Disease relevance of Il1rn

• Glomerular expression of interleukin-1 receptor antagonist and interleukin-1 beta genes in antibody-mediated glomerulonephritis [1].
• Messenger RNA for IL-1ra and IL-1 beta was undetectable by Northern blot in normal glomeruli but increased markedly 4 to 6 hours after induction of nephritis [1].
• IL-1ra (0.1 microgram) also blocked the development of and reversed an established capsaicin-induced hyperalgesia [2].
• Cortical tissues that received rAAV-IL-1ra injections had both significantly smaller total volumes of infarction as well as smaller areas of infarction on each brain slice when compared with the control models [3].
• Gene treatment of cerebral stroke by rAAV vector delivering IL-1ra in a rat model [3].

Psychiatry related information on Il1rn

• However, simultaneous administration of both pentoxifylline and IL-1ra markedly attenuated MF-induced anorexia and body weight loss, but had no effect on the suppression of social behavior [4].
• Pretreatment of rats with IL-1ra, but not with pentoxifylline, significantly attenuated gp120-induced anorexia and loss in body weight, whereas both agents had no effect on gp120-induced reduction in locomotor activity in the open field [5].

High impact information on Il1rn

• Treatment with IL-1ra did not affect the steady state mRNA expression of either IL-1 beta or TNF alpha [6].
• The contribution of IL-1 to leukocyte infiltration in anti-glomerular basement membrane (GBM) antibody (Ab) glomerulonephritis (GN) was examined by the administration of a specific IL-1 receptor antagonist (IL-1ra) [6].
• Interleukin-1 receptor antagonist ameliorates experimental anti-glomerular basement membrane antibody-associated glomerulonephritis [6].
• PMN and monocyte/macrophage infiltration declined 39% (9.8 +/- 1.9 to 6.0 +/- 1.5 PMN/glomerulus, P < 0.001) and 29% (4.9 +/- 0.8 to 3.5 +/- 0.8 ED-1 cells/glomerulus, P = 0.002) with IL-1ra treatment at 4 h, respectively [6].
• These end points were examined: (1) after administration of the locally active steroid budesonide; (2) in congenitally athymic rats; and (3) in rats treated with the interleukin 1 receptor antagonist (IL-1ra) to interleukin 1 beta [7].

Chemical compound and disease context of Il1rn

• Co-administration of the cytokine with the IL-1R antagonist, IL-1ra, or actinomycin D, significantly inhibited the 111In-labeled eosinophil accumulation, and reduced the edema formation, induced by rat rIL-1 [8].
• In the present study, roles of tumor necrosis factor-alpha (TNFalpha) and interleukin-1 beta (IL-1beta) in mediating lipopolysaccharide (LPS)-induced brain injury were investigated by co-administration of LPS with IL-1 receptor antagonist (IL-1ra) or TNFalpha antibody in the 5-day-old rat brain [9].
• METHODS: Both local cerebral blood flow and hypothalamic dopamine release during onset of heatstroke were assessed in saline-treated rats and in rats treated with an IL-1ra [10].
• Influence of the course of brain inflammation on the endogenous IL-1beta/IL-1Ra balance in the model of brain delayed-type hypersensitivity response to bacillus Calmette-Guérin in Lewis rats [11].
• RESULTS: In rats with TNBS-induced colitis, intracerebroventricular infusion of IL-1ra resulted in a 18-fold reduction in PVN 5-HT release compared to vehicle-treated controls [12].

Biological context of Il1rn

• Evaluation of interleukin-1 receptor antagonist (IL-1RA) and tumor necrosis factor binding protein (TNF-BP) in a rodent abscess model of host resistance [13].
• There are few data about kinetics of in vivo synthesis of IL-1ra at tissue level, except in response to bacterial endotoxin [1].
• IRAP inhibited ovulation without significantly affecting PG or steroid production [14].
• At these IC50 doses, the ratios of IRAP/IL-1 were 12.5 and 220 for IL-1 alpha vs. -beta, respectively [15].
• The IL-1 receptor antagonist (IL-1ra) injected intravenously (3 micrograms/rat) or intracisternally (100 ng/rat) reversed the IL-1 beta-induced 47% inhibition of gastric emptying by 100% and 62%, respectively [16].

