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CXCL17 — IRF6

Text-mined interactions from Literome

Si et al., J Immunol 2004 (Acquired Immunodeficiency Syndrome) : Interestingly, although LPS induced IL-8/CXCL8 was dependent on NF-kappaB, the baseline or 15d-PGJ ( 2 ) -mediated IL-8/CXCL8 production was NF-kappaB independent
Dürk et al., Int Immunol 2005 : Pharmacological studies with isotype-selective receptor agonists allowed us to show that 5-HTR(3) subtype up-regulates the LPS induced production of IL-1beta, IL-6 and IL-8/CXCL8 , while it was not involved in TNF-alpha and IL-12p40 secretion
Cassatella et al., Eur J Immunol 2005 : In this study, we show that modulation by IL-10 of LPS induced TNF-alpha, CXCL8/IL-8 and IL-1 receptor antagonist (IL-1ra) mRNA accumulation in neutrophils already expressing a functional IL-10R and antigenic SOCS-3 ( i.e. in `` 4-h cultured '' neutrophils ) occurs with kinetics that are similar to those observed in `` time 0 '' neutrophils, depends on de novo protein synthesis, but does not require SOCS-1, SOCS-3, heme oxygenase and Bcl-3 induction
Hasan et al., BMC immunology 2005 (Tuberculosis...) : BCG-, and LPS induced CXCL8 secretion was comparable between patients and controls
Wehrwein et al., Cardiovascular diabetology 2006 (Diabetes Mellitus, Type 1) : Monocytes were isolated from controls and T1D patients and the LPS stimulated increase of IL-6, CXCL8 , monocyte chemotactic protein 1 ( CCL2, MCP-1 ) and superoxide dismutase ( SOD 2 ), as well as the LPS mediated decrease of apolipoprotein E (Apo E) in primary human monocytes from controls and T1D patients was determined
De Plaen et al., Immunology 2006 : In conclusion, CXCL2 gene is expressed in enterocytes in response to both TNF and LPS
Carvalho et al., Inflammopharmacology 2006 (Disease Models, Animal...) : In vitro data revealed that U. guianensis impaired LPS induced nitric oxide and CXCL8 generation by murine peritoneal macrophages, as well as OVA induced interleukin-5 synthesis by previously sensitized spleen cells
Pioli et al., J Immunol 2007 : In this study, we demonstrate that 17beta-estradiol ( E2 ) attenuates LPS induced expression of CXCL8 in human peripheral blood monocytes
Tamassia et al., Int Immunol 2008 (Sepsis...) : Consistent with the presence of a fully functional IL-10R, modulation of LPS induced CXCL8 , CCL4, tumour necrosis factor-alpha and IL-1ra gene expression was also rapidly induced by IL-10 in septic, but not normal, neutrophils
Anand et al., J Immunol 2008 : In the present study, we determined the role of a nonreceptor proline-rich tyrosine kinase, Pyk2, in LPS induced IL-8 ( CXCL8 ) production in endothelial cells
Farkas et al., Scand J Immunol 2008 : LPS itself significantly augments CXCL-8 production and co-administration of MDP further increases cytokine secretion
Gouwy et al., J Leukoc Biol 2009 : Furthermore, LPS rapidly induced the expression of IL-8/CXCL8 but not of the CCL2 receptor CCR2 in monocytic cells
Hoth et al., J Trauma 2009 (Contusions...) : Injury + LPS showed immune priming observed by lung injury histology and increased bronchoalveolar lavage neutrophilia, lung myeloperoxidase and serum IL-6, CXCL1 , and MIP-2 levels when compared with injury + vehicle or LPS alone
Kim et al., Immune network 2009 : As a result of these properties, we examined the effect of 15d-PGJ ( 2 ) on the LPS induced IL-8/CXCL8 mRNA expression in VSMCs from SHR ... A NAD ( P ) H oxidase inhibitor inhibited the upregulatory effect of 15d-PGJ ( 2 ) on LPS induced IL-8/CXCL8 mRNA expression in SHR VSMCs, and an increase in NAD ( P ) H oxidase activity was detected in SHR VSMCs treated with 15d-PGJ ( 2 ) /LPS ... Our results indicate that the upregulatory effect of 15d-PGJ ( 2 ) on LPS induced IL-8/CXCL8 expression in SHR VSMCs is mediated through the PPARgamma and ERK pathway, and may be related to NAD ( P ) H oxidase activity ... However, p38 inactivation may also play an important role in 15d-PGJ ( 2 ) /LPS induced IL-8/CXCL8 expression in SHR VSMCs
Sheldon et al., PloS one 2010 (Cattle Diseases...) : Endometrial epithelial or stromal cells from wild type but not Toll-like receptor 4 (TLR4) null mice secreted prostaglandin E ( 2 ) and chemokine ( C-X-C motif ) ligand 1 ( CXCL1 ) in response to LPS from EnPEC, highlighting the key role of LPS in PID
Outtz et al., J Immunol 2010 (Inflammation) : Inhibition of Notch signaling decreased induction of the inflammatory cytokines IL-6, IL-12, CXCL10 , MCP-1, monokine induced by IFN-?, and TNF-a in macrophages in response to LPS/IFN-?
Sheldon et al., PloS one 2010 : Stromal and epithelial cells isolated from the endometrium of WT but not Tlr4 ( -/- ) mice, secreted IL-6, CXCL1 , CCL20 and prostaglandin E ( 2 ) in response to LPS , in a concentration and time dependent manner
Wendlandt et al., Innate Immun 2012 : When miR-200b or miR-200c mimics were transfected into the differentiated monocytic THP-1 cell line, the abundance of MyD88 transcripts, as well as LPS induced expression of the pro-inflammatory molecules IL-6, CXCL9 and TNF-a were diminished
Roos et al., Biochem Biophys Res Commun 2012 (Pneumonia) : We hypothesized that C/EBPß in the lung epithelium contributes to lipopolysaccharide (LPS) induced airway neutrophilia and expression of neutrophil chemoattractant chemokine ( C-X-C ) motif ligand ( CXCL)1, as well as the suppressive effects of long acting ß ( 2 ) -agonists ( LABAs ) and glucocorticoids (GCs)
Plumb et al., PloS one 2013 : 17-BMP suppression of LPS induced TNFa, IL-6 and CXCL8 was measured by ELISA and GR phosphorylation was measured by immunohistochemistry and Western blot