Disease relevance of Il1a

• Interleukin-1 alpha, interleukin-1 beta, and tumor necrosis factor gene expression in endotoxin-induced uveitis [1].
• Hepatic ischemia/reperfusion resulted in an enhanced (p < .01) spontaneous release of TNF-alpha (+482%), IL-1 alpha (+33%), and IL-6 (+175%) by KC [2].
• The present study determined the time course and localization of alterations in circulating and tissue pro-inflammatory cytokines (TNF-alpha, IL-1-alpha and -beta) in response to fixed-pressure (40 mm Hg) hemorrhage as well as the associated hanges in circulating neurohormonal and opioid mediators [3].
• Preincubation of hepatoma cells for 1 h with interleukin-1 alpha (IL-1 alpha) alone reduced T-kininogen concentrations by 37%, and this effect was blocked by co-addition of HOE140 [4].
• These data indicate that bone resorption stimulated by bacterial infection is primarily mediated by IL-1 alpha in this model [5].

Psychiatry related information on Il1a

• At the post-puberty stage, however, the interleukin-2-induced abnormal motor activity became undetectable, whereas interleukin-1 alpha-treated rats developed abnormalities in startle response, prepulse inhibition (PPI), and social interaction [6].
• Central effects of tumor necrosis factor alpha and interleukin-1 alpha on nociceptive thresholds and spontaneous locomotor activity [7].
• Interleukin-1 alpha and tumor necrosis factor-alpha induce an increase in pain thresholds in the rat [8].

High impact information on Il1a

• As IL-1 release prostaglandins which sensitize nociceptors in man and in experimental animals, we tested IL-1 alpha and IL-1 beta in rats for hyperalgesic (nociceptive) activity [9].
• The IL-1 receptor antagonist protein completely prevents TNF+LPS-induced inhibition of insulin secretion and attenuates nitrite formation from islets, and neutralization of IL-1 with antisera specific for IL-1 alpha and IL-1 beta attenuates TNF+LPS-induced nitrite formation by islets [10].
• Interleukin 1 alpha causes rapid activation of cytosolic phospholipase A2 by phosphorylation in rat mesangial cells [11].
• Pretreatment of osteoblast-enriched cultures with interleukin 1 alpha (IL-1 alpha) or tumor necrosis factor-alpha (TNF-alpha) synergistically enhanced the mitogenic effect of PDGF-AA coincident with increased binding site occupancy, but neither factor augmented PDGF-BB activity or binding [12].
• Recombinant IL-1 alpha (rIL-1) is a comitogen for glomerular mesangial cells [13].

Chemical compound and disease context of Il1a

• LPS, cachectin, or IL-1 alpha administration produced anorexia; weight loss in these groups was comparable to respective pair-fed animals [14].
• Plasma levels of aspartate aminotransferase (AST), hyaluronic acid (HA), TNF-alpha, IL-1 alpha and three plastanoids, 6-keto prostaglandin (PG) F1 alpha, PGE2 and TXB2, were measured before ischemia insult and 5, 60 and 120 min after reperfusion [15].
• These results suggest that cell-associated IL-1 (IL-1 alpha) is produced continuously in AM from rats with bleomycin-induced pulmonary fibrosis and may be important in regulation of this disorder by inhibiting fibroblast growth [16].
• 2. The febrile responses induced by the I.V. injection of IL-1 alpha (15 micrograms/kg) were completely abolished, and conversely hypothermia occurred, when the animals were pre-treated with a cyclo-oxygenase inhibitor, indomethacin (INDO) [17].
• Tumor necrosis factor alpha, but not interleukin-1 alpha decreases spontaneous locomotor activity evaluated by the Animex test [7].

Biological context of Il1a

• Endotoxin-induced cytokine gene expression in vivo. II. Regulation of tumor necrosis factor and interleukin-1 alpha/beta expression and suppression [18].
• IL-1 alpha slightly increased vascular permeability, whereas recombinant IL-2 and recombinant tumour necrosis factor alpha had no significant effects [19].
• These results suggest a possible anti-inflammatory role of IL-1 alpha via down-regulation of MHC antigen expression by the endothelium [20].
• Interleukin-1 alpha inhibits the effects of gamma-interferon and tumor necrosis factor alpha on the expression of the major histocompatibility antigens by the rat endothelium [20].
• These results suggest that IL-1 alpha and IL-1 beta target resting zone cells, inducing them to differentiate and acquire a phenotype characteristic of the more mature growth zone cells [21].

