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ICAM1 — IL6

Text-mined interactions from Literome

Lauzurica et al., Eur J Immunol 1999 (Disease Models, Animal...) : PDTC treated mice survived despite high IL-1beta and IL-6 levels, induction of VCAM-1 and ICAM-1 expression or leukocyte infiltration in tissues known to be associated with LPS induced shock, indicating that PDTC does not act by modifying these responses
Kuroiwa et al., J Immunol 1999 (Glomerulonephritis) : Ligation of mesangial surface ICAM-1 directly enhanced IL-6 , but not MCP-1, production
Lee et al., J Immunol 2000 (MAP Kinase Signaling System) : ICAM-1 ligation by a mAb to rat ICAM-1 induced mRNA expression of proinflammatory cytokines such as IL-1alpha, IL-1beta, IL-6 , and TNF-alpha ... Examination of cytokine protein production revealed that ICAM-1 ligation results in IL-6 secretion by astrocytes, whereas IL-1beta and IL-1alpha protein is expressed intracellularly in astrocytes ... Studies using pharmacological inhibitors demonstrate that both p38 MAPK and ERK1/2 are involved in ICAM-1 induced IL-6 expression, whereas only ERK1/2 is important for IL-1alpha and IL-1beta expression
Marino et al., J Neuroimmunol 2001 : Membrane ICAM-1 and mRNA expression are absent under basal conditions, but can be induced by IFN-gamma, IL-1beta, IL-4, LPS and IL-6 with different efficiencies and time-courses
Amrani et al., Mol Pharmacol 2001 : Pretreatment of ASM cells with SB203580, a p38 MAPK inhibitor, slightly enhanced TNF alpha induced ICAM-1 expression in a dose dependent manner but partially inhibited secretion of RANTES and IL-6
Wang et al., J Immunol 2003 : Using various deletion constructs of ICAM-1 promoter, we show that ICAM-1 induction by IL-6 requires the activation of NF-kappaB
Detmar et al., J Invest Dermatol 1992 : The effects of recombinant human interleukin 1 alpha (IL-1 alpha), interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6) , granulocyte/macrophage colony stimulating factor ( GM-CSF ) and tumor necrosis factor-alpha (TNF) on the cell proliferation and the expression of intercellular adhesion molecule-1 ( ICAM-1 ) were assessed in cultured human dermal microvascular endothelial cells ( HDMEC )
Giavazzi et al., Cancer Res 1992 (Melanoma) : Tumor necrosis factor, interleukin 1, and gamma-interferon also caused the release of soluble ICAM-1
Andersen et al., Nephrol Dial Transplant 1992 : Furthermore, the in vitro model indicates that ICAM-1 expression is regulated by gamma-interferon and interleukin-1 produced by activated T lymphocytes and macrophages
Walia et al., FASEB J 2003 : We show that pretreatment of cells with TGF-beta1 is associated with a down-regulation of IL-6 induced tyrosine phosphorylation of STAT1 and STAT3 and suppression of ICAM-1 expression ... Furthermore, TGF-beta1 pretreatment resulted in a significant inhibition of IL-6 induced ICAM-1 promoter activity ... TGF-beta mediated inhibition of IL-6 induced ICAM-1 expression was reversed by transfection with dominant negative Smad2 constructs ... In conclusion, we show that : 1 ) TGF-beta receptor Type II is predominantly located on basolateral membrane and receptor stimulation activates Smad pathway ; 2 ) TGF-beta1 down-regulates IL-6 induced tyrosine phoshorylation of STAT1 and STAT3 and ICAM-1 expression ; and 3 ) Smad2 is required for the down-regulation of IL-6 signaling by TGF-beta
Stuyt et al., Immunology 2003 : Selective regulation of intercellular adhesion molecule-1 expression by interleukin-18 and interleukin-12 on human monocytes
