Disease relevance of Il1a

• In vivo biologic and immunohistochemical analysis of interleukin-1 alpha, beta and tumor necrosis factor during experimental endotoxemia. Kinetics, Kupffer cell expression, and glucocorticoid effects [1].
• Therefore, infection of mice with scrapie resulted in significant increases in the expression of the TNF-alpha, IL-1 alpha, and IL-1 beta gene products, whose pattern correlated with the onset and development of molecular and clinical pathological changes [2].
• We conclude that cytokine mRNA expression during the early phases of L. monocytogenes infection in mice is temporally regulated and that IFN-gamma, TNF-alpha, and IL-1 alpha are expressed by cells associated with hepatic granulomas [3].
• Production of tumor necrosis factor alpha, interleukin-1 alpha, and interleukin-6 during murine coccidioidomycosis [4].
• Tumor necrosis factor alpha, interleukin-1 alpha, interleukin-6, and prostaglandin E2 production in murine peritoneal macrophages infected with Ehrlichia risticii [5].

Psychiatry related information on Il1a

• The host defense mechanisms triggered by IL-1 alpha and IL-1 beta differed from one another [6].
• Diurnal variation of heart rate, locomotor activity, and body temperature in interleukin-1 alpha/beta doubly deficient mice [7].
• Peripherally administered IL-1 alpha interferes with scopolamine-induced amnesia in mice [8].
• LPS ip or i.v. produced lethargy, diarrhea, and a dramatic elevation of IL-1 alpha levels in both SB and LB [9].

High impact information on Il1a

• ICE therefore plays a dominant role in the generation of mature IL-1 beta, a previously unsuspected role in production of IL-1 alpha, but has no autonomous function in apoptosis [10].
• Requirement for TNF-alpha and IL-1 alpha in fetal thymocyte commitment and differentiation [11].
• The product of the cloned complementary DNA binds both IL-1 alpha and IL-1 beta in a manner indistinguishable from that of the native T cell IL-1 receptor [12].
• Production of interleukin (IL)-6 in response to IL-1 alpha or tumor necrosis factor (TNF)-alpha was nearly abolished in homozygous mutant (Shp-2(-/)-) fibroblast cells [13].
• MGF also acted synergistically with both IL-3 and IL-1 alpha to promote stem cell proliferation [14].

Chemical compound and disease context of Il1a

• Pretreatment with 250 micrograms of neutralizing antibody to TNF had no effect on IL-1 alpha-induced hemorrhage, whereas TNF-alpha- and LPS-induced hemorrhagic effects were significantly reduced [15].
• Neither IL-4 nor IL-13 further inhibited IL-1 alpha-induced bone resorption in the presence of indomethacin [16].
• Of these cytokines, IL-4 similarly suppressed IL-1 alpha-induced bone resorption, but IL-2 and IL-7 did not [16].
• Actinobacillus actinomycetemcomitans Y4 capsular-polysaccharide-like polysaccharide promotes osteoclast-like cell formation by interleukin-1 alpha production in mouse marrow cultures [17].
• Therefore, the previously reported reduced resistance of vanadate-treated mice to Listeria monocytogenes could be attributed to an inhibitory effect on the production of IL-1 alpha in macrophages [18].

Biological context of Il1a

• In vivo effect of interleukin-1 alpha on hematopoiesis: role of colony-stimulating factor receptor modulation [19].
• Agarose gel electrophoresis of DNA extracted from cells exposed to IL-1 alpha and agonistic anti-Fas showed internucleosomal DNA fragmentation, a hallmark of apoptotic cell death [20].
• The effects of TNF-alpha and IL-1 alpha on glucose uptake and phosphorylation appear to be mediated by the phospholipase A2 signal transduction pathway [21].
• These results demonstrate that TNF-alpha and IL-1 alpha can fundamentally perturb the energy metabolism of astrocytes, possibly impairing their ability to provide adequate energy substrates for neurons [21].
• The additional glucose imported by astrocytes on exposure to TNF-alpha and IL-1 alpha is neither stored as glycogen nor released as glycolytically derived lactate, suggesting that it is processed through the tricarboxylic acid cycle or pentose phosphate pathway [21].

