ng IL-1, the characteristic IL-1-induced febrile and NREMS-promoting effects were completely blocked.

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17

Hannum, Charles H., Carol J. Wilcox, William P. Arend, Fenneke G. Joslin, David J. Dripps, Patricia L. Heimdal, Lyman G. Armes, Andreas Sommer, Stephen P. Eisenberg, and Robert C. Thompson. "Interleukin-1 receptor antagonist activity of a human interleukin-1 inhibitor." Nature 343, no. 6256 (January 1990): 336–40. http://dx.doi.org/10.1038/343336a0.

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18

Cominelli, F., and TT Pizarro. "Interleukin-1 and interleukin-1 receptor antagonist in inflammatory bowel disease." Alimentary Pharmacology & Therapeutics 10, Sup2 (1996): 49–53. http://dx.doi.org/10.1046/j.1365-2036.1996.22164020.x.

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19

Guise, Theresa A., I. Ross Garrett, Lynda F. Bonewald, and Gregory R. Mundy. "Interleukin-1 receptor antagonist inhibits the hypercalcemia mediated by interleukin-1." Journal of Bone and Mineral Research 8, no. 5 (December 3, 2009): 583–87. http://dx.doi.org/10.1002/jbmr.5650080509.

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20

Dinarello, CA. "Interleukin-1 and interleukin-1 antagonism." Blood 77, no. 8 (April 15, 1991): 1627–52. http://dx.doi.org/10.1182/blood.v77.8.1627.1627.

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Abstract The polypeptide cytokine interleukin-1 (IL-1) affects nearly every tissue and organ system. IL-1 is the prototype of the pro-inflammatory cytokines in that it induces the expression of a variety of genes and the synthesis of several proteins that, in turn, induce acute and chronic inflammatory changes. IL-1 is also the prototypic “alarm' cytokine in that it brings about increases in a variety of defense mechanisms, particularly immunologic and hematologic responses. Most studies on the biology of IL-1 have been performed in animals, but human subjects have recently been injected with recombinant IL-1 and the results confirm the two fundamental properties of IL-1 as being both a mediator of disease as well as of host defense. However, in either situation, over or continued production of IL-1 leads to debilitation of normal host functions; therefore, reduction of IL-1 synthesis or its effects becomes a target of therapy in many diseases. In this review, the structure, gene expression, synthesis, and secretion of IL-1 are described. In addition, the two IL-1 surface receptors, possible signal transduction mechanisms, various biologic activities, and production of IL-1 during disease states are discussed. Similarities and differences between IL-1, tumor necrosis factor, and IL-6 are presented. Although various agents for reducing the synthesis and/or for antagonizing the effects of IL-1 have been proposed, the recent cloning of a naturally occurring IL-1 receptor antagonist (IL- 1ra) has opened new experimental and clinical approaches. The ability of this IL-1ra to block the triggering of IL-1 receptors in animals without agonist effects has reduced the severity of diseases such as hemodynamic shock, lethal sepsis, inflammatory bowel disease, experimental arthritis, and the spontaneous proliferation of human leukemic cells.

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21

Dinarello, CA. "Interleukin-1 and interleukin-1 antagonism." Blood 77, no. 8 (April 15, 1991): 1627–52. http://dx.doi.org/10.1182/blood.v77.8.1627.bloodjournal7781627.

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The polypeptide cytokine interleukin-1 (IL-1) affects nearly every tissue and organ system. IL-1 is the prototype of the pro-inflammatory cytokines in that it induces the expression of a variety of genes and the synthesis of several proteins that, in turn, induce acute and chronic inflammatory changes. IL-1 is also the prototypic “alarm' cytokine in that it brings about increases in a variety of defense mechanisms, particularly immunologic and hematologic responses. Most studies on the biology of IL-1 have been performed in animals, but human subjects have recently been injected with recombinant IL-1 and the results confirm the two fundamental properties of IL-1 as being both a mediator of disease as well as of host defense. However, in either situation, over or continued production of IL-1 leads to debilitation of normal host functions; therefore, reduction of IL-1 synthesis or its effects becomes a target of therapy in many diseases. In this review, the structure, gene expression, synthesis, and secretion of IL-1 are described. In addition, the two IL-1 surface receptors, possible signal transduction mechanisms, various biologic activities, and production of IL-1 during disease states are discussed. Similarities and differences between IL-1, tumor necrosis factor, and IL-6 are presented. Although various agents for reducing the synthesis and/or for antagonizing the effects of IL-1 have been proposed, the recent cloning of a naturally occurring IL-1 receptor antagonist (IL- 1ra) has opened new experimental and clinical approaches. The ability of this IL-1ra to block the triggering of IL-1 receptors in animals without agonist effects has reduced the severity of diseases such as hemodynamic shock, lethal sepsis, inflammatory bowel disease, experimental arthritis, and the spontaneous proliferation of human leukemic cells.