Wung et al., J Biomed Sci 2005 : ICAM-1 induction by TNFalpha and IL-6 is mediated by distinct pathways via Rac in endothelial cells ... In this study, the molecular mechanisms of tumor neurosis factor alpha (TNFalpha)- and IL-6 induced ICAM-1 gene expression in endothelial cells ( ECs ) were examined ... ECs infected with adenovirus carrying the dominant negative mutant of Rac ( Ad-RacN17 ) exhibited inhibition in both TNFalpha- and IL-6 induced ICAM-1 expression ... Consistently, ECs transfected with RacN17 inhibited both TNFalpha- and IL-6 induced ICAM-1 promoter activities ... ECs transfected with the dominant negative mutant of Stat3 ( Stat3F ) demonstrated that Stat3 was required for IL-6 induced ICAM-1 gene expression ... Our data strongly indicated that ICAM-1 gene induction by TNFalpha and IL-6 is mediated mainly via NFkappaB and Stat3, respectively and Rac1 appears to play a central role in modulating cytokine induced ICAM-1 expression in ECs
Wung et al., Life Sci 2005 : Resveratrol suppresses IL-6 induced ICAM-1 gene expression in endothelial cells : effects on the inhibition of STAT3 phosphorylation ... In this study we tested the effects of resveratrol upon both IL-6 induced ICAM-1 gene expression and its underlying signaling pathways in endothelial cells ( ECs ) ... Resveratrol was found to inhibit both TNFalpha- and IL-6 induced ICAM-1 gene expression at the promoter, transcriptional and protein levels ... In summary, we demonstrate for the first time that resveratrol inhibits IL-6 induced ICAM-1 gene expression, in part, by interfering with Rac mediated pathways via the attenuation of STAT3 phosphorylation
Yang et al., J Mol Cell Cardiol 2006 (Shock, Hemorrhagic...) : Thus, IL-6 mediated upregulation of cardiac NF-small ka, CyrillicB, ICAM-1 , CINC-1, -3, and MPO activity likely contributes to altered cardiac function following T-H and neutralization of IL-6 therefore appears to be an effective and novel adjunct for improving organ/cell function under those conditions
Chen et al., Br J Pharmacol 2006 : Mag pretreatment of these ECs dose dependently suppressed IL-6 induced promoter activity of intracellular cell adhesion molecule ( ICAM)-1 that contains functional IL-6 response elements (IREs)
Chen et al., Exp Eye Res 2006 (Translocation, Genetic) : We used flow cytometry and an ARPE-19 cell model to determine the effect of GS on the production of ICAM-1 in response to IL-1beta, IL-6 , tumor necrosis factor (TNF)-alpha plus IL-1beta, TNF-alpha plus IL-6, and TNF-alpha plus interferon (IFN)-gamma ... GS downregulated the production of ICAM-1 induced by IL-1beta, IL-6 , TNF-alpha, and IFN-gamma at the protein level in a dose dependent manner
Moreira et al., Am J Pathol 2006 (Disease Susceptibility...) : Expression of ICAM-1 was up-regulated on T lymphocytes after infection with the fungus, and its expression was dependent on interferon-gamma, tumor necrosis factor-alpha, and interleukin-12
Kempf et al., J Mol Med (Berl) 2007 (Hyperglycemia...) : Using quantitative real-time PCR, we could show that the expression of intercellular adhesion molecule 1 ( ICAM-1 ), tumor necrosis factor alpha (TNF-alpha), and interleukin 6 (IL-6) significantly increased in peripheral blood leukocytes from `` MetS '' subjects ( n=39 ) compared to `` no MetS '' subjects ( n=35 ) 2 h after an oral glucose tolerance test ( ICAM-1 +52 %, TNF-alpha +107 %, and IL-6 +38 % ) and also in vitro after 72 h cultivation in high-glucose medium ( ICAM-1 +74 %, TNF-alpha +71 %, and IL-6 +44 % )