Anatomical context of Il1a

• Adherent monocytes from mice harboring a disrupted ICE gene (ICE-/-) did not export IL-1 beta or interleukin-1 alpha (IL-1 alpha) after stimulation with lipopolysaccharide [22].
• To determine the mechanism(s) by which interleukin-1 (IL-1) promotes granulopoiesis in vivo, we examined the effect of in vivo administration of IL-1 alpha on colony-stimulating factor (CSF) receptor expression on bone marrow cells (BMCs) and whether this directly correlated with progenitor cell responsiveness [19].
• We used highly purified murine granulocyte-macrophage progenitor cells (CFU-GM, up to 92% cloning efficiency) to assess the effects of IL-1 alpha on the proliferation, differentiation, and survival of these cells [23].
• No secretion of interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor-alpha was detected by any of the stromal cell lines [24].
• When either TNF alpha or GM-CSF was neutralized by monoclonal antibodies the addition of IL-1 alpha resulted in a significant increase in BFU-E growth [25].

Associations of Il1a with chemical compounds

• In vivo control of differentiation of myeloid leukemic cells by cyclosporine A and recombinant interleukin-1 alpha [26].
• Thus, IL-10 may induce a ribonuclease active on cytokine transcripts or may induce a protein that enhances the susceptibility of TNF, IL-1 alpha, and IL-1 beta mRNAs to ribonucleolytic action [27].
• Pretreatment with 4 mg/kg dexamethasone significantly decreased Kupffer cell expression of TNF and IL-1 alpha (about 80% and 60% suppression, respectively) but had less effect on IL-1 beta expression (about 30% suppression) [1].
• Tumor necrosis factor-alpha and interleukin-1 alpha enhance glucose utilization by astrocytes: involvement of phospholipase A2 [21].
• Uterus from ovariectomized mice contained little or no cytokine activity, and systemic administration of estrogen or progesterone resulted in the induction of IL-1 alpha and IL-1 beta mRNA expression [28].

Regulatory relationships of Il1a

• Thus, IL-1 alpha directly and indirectly stimulates the growth and differentiation of purified progenitors through the type I IL-1R but not the type II IL-1R [29].
• IL-18 induced intracellular expression of IL-1 alpha and proIL-1 beta, and release of IL-6 from mixed glia [30].
• Tumor necrosis factor alpha and interleukin-1 alpha inhibit through different pathways interferon-gamma-induced antigen presentation, processing and MHC class II surface expression on astrocytes, but not on microglia [31].
• Moreover, all three fractions were found to increase the expression of IL-1-alpha mRNA while PH-I C showed the most potent activating effect on the expression of IL-1-beta mRNA [32].
• Secretion of IL-6 by USC was stimulated by IL-1 alpha, and coculture studies demonstrated the ability of UEC to stimulate a several-fold increase in IL-6 secretion by USC [33].

Other interactions of Il1a

• The addition of IL-1 alpha to culture stimulated the release of both TNF alpha and GM-CSF and acted synergistically with both cytokines, resulting in a dose-dependent suppression of BFU-E and stimulation of CFU-GM growth [25].
• The results demonstrated that IL-1 alpha does not directly influence the proliferation or differentiation of purified CFU-GM in the presence of plateau concentrations of purified natural or recombinant CSFs, and IL-1 alpha lacks intrinsic CSF activity of its own [23].
• The direct synergistic effect of IL-1 alpha on CSF-1-induced progenitor growth was observed in all progenitor populations examined (Lin-, Lin-Thy-1+, and Lin-Thy-1-) and was inhibited by MoAb 35F5 [29].
• Interferon-gamma and interleukin-1 alpha induce transient translocation of protein kinase C activity to membranes in a B lymphoid cell line. Evidence for a protein kinase C-independent pathway in lymphokine-induced cytoplasmic alkalinization [34].
• However, IL-1 alpha and IL-6 mRNA levels in diestrous epithelial cells, like those in D1 epithelial cells, increased in culture [35].

Analytical, diagnostic and therapeutic context of Il1a

• Furthermore, the quantitative comparison of cytokine transcripts in cLC vs cKC using Northern blot analysis and mRNA detection on the single cell level using in situ hybridization confirmed that cLC generate IL-6, whereas cKC synthesize IL-1 alpha and GM-CSF [36].
• METHODS: Male DBA/1 mice with collagen-induced arthritis were treated with antibodies against murine TNF alpha and IL-1 alpha/beta at different time points of the disease [37].
• Western immunoblots of 100-fold concentrated CM demonstrated only a single 33 kD band with an antiserum to murine IL-1 beta and no bands with an antiserum to murine IL-1 alpha [38].
• Surface Fas expression was detected by immunofluorescence flow cytometry using a non-cytolytic anti-Fas monoclonal antibody after 6 or 12 h of incubation with 10(3) U/l of IL-1 alpha [20].
• Activity in the CM eluted from a gel filtration column with a peak Mr of 16-18 kD (the Mr of mature murine IL-1 alpha and beta is 17 kD) [38].

References