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22

Khalilzadeh, Omid, Mehdi Anvari, Alireza Esteghamati, Mahdi Mahmoudi, Maryam Tahvildari, Armin Rashidi, Farideh Khosravi, and Aliakbar Amirzargar. "Graves' ophthalmopathy and gene polymorphisms in interleukin-1α, interleukin-1β, interleukin-1 receptor and interleukin-1 receptor antagonist." Clinical & Experimental Ophthalmology 37, no. 6 (August 2009): 614–19. http://dx.doi.org/10.1111/j.1442-9071.2009.02093.x.

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23

Granowitz, E. V., B. D. Clark, J. Mancilla, and C. A. Dinarello. "Interleukin-1 receptor antagonist competitively inhibits the binding of interleukin-1 to the type II interleukin-1 receptor." Journal of Biological Chemistry 266, no. 22 (August 1991): 14147–50. http://dx.doi.org/10.1016/s0021-9258(18)98655-2.

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24

Serdaroğlu, Gul, Asude Alpman, Ayse Tosun, Sacide Pehlıvan, Ferda Özkınay, Hasan Tekgül, and Sarenur Gökben. "Febrile Seizures: Interleukin 1β and Interleukin-1 Receptor Antagonist Polymorphisms." Pediatric Neurology 40, no. 2 (February 2009): 113–16. http://dx.doi.org/10.1016/j.pediatrneurol.2008.10.004.

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25

Beamer, Nancy B., Bruce M. Coull, Wayne M. Clark, J. Samantha Hazel, and Jenny R. Silberger. "Interleukin-6 and interleukin-1 receptor antagonist in acute stroke." Annals of Neurology 37, no. 6 (June 1995): 800–805. http://dx.doi.org/10.1002/ana.410370614.

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26

Miller, Lauri J., Scott H. Kurtzman, Kathleen Anderson, Yanping Wang, Marra Stankus, Maria Renna, Richard Lindquist, George Barrows, and Donald L. Kreutzer. "Interleukin-1 Family Expression in Human Breast Cancer: Interleukin-1 Receptor Antagonist." Cancer Investigation 18, no. 4 (January 2000): 293–302. http://dx.doi.org/10.3109/07357900009012171.

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27

Arend, W. P. "Interleukin 1 receptor antagonist. A new member of the interleukin 1 family." Journal of Clinical Investigation 88, no. 5 (November 1, 1991): 1445–51. http://dx.doi.org/10.1172/jci115453.

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28

Firestein, Gary S., David L. Boyle, Carolyn Yu, Mary M. Paine, Teri D. Whisenand, Nathan J. Zvaifler, and William P. Arend. "Synovial interleukin-1 receptor antagonist and interleukin-1 balance in rheumatoid arthritis." Arthritis & Rheumatism 37, no. 5 (May 1994): 644–52. http://dx.doi.org/10.1002/art.1780370507.

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29

Uludag, Irem Fatma, Sule Bilgin, Yasar Zorlu, Gamze Tuna, and Guldal Kirkali. "Interleukin-6, interleukin-1 beta and interleukin-1 receptor antagonist levels in epileptic seizures." Seizure 22, no. 6 (July 2013): 457–61. http://dx.doi.org/10.1016/j.seizure.2013.03.004.