Chen et al., J Ocul Pharmacol Ther 2006 : We used flow cytometry and either primary cultured human conjunctival cells or the Chang conjunctival cell model to determine the effects of glucosamine sulfate on the production of ICAM-1 in response to tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-1beta, IL-6 , TNF-alpha plus IFN-gamma, or TNF-alpha plus IL-1beta
Yang et al., J Mol Cell Cardiol 2007 (Disease Models, Animal...) : Thus, IL-6 mediated up-regulation of cardiac NF-kappaB, ICAM-1 , CINC-1, -3, and MPO activity likely contributes to altered cardiac function following trauma-hemorrhage
Wong et al., Am J Respir Cell Mol Biol 2007 (MAP Kinase Signaling System) : Peptidoglycan ( PGN ) ( TLR2 ligand ), flagellin ( TLR5 ligand ), and Imiquimod R837 ( TLR7 ligand ) could significantly upregulate cell surface expression of intercellular adhesion molecule (ICAM)-1 and CD18, and induce the release of IL-1beta, IL-6 , IL-8, growth related oncogene ( GRO ) -alpha, and superoxides of eosinophils
Gustavsson et al., Retina 2008 (Diabetes Mellitus, Experimental...) : Ischemia induced increased expressions of TNF-alpha ( P < or= 0.012 ), IL-1beta ( P < or= 0.017 ), ICAM-1 ( P < or= 0.025 ), and IL-6 ( P = 0.012 ), and diabetes induced increased expression of caspase-1 ( P < or= 0.046 ), VCAM-1 ( P < or= 0.027 ), ICAM-1 ( P < or= 0.016 ), IL-1beta ( P = 0.016 ), and IL-6 ( P = 0.041 )
Shelton et al., J Biol Chem 2009 (Diabetes Complications...) : Also, pure interleukin-6 increased Grx1 and ICAM-1 in the rMC-1 cells
Rudnicka et al., Eur J Immunol 2009 (Arthritis, Rheumatoid) : Stimulation of BM CD20 ( + ) B cells by CpG containing oligodeoxynucleotide enhanced expression of activation markers ( CD86 and CD54 ) triggered IL-6 and TNF-alpha secretion and cell proliferation
Krutmann et al., J Invest Dermatol 1990 : Stimulation of cells with recombinant human ( rh ) interleukin (IL) 1 alpha, rhIL-4, rhIL-5, rhIL-6, rh granulocyte/macrophage colony stimulating factor ( GM-CSF ), rh interferon alpha ( rhIFN alpha ), and rh transforming growth factor beta ( TGF beta ) did not increase ICAM-1 surface expression
Suzuki et al., J Dent Res 2009 (Gingival Overgrowth) : In human gingival fibroblasts, cyclosporin alone did not induce evident inflammatory responses, but augmented the expression of CD54 and the production of interleukin (IL)-6 and IL-8 induced by TLR ligands, whereas phenytoin attenuated those responses
Suzuki et al., Clin Exp Immunol 2011 : SW982 cells expressed high levels of ICAM-1 originally, and ICAM-1 expression was increased significantly by IL-6+sIL-6R
Yoon et al., PloS one 2011 (Graves Disease...) : Quercetin significantly attenuated intercellular adhesion molecule-1 ( ICAM-1 ), interleukin (IL) -6, IL-8, and cyclooxygenase (COX) -2 mRNA expression, and inhibited IL-1ß induced increases in ICAM-1, IL-6 , and IL-8 mRNA
Giwa et al., Neurology 2012 (Cerebral Small Vessel Diseases) : Endothelial dysfunction is a possible causal factor, and circulating markers of endothelial activation ( intercellular adhesion molecule-1 , thrombomodulin ) and inflammation ( interleukin [ IL]-6 ) are elevated in patients with SVD
Birukova et al., Am J Physiol Lung Cell Mol Physiol 2012 (Acute Lung Injury...) : 18 % CS also increased IL-6 induced ICAM-1 expression by pulmonary EC and neutrophil adhesion, which was attenuated by Y-27632
