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The immune and lymphatic systems, infection and sepsis
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Michelle Treacy, Caroline Smales, Helen Dutton
Resolving inflammation does not occur simply as a result of stopping the pro-inflammatory response, rather, it is an active and synchronised process dependent on anti-inflammatory cytokines (those that suppress the immune system by inhibiting cytokine production). Anti-inflammatory cytokines include interleukin-1 receptor antagonist, interleukins-4, -6 and -10. Some cytokines have both pro-inflammatory and anti-inflammatory effects; it depends on the receptor they activate, see Table 12.7 for their clinical effect.
Immune Modulation In Sepsis
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Janet M. J. Hammond, Peter D. Potgieter
Interleukin 1 receptor antagonist (IL-1ra) is a naturally occurring 17- to 22-kDa protein synthesized by a variety of inflammatory cells, which exhibits homology with IL-1β and is a part of the body’s normal mechanism for controlling acute inflammation. Increased concentrations of this endogenous cytokine antagonist are detected in human sepsis or experimental inflammation, and the molecule has no intrinsic agonist properties, even at increased concentrations. It inhibits IL-1 by competing with it for cell receptor sites [199]. A recombinant 17-kDa form has been produced and has been found to prevent shock and reduce mortality rate in several rodent and baboon models of sepsis [200]. Increased survival rates of animals challenged with endotoxin or gram-negative bacteria and improvement in hemodynamic parameters in animals challenged with gram-positive bacteria have been observed when IL-1ra has been administered before or up to 3 hours after the septic challenge [201].
Treatment of Rheumatoid Arthritis
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Stuart Weisman, Arthur Kavanaugh
In rheumatoid arthritis, IL-lβ is present in large quantities in the synovial fluid and synovial tissue.47 Interleukin-1 β can stimulate metalloproteinase expression, adhesion molecule expression, secretion of other cytokines, and prostaglandin production. Interleukin 1 receptor antagonist is a naturally occurring competitive inhibitor for IL-la and IL-lβ. IL-1 Ra binds to the IL-1R1 (interleukin-1 receptor) without transducing a signal, thus blocking the ability of interleukin la or 1 β to bind to the receptor. In November 2001, anakinra was approved for the treatment of rheumatoid arthritis. Anakinra is a recombinant form of the naturally occurring interleukin-1 receptor antagonist (ILl-Ra) produced using E. coli.
Amyloid nomenclature 2022: update, novel proteins, and recommendations by the International Society of Amyloidosis (ISA) Nomenclature Committee
Published in Amyloid, 2022
Joel N. Buxbaum, Angela Dispenzieri, David S. Eisenberg, Marcus Fändrich, Giampaolo Merlini, Maria J. M. Saraiva, Yoshiki Sekijima, Per Westermark
Interleukin-1 is a prominent proinflammatory cytokine which is over-expressed in a number of inflammatory diseases, e.g. in auto-inflammatory disorders and in rheumatoid arthritis. Interleukin-1 receptor antagonist protein is expressed as a 177 aa protein including a 25 aa signal peptide. Anakinra is a recombinant analog, which binds to the IL-1 receptor and thereby exerts anti-inflammatory properties and is used therapeutically in rheumatoid arthritis and a variety of inflammatory disorders. The drug is given subcutaneously with one daily dose 100 mg which may vary according to the patients’ clinical status. In a recent report two patients were described with pronounced localised subcutaneous amyloid deposits at the site of injections [21]. Mass spectrometric analyses showed these to be of Interleukin-1 receptor antagonist protein nature. The name of the amyloid fibril protein is AIL1RAP.
Changes in health-related outcomes among colorectal cancer patients undergoing inpatient rehabilitation therapy: a systematic review of observational and interventional studies
Published in Acta Oncologica, 2021
Sophie Scherer, Lina Jansen, Daniel Boakye, Michael Hoffmeister, Hermann Brenner
Results from two studies suggest that the intensity of endurance training during rehabilitative treatment could influence immune response [41] and the level of oxidative stress [42]. Both studies compared 2-week aerobic exercise with lower (30–40% × maximal exercise capacity) and higher intensity (50–60%/55–65%). A significant reduction in oxidative stress levels measured by urinary 8-Oxo-2′-deoxyguanosine was observed from before treatment to after treatment in the lower exercise intensity group in comparison to no significant reduction in the higher-intensity group [42]. A significant decrease in anti-inflammatory cytokines (Lipopolysaccharide-stimulated interleukin-1 receptor antagonist) was observed in the higher-intensity group in comparison to no significant change in the lower-intensity group [41]. The potential benefit for both outcomes, with respect to infection rate, anti-tumor response, and survival, is unknown hitherto as pointed out by the authors.
A positive association between interleukin-1 receptor antagonist and insulin resistance in postmenopausal women
Published in Gynecological Endocrinology, 2018
Chii-Min Hwu, Hung-Hsiang Liou, Chung-Jen Lee, Bang-Gee Hsu
Interleukin-1 receptor antagonist (IL-1Ra) is a naturally occurring protein of the inteleukin-1 (IL-1) family [1]. Evidence indicates that circulating IL-1Ra competitively inhibits IL-1 binding to the IL-1 receptor without initiating cellular signal transduction, thus, antagonizing the inflammatory effects of IL-1 [1,2]. Plasma IL-1Ra concentrations gradually increase from normoglycemic through prediabetes to type 2 diabetes mellitus (DM) [3]. Insulin resistance and β-cell dysfunction are two major pathophysiological features of type 2 DM and both are present very early in the natural history of the disease [4]. Fève and Bastard proposed that IL-1Ra could have a dual effect on insulin resistance and insulin secretion, namely, modulation of both insulin sensitivity and β-cell capacity [5].