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CSF3 — IL1A

Text-mined interactions from Literome

Nakata et al., Cancer Sci 2003 (Disease Progression...) : Inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-1beta stimulated the expression of G-CSF , GM-CSF, and cyclooxygenase (COX)-2 in the two cell lines
Suzuki et al., Br J Cancer 1992 : These results indicate that IL-1 alpha regulates G-CSF and IL-6 production in these tumour cell lines, and suggest that the IL-1 production plays an important role in CSF producing tumours
Segal et al., Blood 1992 : Moreover, IL-1 induced GM-CSF or G-CSF expression does not depend on expression of the other factor
Leizer et al., Blood 1990 : The transcription inhibitor, actinomycin D, and protein synthesis inhibitor, cycloheximide, inhibited the increase in GM-CSF and G-CSF production induced by IL-1 and TNF
Tweardy et al., J Neuroimmunol 1991 (HIV Infections) : We have recently demonstrated that IL-1 alpha and beta induced the production of GM-CSF and G-CSF by two human astroglial cell lines
Falkenburg et al., Blood 1991 : Interleukin-1 (IL-1) combined with fetal bovine serum ( FBS ) strongly induces the expression of macrophage-CSF (M-CSF), granulocyte-CSF (G-CSF) , and granulocyte-macrophage-CSF (GM-CSF) in fibroblasts ... G-CSF mRNA expression was induced by IL-1 , and not by FBS ... IL-1 induced G-CSF expression was completely prevented in these cells by pretreatment with cycloheximide, illustrating that, for this effect, intermediate protein synthesis was required
Shieh et al., J Immunol 1991 : In vitro, G-CSF induced a greater than 1.5-fold increase in IL-1 binding to BMC after 8 h, suggesting that up-modulation of IL-1 binding in vivo required G-CSF and other influences ... Inasmuch as IL-1 induces the secretion of G-CSF and glucocorticoids in vivo, this synergistic induction may play an important, as yet unknown, role in the inflammatory cascade
Galy et al., J Immunol 1991 : IL-1 alpha strongly up-regulated the production of granulocyte-macrophage CSF (GM-CSF), granulocyte CSF (G-CSF) , IL-6, and IL-8, as measured by specific immunoenzymetric assays and by increased steady state mRNA levels ... Only IFN-gamma, and not IL-4, suppressed the IL-1 induced G-CSF and IL-8 production, as shown at both the protein and mRNA levels
Shieh et al., J Immunol 1991 : 125I-G-CSF bound to PEM has a half-life of 30 min at 37 degrees C. Preincubation of PEM with murine rTNF, murine recombinant granulocyte-macrophage CSF, CSF-1, or G-CSF for 30 min at 37 degrees C resulted in partial reduction of 125I-G-CSF binding capacity, whereas IL-1 or IFN-gamma did not inhibit G-CSF binding
Sauter et al., Cancer Biol Ther 2011 : Studies with IL-1R-deficient mice demonstrate that IL-1 signaling plays a role in doxorubicin induced increases in IL-6 and GCSF
Wang et al., Int J Oncol 1995 : We report that all-trans retinoic acid ( tRA ) synergizes with LPS to enhance the production of granulocyte colony stimulating factor ( G-CSF ) in PMA treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta) , and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA
Cain et al., PloS one 2011 (Inflammation...) : Here, we show in mice that alum triggers emergency granulopoiesis through the IL-1RI dependent induction of G-CSF
Shih et al., PloS one 2012 : The expression of granulocyte colony stimulating factor ( G-CSF ), the major regulator of neutrophil maturation, by human fibroblast-like synoviocytes ( FLS ) can be stimulated by the inflammatory cytokine interleukin-1ß (IL-1ß) ... The aims of this study were to identify the signaling pathways involved in IL-1ß stimulated G-CSF production and to determine whether this process was inhibited by aciculatin ( 8- ( ( 2R,4S,5S,6R ) -tetrahydro-4,5-dihydroxy-6-methyl-2H-pyran-2-yl ) -5-hydroxy-2- ( 4-hydroxyphenyl ) -7-methoxy-4H-chromen-4-one ), the major bioactive component of Chrysopogon aciculatus ... Whether aciculatin inhibited IL-1ß stimulated G-CSF expression, and if so, how, were evaluated using western blot assay, an electrophoretic mobility shift assay, and a reporter gene assay ... Aciculatin markedly inhibited G-CSF expression induced by IL-1ß ( 10 ng/mL ) in a concentration dependent manner ( 1-10 µM ) ... Our results show that aciculatin inhibits IL-1ß stimulated G-CSF expression and the subsequent neutrophil differentiation, suggesting that it might have therapeutic potential for inflammatory arthritis