Takahashi et al., J Periodontol 1994 (Gingivitis) : The levels of ICAM-1 expression were enhanced in a dose- and time dependent manner by IL-1 beta, TNF-alpha, or IFN-gamma, but not by IL-6 or IL-8
Ikeda et al., J Cardiovasc Pharmacol 1994 : In ELISA analysis, ICAM-1 molecule expression on myocytes was significantly stimulated by TNF-alpha ( 100 U/ml ), but not by IL-6 ( 100 U/ml ) or IL-8 ( 100 ng/ml ) dose dependently
Hutchins et al., Int J Cancer 1994 (Breast Neoplasms) : Regulation of ICAM-1 ( CD54 ) expression in human breast cancer cell lines by interleukin 6 and fibroblast derived factors ... Tumour necrosis factor (TNF)alpha, interleukin (IL)1 alpha, IL1 beta and IL6 also up-regulated the expression of CD54 in all the cell lines but CD40 was unaffected
Sano et al., Mol Cell Biochem 1994 : Cellular expression of ICAM-1 was drastically induced by TNF or interleukin-1 stimulation, and the moderate expression with delayed-action was observed only by lipopolysaccharide stimulation
Bloom et al., Clin Exp Immunol 1995 (Colitis) : Expression of ICAM-1 by cell lines HT29 and int407 was increased by proinflammatory cytokines interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and IL-1 but not by IL-6
Shrikant et al., J Immunol 1995 : Thus, both IL-10 and IL-6 can inhibit ICAM-1 expression by glial cells, although they do so by contrasting mechanisms
Mickelson et al., Hepatology 1995 (Adenocarcinoma...) : IFN gamma- and IL-6 induced ICAM-1 mRNA synthesis was not different from unstimulated A549 cells
Wake et al., Blood 1995 (Bone Resorption...) : We report the following novel features of homotypic adhesion via leukocyte function associated antigen-1 ( LFA-1 ) /intracellular adhesion molecule-1 ( ICAM-1 ) pathway that suggest a role for it in cytokine production and rapid proliferation of ATL cells : ( 1 ) ATL cells show clustering in a calcium dependent manner, even at the higher concentration ; ( 2 ) ATL cells consistently and highly express ICAM-1 and an active form of LFA-1, whereas integrin expression, except for LFA-1, is rather lower compared with that of normal CD4+ T cells ; ( 3 ) ATL cells make conjugate formation within 6 minutes and clustering within 48 hours, both of which are inhibited by the addition of monoclonal antibodies ( MoAbs ) against LFA-1 and ICAM-1 ; ( 4 ) spontaneous mRNA transcription and protein secretion of both interleukin-1 and parathyroid hormone related protein are observed consistently in ATL cells, and these productions are inhibited by anti-LFA-1 and anti-ICAM-1 MoAbs but are markedly increased by cross linking of LFA-1 and ICAM-1 by the immobilized specific MoAbs ; and ( 5 ) proliferative responses of ATL cells are also inhibited by these MoAbs
Campbell et al., J Urol 1994 (Carcinoma, Transitional Cell...) : In contrast, interleukin-1 and phorbol myristate acetate exhibited variable effects on ICAM-1 expression, and interferon-alpha had no effect
Shrikant et al., J Neuroimmunol 1994 (Encephalomyelitis, Autoimmune, Experimental) : Regulation of intercellular adhesion molecule-1 gene expression by tumor necrosis factor-alpha, interleukin-1 beta, and interferon-gamma in astrocytes
Caldenhoven et al., J Biol Chem 1994 : ICAM-1 is expressed on cells of many lineages and is induced by interleukin-6 (IL-6) and interferon-gamma (IFN-gamma)
Czech et al., J Invest Dermatol 1993 (Hypersensitivity, Immediate) : Cytokine induced ICAM-1 expression was specific, because IL-1 alpha, IL-1 beta, IL-2, IL-4, IL-6 , IL-7, IL-8, C5a, and platelet activating factor did not significantly affect eosinophil ICAM-1 surface expression