Anatomical context of Il1a

• Interleukin 1 alpha at the dose of 10.0 micrograms/kg body wt increased the proliferation of thyroid follicular cells (p < 0.05) [22].
• Interleukin-1 beta but not interleukin-1 alpha, induces acute inflammation-like changes in the testicular microcirculation of adult rats [23].
• We have evaluated the effects of IL-6 and IL-1 alpha as well as extracellular zinc and glucocorticoid hormone on metallothionein gene expression and cellular zinc accumulation in rat hepatocyte monolayer cultures [24].
• Interleukin-1 induces interleukin-1 alpha and interleukin-1 beta gene expression in synovial fibroblasts and peripheral blood monocytes [25].
• IL-1 alpha also stimulated alkaline phosphatase specific activity and inhibited [35S]-sulfate incorporation by resting zone chondrocytes, but had no affect on growth zone chondrocytes [21].

Associations of Il1a with chemical compounds

• Dexamethasone pretreatment prevents the LPS-induced appearance of IL-1 alpha mRNA and suppresses but does not completely inhibit the appearance of IL-1 beta mRNA [18].
• IL-1 alpha gene expression began to increase (about 10-fold greater than that of the control) as early as 1 hour after the LPS treatment, reached a peak (about 100-fold) at 3 to 6 hours [1].
• The expression of IL-1 alpha by fibers (crocidolite, chrysotile, TW, and RCF) may be a good indicator of the pathologic potential of fibers [26].
• We have studied the effect of different doses of interleukin 1 alpha (IL-1 alpha) and IL-1 beta (given twice daily ip) alone or together with antihuman IL-1 receptor antibody (aIL-1ra) on the proliferation of thyroid follicular cells and thyroid hormone levels in male Wistar rats [22].
• All the other factors studied--histamine, serotonin, bradykinin, interleukin-1 alpha (IL-1 alpha), and a partially purified interleukin-1 alpha-like factor (tIL-1) from rat testis--did not induce any acute signs of increased vascular permeability or inflammatory response after local injection [23].

Regulatory relationships of Il1a

• Dexamethasone (5 mumol l-1) prevented the IL-1 alpha-induced increase in COX-2 steady-state mRNA [27].
• Interleukin 1 alpha (IL-1 alpha) stimulates prostaglandin production and cyclooxygenase activity in endometrial stromal cells isolated from the uteri of ovariectomized rats that have been sensitized for the decidual cell reaction [27].
• Finally, TNF alpha-induced class I MHC expression was inhibited strongly by IL-1 alpha [20].
• Juxtacrine effects of IL-1 alpha precursor promote iNOS expression in vascular smooth muscle cells [28].
• This inhibitor reduced basal and IL-1 alpha- and LPS-stimulated IL-6 production [29].

Other interactions of Il1a

• Expression of IL-1 beta and TNF genes showed a pattern similar to that of IL-1 alpha [1].
• The increase of IL-1 alpha and TNF-alpha mRNA in AM peaked at 1 month and 3 days after exposure to crocidolite or TW, respectively [26].
• The aim of the present study was to examine the effect of IL-1 alpha on the amount of cyclooxygenase mRNA and protein in these cells [27].
• These data demonstrate that IL-1 alpha increases steady-state concentrations of COX-2 mRNA and protein in endometrial stromal cells isolated from the uteri of rats that have been sensitized for decidualization [27].
• At these IC50 doses, the ratios of IRAP/IL-1 were 12.5 and 220 for IL-1 alpha vs. -beta, respectively [30].

Analytical, diagnostic and therapeutic context of Il1a

• The levels of IL-1 alpha, IL-1 beta, and TNF gene expression in the iris-ciliary body (ICB) were quantified by a semiquantitative polymerase chain reaction (PCR) method; in situ hybridization histochemistry was carried out to localize the gene transcripts [1].
• Experiments were performed employing both enzyme-linked immunoassay (ELISA) and fluorescence-activated cell-sorting (FACS) techniques and recombinant cytokines: interleukin-1 alpha (IL-1 alpha), tumor necrosis factor alpha (TNF alpha), and gamma-interferon (tau IFN) [20].
• In Northern blot analysis, ICAM-1 mRNA was slightly detectable in unstimulated SMC, but its expression was clearly observed following exposure to IL-1 alpha or MCP-1 [31].
• Development and application of radioimmunoassays for interleukin-1 alpha and interleukin-1 beta [32].
• Treatment with IL-1 alpha (20 ng ml-1) for 24 h significantly increased steady-state concentrations of cyclooxygenase 2 (COX-2) mRNA and protein in the cells, as determined by northern and western blot analyses, respectively [27].

References