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30

Yuan, S., P. M. Roos, and S. C. Larsson. "Interleukin‐1 receptor antagonist, interleukin‐2 receptor alpha subunit and amyotrophic lateral sclerosis." European Journal of Neurology 27, no. 10 (June 8, 2020): 1913–17. http://dx.doi.org/10.1111/ene.14338.

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31

Murata, Minako, Carol Trahan, Junichi Hirahashi, Henry J. Mankin, and Christine A. Towle. "Intracellular Interleukin-1 Receptor Antagonist in Osteoarthritis Chondrocytes." Clinical Orthopaedics and Related Research 409 (April 2003): 285–95. http://dx.doi.org/10.1097/01.blo.0000059582.08469.ac.

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32

Sönnichsen, Astrid, Ieva Saulite, Johanna Mangana, Katrin Kerl, Tarun Mehra, Ignatova Desislava, Yun-Tsan Chang, et al. "Interleukin-1 receptor antagonist (anakinra) for Schnitzler syndrome." Journal of Dermatological Treatment 27, no. 5 (February 10, 2016): 436–38. http://dx.doi.org/10.3109/09546634.2015.1136048.

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33

Bigler, Carl F., David A. Norris, William L. Weston, and William P. Arend. "Interleukin-1 Receptor antagonist Production by Human Keratinocytes." Journal of Investigative Dermatology 98, no. 1 (January 1992): 38–44. http://dx.doi.org/10.1111/1523-1747.ep12494196.

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34

Bry, K., K. Teramo, U. Lappalainen, F. Waffarn, and M. Hallman. "Interleukin-1 receptor antagonist in the fetomaternal compartment." Acta Paediatrica 84, no. 3 (March 1995): 233–36. http://dx.doi.org/10.1111/j.1651-2227.1995.tb13620.x.

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35

Arend, W. P. "Biological role of interleukin 1 receptor antagonist isoforms." Annals of the Rheumatic Diseases 59, no. 90001 (November 1, 2000): 60i—64. http://dx.doi.org/10.1136/ard.59.suppl_1.i60.

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36

Sehouli, Jalid, and Alexander Mustea. "Interleukin‐1 Receptor Antagonist Gene Polymorphism and Cancer." Clinical Infectious Diseases 34, no. 11 (June 2002): 1535–36. http://dx.doi.org/10.1086/340530.

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37

Semana, G., J. Yaouanq, M. Alizadeh, M. Clanet, and G. Edan. "Interleukin-1 receptor antagonist gene in multiple sclerosis." Lancet 349, no. 9050 (February 1997): 476. http://dx.doi.org/10.1016/s0140-6736(05)61188-9.

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38

Arend, William P. "Interleukin-1 receptor antagonist: Discovery, structure and properties." Progress in Growth Factor Research 2, no. 4 (January 1990): 193–205. http://dx.doi.org/10.1016/0955-2235(90)90018-f.

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39

Geiger, R., H. Ellemunter, F. M. Fink, M. Falk, and H. Tilg. "Circulating interleukin-1 receptor antagonist levels in neonates." European Journal of Pediatrics 155, no. 9 (September 1996): 811–14. http://dx.doi.org/10.1007/bf02002913.

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40

Gillespie, Shannon L., Jeremy L. Neal, Lisa M. Christian, Laura A. Szalacha, Donna O. McCarthy, and Pamela J. Salsberry. "Interleukin-1 Receptor Antagonist Polymorphism and Birth Timing." Nursing Research 66, no. 2 (2017): 95–104. http://dx.doi.org/10.1097/nnr.0000000000000200.

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41

Brett, PM, F. Herbst, N. Yasuda, JY Yiannakou, RJ Nicholls, and PJ Ciclitira. "Interleukin 1 Receptor Antagonist Vntr Polymorphism and Pouchitis." Clinical Science 90, s34 (February 1, 1996): 9P. http://dx.doi.org/10.1042/cs090009pa.

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42

Mulero, Julio J., Ann M. Pace, Sarah T. Nelken, Deborah B. Loeb, Tanis R. Correa, Radoje Drmanac, and John E. Ford. "IL1HY1: A Novel Interleukin-1 Receptor Antagonist Gene." Biochemical and Biophysical Research Communications 263, no. 3 (October 1999): 702–6. http://dx.doi.org/10.1006/bbrc.1999.1440.