Kim et al., J Korean Med Sci 1993 (Melanoma) : IL-6 did not increase ICAM-1 expression on HUVEC
Ohteki et al., Immunol Lett 1993 (Arthritis, Rheumatoid...) : These data suggest that ICAM-1 expressed on the hepatic sinusoidal endothelial cells in MRL/lpr mice is induced by IL-6 , which is produced by hepatic MNC, and that such ICAM-1 may be responsible for the saturation of inflammatory cells and the proliferation of lymphocytes in the liver of MRL/lpr mice
Bajaj et al., Cancer Lett 1993 (Breast Neoplasms) : Interleukin-6 and tumour necrosis factor alpha synergistically block S-phase cell cycle and upregulate intercellular adhesion molecule-1 expression on MCF7 breast carcinoma cells ... The individual effect of IL-6 resulted in down-regulation of ICAM-1 expression ( 30-35 % ), while TNF alpha always upregulated ICAM-1 ( 1.5 to 4-fold increase ) ... The combined effect of IL-6 and TNF alpha consistently caused an increased expression of ICAM-1 , which was greater than the sum of each one alone and also sustained for 72 h following cytokine withdrawal
Deisher et al., Life Sci 1993 (Second Messenger Systems) : Surface protein expression of vascular cell adhesion molecule-1, endothelial leukocyte adhesion molecule-1, or intercellular adhesion molecule-1 , which is induced by tumor necrosis factor, interleukin-1 , and lipopolysaccharide, was not induced by pentoxyfilline, a phosphodiesterase inhibitor, nor by dibutyryl cyclic adenosine monophosphate
Lai et al., Int J Cancer 1993 (Fibrocystic Breast Disease) : Possible regulation of soluble ICAM-1 levels by interleukin-1 in a sub-set of breast cysts
Nosé et al., J Card Surg 1993 (Myocardial Reperfusion Injury) : Interleukin-6 (IL-6) , along with IL-1 and tumor necrosis factor-alpha (TNF-alpha), induces the expression of intracellular adhesion molecule-1 ( ICAM-1 ) in myocytes and endothelial cells, respectively
Baumgartner-Parzer et al., Diabetologia 1995 : Stimulation of confluent HUVECs, kept in 30 vs 5 mmol/l glucose for 13 +/- 1 days, with 20 U/ml interleukin-1 for 24 h ( ICAM-1 ) and 4 h ( endothelial leukocyte adhesion molecule 1 ) resulted in reduced ICAM-1 ( 84.8 +/- 27.0 %, p < 0.05 ) and endothelial leukocyte adhesion molecule-1 ( 87.6 +/- 22.4 %, p < 0.05 ) expression vs control cells, while that of PECAM ( t : 24 h ) and vascular cell adhesion molecule-1 ( t : 16 h ) remained unchanged
Del Papa et al., Arthritis Rheum 1996 (Wegener Granulomatosis) : We found that AECA IgG from WG patients do not display any significant cytotoxicity but are able to up-regulate the expression of E-selectin, intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 and to induce the secretion of IL-1 beta, IL-6 , IL-8, and MCP-1 ... We found that AECA IgG from WG patients do not display any significant cytotoxicity but are able to up-regulate the expression of E-selectin, intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 and to induce the secretion of IL-1 beta, IL-6 , IL-8, and MCP-1
Perretti et al., Biochem Biophys Res Commun 1996 : This opposite modulatory role of interleukin-1 and dexamethasone on intercellular adhesion molecule-1 expression was also, for the first time, observed in vivo using mouse peritoneal macrophages : a four-fold increase in intercellular adhesion molecule-1 expression was measured after local administration of the cytokine ( 5 micrograms/kg ) and this effect was greatly inhibited ( > 70 % ) by co-injection with 1 microgram dexamethasone
