Gene interactions and pathways from curated databases and text-mining

◀ Back to IL8

ICAM1 — IL8

Text-mined interactions from Literome

Li et al., J Invest Dermatol 2000 (Vitiligo) : After incubation of IgG anti-melanocyte antibodies with cultured melanocytes, the results revealed : ( i ) IgG anti-melanocyte antibody stimulated HLA-DR expression on melanocytes ; ( ii ) intercellular adhesion molecule-1 expression on melanocytes was significantly induced by IgG anti-melanocyte antibodies ; and ( iii ) IgG anti-melanocyte antibodies induced an increase in interleukin-8 release from melanocytes
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
Stuyt et al., Immunology 2003 : Selective regulation of intercellular adhesion molecule-1 expression by interleukin-18 and interleukin-12 on human monocytes
Böhm et al., Exp Dermatol 2004 : Functional studies have shown that alpha-MSH exerts anti-inflammatory actions in human fibroblastic skin cells by suppressing interleukin-1 (IL-1) induced IL-8 production, activation of the transcription factor activator protein-1 (AP-1) and induction of intercellular adhesion molecule-1 by interferon-alpha
Manna et al., J Biol Chem 2005 : IL-8 induces NF-kappaB dependent reporter gene expression as well as ICAM-1 , VCAM-1, and Cox-2 expression
Egusa et al., Infect Immun 2005 : Intercellular adhesion molecule 1-dependent activation of interleukin 8 expression in Candida albicans infected human gingival epithelial cells
Relova et al., Cell Biol Int 2005 : The study aimed at investigating the effects of interleukin (IL)-4, IL-8 , IL-13 and interferon-gamma (IFN-gamma) on cell viability and intracellular adhesion molecule (ICAM)-1 and zonula occludens protein (ZO)-1 expression on cultured human basal and columnar airway epithelial cells
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
Wang et al., J Immunol 2006 : ICAM-1 engagement by HRV and cross linking Abs also induced phosphorylation of p38 in a Syk dependent manner, and conversely, knockdown of Syk by short interfering ( si ) RNA substantially diminished p38 activation and IL-8 gene expression
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
Pazdrak et al., J Immunol 2008 : Importantly, we found that inhibition of ICAM-1 in activated eosinophils blocked GM-CSF induced expression of c-fos, c-myc, IL-8 , and TNF-alpha
Li et al., American journal of physiology. Renal physiology 2009 (MAP Kinase Signaling System) : IL-8 increased ICAM-1 expression only via the CXCR-1 receptor, which in turn resulted in activation of the p38 mitogen activated protein kinase ( MAPK ) pathway ; neither the extracellular signal related kinase ( ERK ) 1/2 MAPK pathway nor the stress activated protein kinase ( SAPK ) /c-Jun NH ( 2 ) terminal kinase ( JNK ) pathway was involved ... We conclude that in human renal PTCs, IL-8 upregulates ICAM-1 production by engaging the CXCR-1 receptor and p38 MAPK signaling pathway
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
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
Kuai et al., World J Gastroenterol 2012 (Neoplasm Invasiveness...) : IL-8 increased NF-?B and Akt activities and adhesion molecules ICAM-1 , VCAM-1, and CD44 expression in GC cells
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
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
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
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
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
Bryant et al., Infect Immun 1996 : PLC strongly induced expression of ELAM-1, ICAM-1 , and IL-8, while PFO stimulated early ICAM-1 expression but did not promote ELAM-1 expression or IL-8 synthesis ... PLC strongly induced expression of ELAM-1, ICAM-1, and IL-8 , while PFO stimulated early ICAM-1 expression but did not promote ELAM-1 expression or IL-8 synthesis
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
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
Viac et al., Arch Dermatol Res 1996 : Human keratinocytes derived from skin obtained during plastic surgery were cultured in defined medium ( MCDB 153 ) and were stimulated by SP. Flow cytometry analysis showed that SP ( 10 ( -7 ) and 10 ( -5 ) M ) as well as the specific NK1 agonist Sar9Met ( O2 ) 11SP ( Sar Met ) induced a slight but significant expression of ICAM-1 at the cell surface during treatment periods of 24 h and 48 h. SP ( 10 ( -5 ) M ) also induced a significant but transient increase in the production of IL-1alpha, IL-1beta, IL-1 receptor antagonist and IL-8 which was detectable by ELISA techniques 6 h after stimulation
Nagendra et al., Am J Physiol 1997 : Detailed studies with IFN-gamma stimulated ( 100 U/ml ) C3A cells revealed that this adhesion involved CD11a/CD18 [ lymphocyte function associated antigen-1 ( LFA-1 ) ] and CD54 and was dependent on low levels of IL-8 produced by the stimulated hepatocytes
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
Ishii et al., Nihon Kyobu Shikkan Gakkai Zasshi 1996 (Lung Diseases) : N-acetylcysteine, an antioxidant, decreased the TNF alpha induced expression of intercellular adhesion molecule-1 on cultured epithelial cells from human bronchi ( BEAS-2A ), and inhibited IL-8 production by those cells
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
Bianco et al., Monaldi Arch Chest Dis 1998 (Asthma...) : In addition, IFN gamma appeared to completely override the ICAM-1 upregulation induced by IL-1 beta, IL-8 and TNF alpha, during HRV infection
Sano et al., Biochem Biophys Res Commun 1998 : Cross linking of intercellular adhesion molecule-1 induces interleukin-8 and RANTES production through the activation of MAP kinases in human vascular endothelial cells ... Cross linking of ICAM-1 induced IL-8 and RANTES mRNA expressions and increased their protein synthesis and secretions in endothelial cells ... Finally, the specific MEK inhibitor PD98059 inhibited ICAM-1 induced IL-8 and RANTES production in endothelial cells ... Taken together, these results indicate that stimulation of ICAM-1 induces IL-8 and RANTES production through the activation of 44- and 42-kDa MAP kinases in endothelial cells, suggesting that ICAM-1 induced chemokine production in endothelial cells would further attract and activate leukocytes to induce intense inflammation