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43

Geiger, R., H. Ellemunter, F. M. Fink, M. Falk, and H. Tilg. "Circulating interleukin-1 receptor antagonist levels in neonates." European Journal of Pediatrics 155, no. 9 (August 9, 1996): 811–14. http://dx.doi.org/10.1007/s004310050493.

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44

Meyer, Nuala J., John P. Reilly, Brian J. Anderson, Jessica A. Palakshappa, Tiffanie K. Jones, Thomas G. Dunn, Michael G. S. Shashaty, Rui Feng, Jason D. Christie, and Steven M. Opal. "Mortality Benefit of Recombinant Human Interleukin-1 Receptor Antagonist for Sepsis Varies by Initial Interleukin-1 Receptor Antagonist Plasma Concentration*." Critical Care Medicine 46, no. 1 (January 2018): 21–28. http://dx.doi.org/10.1097/ccm.0000000000002749.

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45

Barton, Parrin T., Stefan Gerber, Daniel W. Skupski, and Steven S. Witkin. "Interleukin-1 Receptor Antagonist Gene Polymorphism, Vaginal Interleukin-1 Receptor Antagonist Concentrations, and Vaginal Ureaplasma urealyticum Colonization in Pregnant Women." Infection and Immunity 71, no. 1 (January 2003): 271–74. http://dx.doi.org/10.1128/iai.71.1.271-274.2003.

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ABSTRACT Ureaplasma urealyticum is the microorganism most frequently isolated from amniotic fluids of women in preterm labor. The relationship between vaginal colonization with U. urealyticum, vaginal interleukin-1 receptor antagonist (IL-1ra) levels, and the IL-1ra genotype in pregnant women was examined. Vaginal specimens, obtained with a cotton swab from 207 women in their first trimester of pregnancy, were tested for IL-1ra concentrations by enzyme-linked immunosorbent assay and for U. urealyticum and IL-1ra genotypes by PCR. U. urealyticum was detected in 85 (41.1%) women. The median IL-1ra level was 450 ng/ml in women positive for U. urealyticum, as opposed to 225 ng/ml in women negative for this microorganism (P < 0.0001). Sixty-two percent of the 16 women who were homozygous for allele 2 of the IL-1ra gene (IL-1RN*2) were colonized with U. urealyticum, as opposed to 47% of the 49 women who were IL-1RN*1/IL-1RN*2 heterozygotes and 34% of the 133 women who were IL-1RN*1 homozygotes (P < 0.05). Median IL-1ra levels were 750 ng/ml in IL-1RN*2 homozygotes, 300 ng/ml in IL-1RN*1/IL-1RN*2 heterozygotes, and 250 ng/ml in IL-1RN*1 homozygotes (P = 0.02). The vast majority of subjects had an uneventful pregnancy and delivered a healthy infant at term. The IL-1ra genotype or U. urealyticum colonization was unrelated to birth weight. Pregnant women who are colonized with U. urealyticum during the first trimester have elevated vaginal IL-1ra concentrations and a higher prevalence of the IL-1RN*2 homozygote genotype than do noncolonized women.

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46

van Minkelen, Rick, Stephanie Bezzina Wettinger, Marieke C. H. de Visser, Hans L. Vos, Pieter H. Reitsma, Frits R. Rosendaal, Rogier M. Bertina, and Carine J. M. Doggen. "Haplotypes of the interleukin-1 receptor antagonist gene, interleukin-1 receptor antagonist mRNA levels and the risk of myocardial infarction." Atherosclerosis 203, no. 1 (March 2009): 201–5. http://dx.doi.org/10.1016/j.atherosclerosis.2008.06.029.

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47

Richter, Frank, Annett Eitner, Johannes Leuchtweis, Reinhard Bauer, Alfred Lehmenkühler, and Hans-Georg Schaible. "Effects of interleukin-1ß on cortical spreading depolarization and cerebral vasculature." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (July 20, 2016): 1791–802. http://dx.doi.org/10.1177/0271678x16641127.