Anatomical context of Il1rn

• The maximum mRNA levels of IL-1 beta were 15-fold higher than pre-IMS levels, whereas those of IL-1Ra were 250-fold higher in the hypothalamus [17].
• Biotinylated IL1ra also labeled smooth muscle and endothelial cells of blood vessels and lymphoid tissues [18].
• The purpose of this study was to examine the kinetics of local expression of IL-1ra gene in relation to IL-1 beta gene in a model of anti-glomerular basement membrane antibody-mediated glomerulonephritis [1].
• Expression of these mRNA in noninflamed tissues, spleens and lungs, was different, particularly increase in IL-1ra mRNA was more substantial than that of IL-1 beta [1].
• 5 Neutrophil migration induced by LPS or BK was reduced by interleukin-1 receptor antagonist (IL-1ra) (1 mg kg(-1)), sheep anti-rat TNF serum (anti-TNF serum) (0.3 ml cavity(-1)), and the nonspecific selectin inhibitor fucoidin (10 mg kg(-1)) [19].

Associations of Il1rn with chemical compounds

• The natural IRAP inhibited ovulation (7.8 +/- 3.9 ovulations vs. 12.4 +/- 1.5; P < 0.04) in PMSG-stimulated ovaries given LH and IBMX as the ovulatory trigger compared to that in controls [14].
• OHSCs obtained from rats were excitotoxically lesioned after 6 days in vitro by application of N-methyl-D-aspartate (NMDA) and treated with IL-1beta (6 ng/mL) or IL-1ra (40, 100 or 500 ng/mL) for up to 10 days [20].
• In addition, a few neurons expressing IL-1ra mRNA were observed in the piriform cortex and amygdala following kainic acid injection [21].
• Triphenyltetrazolium chloride (TTC) staining of viable brain tissue revealed that the rAAV-delivered IL-1ra gene could rescue the brain tissues from ischemia-induced injury [3].
• In hepatocytes, the NO formation induced by IL-l beta was blocked by both the NO synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA) and by IL-1 receptor antagonist (IL-1ra) [22].

Physical interactions of Il1rn

• Interleukin-1 receptor antagonist (IL-1ra) competes with IL-1 for binding of the IL-1 receptor, but does not elicit a cellular immune response [23].

Regulatory relationships of Il1rn

• IL-1 beta-induced current reduction could not be abolished by the interleukin-1 receptor antagonist, indicating that the electrophysiological effects of IL-1 beta are independent of interleukin-1 receptor I (IL-1RI) activation [24].
• IL-1ra attenuated the sepsis-induced decrease in plasma IGF-I and completely prevented the changes in IGF-I observed in liver, kidney, and the gastrocnemius [25].
• Moreover, when IL-1 receptor activity was inhibited using an adenoviral vector that expresses the IL-1 receptor antagonist (IL-1ra) in the hippocampus, both short-term and long-term memory retention scores were facilitated [26].
• Excitotoxic damage due to striatal infusion of an NMDA-receptor agonist (cis-2,4-methanoglutamate) was also markedly inhibited (71%) by injection of the IL-1ra [27].

Other interactions of Il1rn

• 3. After the biosynthesis of IL-1 beta has peaked, IL-1Ra may contribute to attenuation of the IL-1 activity which has been enhanced by IMS [17].
• 3. At 1 microgram ml-1, the specific IL-1 receptor antagonist, IRAP, antagonised the effect induced by, 10 ng ml-1 IL-1 [28].
• Contralateral, non-grafted corneas showed constitutive mRNA expression for interleukin-1 receptor antagonist and in a few samples also monocyte chemotactic protein-1 and macrophage inflammatory protein-2 mRNA was found [29].
• A detectable level of TGF-beta 1 was found 8 h after stimulation and a plateau was reached at 72 h with a maximal increase of 5-fold and was inhibited by IL-1 receptor antagonist (IL-1ra) [30].
• They were rich in interleukin-1, interleukin-1 receptor antagonist and interleukin-6 [31].

Analytical, diagnostic and therapeutic context of Il1rn

• Immobilization stress increases mRNA levels of interleukin-1 receptor antagonist in various rat brain regions [17].
• In situ hybridization showed that IL-1 beta mRNA increased diffusely within glomeruli, while IL-1ra mRNA was expressed more discretely [1].
• An accumulation of IL-1ra in cortical tissues of rAAV-IL-1ra-injected animals was confirmed by ELISA [3].
• Adult male rats were perfused via an intra-aortic cannula with either A beta alone, interleukin-1 receptor antagonist (IL-1 ra) plus A beta, tumor necrosis factor-binding protein (TNF-bp) plus A beta or sterile saline [32].
• The IL-1ra was found to inhibit LPS-induced acute inflammation (P greater than 0.0001) as measured by the number of neutrophils recovered in bronchoalveolar lavage [33].

References