Schaafsma et al., Blood 1989 : Neutralization experiments with an anti-G-CSF monoclonal antibody showed that IL-1 induced G-CSF production was responsible for the synergy with GM-CSF
Ogawa et al., Hematol Oncol Clin North Am 1989 : Available evidence indicates that the effects of IL-1 on stem cells are indirectly mediated in part by IL-6 and G-CSF
Zsebo et al., Blood 1988 : G-CSF radioimmunoassay of endothelial cell culture supernatants and Northern blot analysis of endothelial cell cytoplasmic RNA for GM-CSF gene transcripts confirmed that IL 1 induced expression of both G-CSF and GM-CSF genes
Caldwell et al., J Cell Physiol 1994 : We further show that IL-1 alpha and TNF alpha synergistically stimulate production of GM-CSF and G-CSF by a clonal stroma derived cell strain
Watari et al., Stem Cells 1994 : Induction of G-CSF by interleukin 1 (IL-1) and lipopolysaccharide (LPS) was compared using enzyme immunoassay in various kinds of stromal cells ... IL-1 and LPS stimulated similar levels of G-CSF production by primary bone marrow stromal cells which consisted of various types of cells
Tsuyuoka et al., Eur J Cancer 1994 (Lung Neoplasms) : These results indicate that CSF producing tumours can be characterised by their constitutive IL-1 production, IL-1 receptor expression and IL-1 dependent excess production of G-CSF and IL-6
Caldwell et al., Blood 1995 : Taken together, these results raise the possibility that IL-1 alpha cross-induction of TNF receptors may contribute to the biochemical mechanisms underlying the synergistic stimulation of G-CSF and GM-CSF production by IL-1 alpha and TNF alpha
Aman et al., Blood 1994 : Production of granulocyte-macrophage colony stimulating factor ( GM-CSF ), granulocyte-CSF (G-CSF) , and interleukin-1 beta (IL-1 beta) in stromal cell layers was induced by incubation with IL-1 alpha , tumor necrosis factor (TNF), or lipopolysaccharide (LPS)
Moses et al., Blood 1996 (HIV Infections) : Although HIV infected stromal cultures enriched for MVEC constitutively express normal levels of interleukin (IL)-4, IL-6, granulocyte ( G)-colony stimulating factor (CSF), granulocyte-macrophage (GM)-CSF, tumor necrosis factor (TNF)-alpha, transforming growth factor ( TGF ) -beta, and Steel factor, IL-1 alpha induced release of IL-6 and G-CSF is significantly reduced in these cultures
Haynesworth et al., J Cell Physiol 1996 : In contrast, IL-1 alpha increased the expression of G-CSF , M-CSF, LIF, IL-6 and IL-11 and induced the expression of GM-CSF
Ogawa et al., Am J Hematol 1996 : Interleukin-1 (IL-1) induced a dose dependent production of G-CSF , and the production reached a plateau at 50 U/ml of IL-1
Lai et al., Blood 1996 (Acute-Phase Reaction...) : In human hepatoma HepG2 and Hep3B cells, IL-1 beta induced production of the granulocyte colony stimulating factor ( G-CSF ) in a dose dependent manner
Wang et al., Biochem Biophys Res Commun 1996 (Leukemia, Monocytic, Acute) : Finally, we demonstrated that RA can also enhance IL-1 induced G-CSF production in primary monocytes of human peripheral blood
Rinehart et al., Exp Hematol 1997 : Analysis of the cytokines produced by mononuclear cell subpopulations demonstrated that HCS markedly enhanced IL-1 induced monocyte secretion of granulocyte (G)-CSF ... HCS alone had no effect on G-CSF secretion or mRNA expression while IL-1+HCS resulted in a 3-fold increase in G-CSF mRNA levels
Eissner et al., Br J Haematol 1997 : This could be explained, at least in part, by an increased autocrine G-CSF production by endothelial cells in response to IL-1 and exogenous G-CSF
Majumdar et al., J Cell Physiol 1998 : Steady-state levels of IL-11 and IL-12 mRNA were found to be greater in MSCs. Addition of IL-1alpha induced steady-state levels of G-CSF and GM-CSF mRNA in both cell preparations