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During brain damage and ischemia, the cytokine interleukin-1ß is rapidly upregulated due to activation of inflammasomes. We studied whether interleukin-1ß influences cortical spreading depolarization, and whether lipopolysaccharide, often used for microglial stimulation, influences cortical spreading depolarizations. In anaesthetized rats, cortical spreading depolarizations were elicited by microinjection of KCl. Interleukin-1ß, the IL-1 receptor 1 antagonist, the GABAA receptor blocker bicuculline, and lipopolysaccharide were administered either alone or combined (interleukin-1ß + IL-1 receptor 1 antagonist; interleukin-1ß + bicuculline; lipopolysaccharide + IL-1 receptor 1 antagonist) into a local cortical treatment area. Using microelectrodes, cortical spreading depolarizations were recorded in a non-treatment and in the treatment area. Plasma extravasation in cortical grey matter was assessed with Evans blue. Local application of interleukin-1ß reduced cortical spreading depolarization amplitudes in the treatment area, but not at a high dose. This reduction was prevented by IL-1 receptor 1 antagonist and by bicuculline. However, interleukin-1ß induced pronounced plasma extravasation independently on cortical spreading depolarizations. Application of lipopolysaccharide reduced cortical spreading depolarization amplitudes but prolonged their duration; EEG activity was still present. These effects were also blocked by IL-1 receptor 1 antagonist. Interleukin-1ß evokes changes of neuronal activity and of vascular functions. Thus, although the reduction of cortical spreading depolarization amplitudes at lower doses of interleukin-1ß may reduce deleterious effects of cortical spreading depolarizations, the sum of interleukin-1ß effects on excitability and on the vasculature rather promote brain damaging mechanisms.

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48

De Simoni, M. G., A. De Luigi, L. Gemma, M. Sironi, A. Manfridi, and P. Ghezzi. "Modulation of systemic interleukin-6 induction by central interleukin-1." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 4 (October 1, 1993): R739—R742. http://dx.doi.org/10.1152/ajpregu.1993.265.4.r739.

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Centrally administered interleukin (IL)-1 [both alpha and beta forms, 200 ng/rat intracerebroventricularly (icv)] results in a larger increase in serum IL-6 than after systemic injection, indicating the brain's role in the acute phase response. This action was prevented by the IL-1-receptor antagonist IL-1Ra (20 micrograms/rat icv). Neither antiserum against corticotropin-releasing factor (CRF) nor the alpha-helical-CRF antagonist (25 micrograms/rat icv) affected IL-6 induction by central IL-1 beta, which, however, was significantly prevented by the synthetic glucocorticoid dexamethasone [3 mg/kg intraperitoneally (ip)]. Naloxone, the opiate antagonist, but not naloxone methiodide, its quaternary salt that does not penetrate the blood-brain barrier (both administered at 10 mg/kg ip), antagonized this action of IL-1 beta. After intracerebroventricular IL-1 beta, IL-6 levels in brain areas (striatum, hippocampus, hypothalamus) were extremely low, suggesting that the brain does not significantly contribute to IL-6 synthesis in this condition. The results show that induction of high serum IL-6 levels by central IL-1 beta is mediated by brain IL-1 receptors and is sensitive to inhibition by corticosteroids. The inhibitory effect of naloxone suggests that central opiates are required for this action of IL-1 beta.

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Chung-Ming Huang, Fuu-Jen Tsai, Jer. "Interleukin-1ßand interleukin-1 receptor antagonist gene polymorphisms in rheumatoid arthritis." Scandinavian Journal of Rheumatology 30, no. 4 (January 2001): 225–28. http://dx.doi.org/10.1080/030097401316909576.

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Thi-Ngo, Kim-Hang, Duy Nguyen-Le, Thanh Nguyen-Phuoc, Thuoc Linh Tran, and Hieu Tran-Van. "Cloning, Expression and Purification of Recombinant Interleukin 1 Receptor Antagonist (IL-1RA) in Escherichia coli." SSR Institute of International Journal of Life Sciences 6, no. 3 (May 2020): 2528–35. http://dx.doi.org/10.21276/ssr-iijls.2020.6.3.1.

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