Disease relevance of IL6

• IL-6 signaling is activated during human chronic atrophic gastritis with Helicobacter pylori infection, and aberrant Stat3 signaling activation gives rise to mouse gastric tumors [1].
• Delayed-type hypersensitivity (DTH) reaction, serum levels of interleukin-6 (IL-6) and anti-proteoglycan IgG titres were significantly reduced in STAT-1 decoy ODN-treated mice, whereas mBSA, collagen type I and type II specific immunoglobulins were not significantly affected [2].
• In fact, stimulation with M. avium subsp. paratuberculosis tended to reduce the differential expression observed in infected and uninfected cows for genes encoding IFN-gamma, IL-1alpha, and IL-6 [3].
• Several strains of the closely related Mycobacterium avium, and the unrelated saprophyte, Mycobacterium phlei, had somewhat less ability to stimulate TNF-alpha and IL-6 mRNA expression [4].
• The cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) have been associated with granuloma formation and wasting in other disease syndromes [4].

High impact information on IL6

• METHODS: Biotinylated antibodies against alpha-fetoprotein (AFP), interleukin-6 (IL-6), and carcinoembryonic antigen [(CEA); 0.1 g/L each in 15 mmol/L phosphate-buffered saline (PBS) containing 0.1 mL/L Tween 20] were attached to a microcolumn packed with streptavidin-coated particles [5].
• Murine bone marrow-derived dendritic cells were activated to secrete interleukin-6 (IL-6), IL-12, and tumor necrosis factor upon exposure to antigen-free TPL liposomes [6].
• Although the activity of phosphatidylinositol dimannoside was little influenced by palmitoylation of mannose at C-6, a further palmitoylation at inositol C-3 diminished the induction levels of IL-6 and IL-12 [6].
• Suboptimal doses of IL17 synergised potently with TNFalpha, IL1, OSM, and IL6 to promote collagen degradation [7].
• IL-6 and its soluble receptor augment aggrecanase-mediated proteoglycan catabolism in articular cartilage [8].

Chemical compound and disease context of IL6

• Muramyl dipeptide (MDP) and Escherichia coli LPS also stimulated TNF-alpha and IL-6 mRNA expression [4].
• Cytokines such as interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF) play key roles in the regulation of acute phase response in the species studied to date [9].

Biological context of IL6

• IL6, secreted from epithelial cells or macrophages, induces WNT5A upregulation in mesenchymal cells [1].
• IL-6 was also a more potent inhibitor of cell proliferation in cultures of cells from small (55% inhibition) than from large (32% inhibition) follicles [10].
• Using mutant reporter genes, we demonstrate that although mutation in the NF-kappa B element produces the major loss of induction, both NF-kappa B and C/EBP elements are necessary for maximal transcriptional activation of the bovine IL-6 gene [11].
• The interleukin-6 (IL-6) gene expression in bovine monocytes is highly induced following bacterial lipopolysaccharide (LPS) stimulation [11].
• Recombinant IL-6 production in JM109 (DE3) and BL21 (DE3) pLysS bacterial system is substantially enhanced by supplementation of rare codon tRNAs through co-transformation with a second plasmid [12].

Anatomical context of IL6

• Therefore, in the present study we determined if TMA and TMA conjugated to serum albumin induced the production of the macrophage mediators nitric oxide (NO), tumour necrosis factor (TNF), and interleukin 6 (IL-6) in vitro using the rat AM cell line NR8383 and primary AMs derived from TMA-sensitized and naïve Brown Norway rats [13].
• IL6-induced WNT5A activates canonical WNT signaling for autocrine proliferation of human synovial fibroblasts in rheumatoid arthritis [1].
• Thus, it appears that less differentiated granulosa cells (small follicles) are more sensitive to IL-6 than are highly differentiated granulosa cells (large follicles) [10].
• We have investigated the involvement of interleukin 6 (IL-6), a growth-regulatory molecule for vascular smooth muscle cells (SMC), in the development of atherosclerotic lesions of Watanabe heritable hyperlipidemic (WHHL) rabbits [14].
• BBEC pre-incubated with IL-6 for 4 h also showed an increase in adhesion of lymphocytes, and cells pretreated with 100 ng/ml IL-6 showed a 3-fold increase in lymphocyte adherence [15].

Associations of IL6 with chemical compounds

• EGCG and catechin had no significant effects in primary WBC on the expression pattern of the proinflammatory cytokines IL1beta and IL6 and on the expression of the housekeeping genes GAPDH and histon H3 [16].
• In comparison, all doses of IL-6 inhibited (p < 0.05) FSH-induced estradiol production in cultures of cells from small follicles; maximal inhibition was achieved (75% decrease) with > or = 10 ng/ml [10].
• To investigate the mechanism of the suppression induced by IL-6, we studied its effect upon PGI2 synthesizing enzymes [17].
• The effect of interleukin 6 (IL-6) upon arachidonic acid (AA) metabolism was studied in cultured bovine vascular endothelial cells (BVECs) [17].
• IL-6 also potentiated the cortisol release stimulated by the adenylyl cyclase activator forskolin [18].

Other interactions of IL6

• Increases in transcripts for the IL6 (29 and 34 dpi) and IL10 (21, 25, and 29 dpi) genes were detected that were higher in the Boran compared with N'Dama [19].
• STAT and MAPK pathways play a crucial role in IL-6/sIL-6R modulation of these enzymes, suggesting that new strategies in the treatment of osteoarticular diseases might target these transduction cascades [20].

Analytical, diagnostic and therapeutic context of IL6

• Using RT-PCR techniques we have previously detected the aberrant expression of FGF4, FGFr2 and IL6 in a significant proportion of bovine granulosa cell-derived nuclear transfer embryos, which correlated with a limited developmental potential in vivo [21].
• These findings support the premise that IL-6 is an important autocrine and/or paracrine regulator of SMC proliferation and of pathogenesis of atherosclerosis in this animal model [14].
• In the present study, bovine articular cartilage explants were maintained in a model organ culture system in the presence or absence of IL-1alpha or TNF-alpha, and under co-stimulation with or without IL-6 and/or sIL-6R [8].
• In in situ hybridization analysis, quite low levels of IL-6 mRNA were expressed in 'quiescent' SMC cultured from WHHL rabbits; however, high levels of IL-6 mRNA were induced in SMC exposed to 10% fetal bovine serum (FBS), suggesting that growth-stimulated SMC themselves can synthesize IL-6 [14].
• The release of IL-1 and IL-6 by EC was measured by enzyme-linked immunosorbent assay [22].

References