Tanaka et al., J Bone Miner Res 1995 : We first demonstrate that cellular adhesion by which osteoblasts communicate with opposing cells in bone milieu is involved in the osteoblast activation : ( a ) purified human osteoblasts obtained from osteoarthritis patients expressed particular adhesion molecules, ICAM-1, VCAM-1, and LFA-3 ; ( b ) toe osteoblasts adhered to T cells which were used as representative adhesive partners, since T cells possess all the receptors to these adhesion molecules ; ( c ) mRNA transcription and secretion of IL-1beta and IL-6 were induced in the osteoblasts by the cellular adhesion to T cells and they were reduced by interrupting the adhesion ; ( d ) cross linking of ICAM-1 and VCAM-1 on the osteoblasts induced IL-6 secretion from the osteoblasts
Shu et al., Thymus 1996 : Recombinant IL-1, anti ICAM-1 , and anti LFA-3 alone and collectively induced modest but significant increases in the secretions of 14C labelled peptides and of IL-6 and IL-8 which were not inhibited by HC
Ikeda et al., Cytokine 1996 : ICAM-1 expression on mesangial cells was stimulated significantly by IL-1 beta, but not by IL-6 nor IL-8, in a dose dependent manner
Ikeda et al., J Am Soc Nephrol 1996 : In an enzyme linked immunosorbent assay, interleukin 1 beta ( IL-1 beta ; 10 ng/mL ) increased ICAM-1 molecule expression on cultured rat mesangial cell surface in a time dependent manner
Yu et al., J Invest Dermatol 1997 (Vitiligo) : Immunologically, IL-6 can enhance melanocyte ICAM-1 expression, which may increase leukocyte-melanocyte attachment and cause melanocyte damage in vitiligo
Paolieri et al., Allergy 1997 : IL-4, IL-6 , IL-8, IL-10, and TGF-beta 1 did not affect either ICAM-1 expression or sICAM-1 release
Gaugler et al., Int J Radiat Biol 1997 : Interleukin-6 (Il-6) or other soluble factors released by irradiation were not involved in the enhanced ICAM-1 expression by irradiation
De Cesaris et al., J Biol Chem 1998 : SB203580, a highly specific p38 inhibitor, does not affect ICAM-1 and VCAM-1 expression, but strongly inhibits IL-6 production
Wang et al., Circ Res 1998 : Cardiac graft intercellular adhesion molecule-1 ( ICAM-1 ) and interleukin-1 expression mediate primary isograft failure and induction of ICAM-1 in organs remote from the site of transplantation
Baba et al., Mol Pharmacol 1998 : Interestingly, K-37 and K-38 could suppress the production of tumor necrosis factor alpha and interleukin 6 in phytohemagglutinin stimulated peripheral blood mononuclear cells and the expression of intercellular adhesion molecule 1 in tumor necrosis factor alpha stimulated human umbilical vein endothelial cells at their nontoxic concentrations
Oh et al., J Immunol 1998 (Astrocytoma) : IL-6, the soluble form of the IL-6R ( sIL-6R ), or both IL-6 plus sIL-6R, had no effect on VCAM-1 or ICAM-1 gene expression ... Interestingly, the IL-6/sIL-6R complex inhibited TNF-alpha induced VCAM-1 gene expression but did not affect TNF-alpha induced ICAM-1 expression
Miyazawa et al., J Biochem 1998 (Arthritis, Rheumatoid) : IL-1beta enhanced the production of IL-6 and stromelysin-1, and the surface expression of ICAM-1 , in a manner similar to that in the parental FLSs. SB203580, a specific inhibitor of p38 MAP kinase, significantly inhibited IL-1beta induced IL-6 and stromelysin-1 production by both parental FLSs and MH7A cells ; although PD098059, an inhibitor of the p42/p44 MAP kinase pathway, did not affect it