Disease relevance of IL6

• IL-2 mRNA was localized to endothelial cells (EC) and leukocytes and in close relation to ganglion cells (GC): IL-6 mRNA in EC, smooth muscle cells (SMC), and GC: HSP70 mRNA in EC and SMC; and IFN-gamma mRNA in leukocytes [1].
• Interleukin-6 (IL-6) is a pleiotropic cytokine that regulates the immune response, acute-phase reaction, and hematopoiesis [2].
• Interleukin-6 (IL-6), a multifocal cytokine produced by lymphoid and non-lymphoid cells, regulates immune responses, acute-phase reactions against bacterial infections, and haematopoiesis [3].
• RESULTS: Bilateral hind limb I/R injury increased significantly intestinal mucosal acidosis, intestinal permeability, portal endotoxemia, plasma IL-6 concentrations, circulating phagocytic cell priming and pulmonary leukosequestration, edema, capillary-alveolar protein leak, and impaired gas exchange [4].
• Taken together, these findings show that bacterial products (LPS), IL-6, RA, and Salmonella infection enhance the expression of the cathelicidins, PR-39 and protegrin, in bone marrow progenitor cells, and we suggest that extrinsic modulation of this innate host defense mechanism may be possible [5].

Psychiatry related information on IL6

• Intrapancreatic ET-1 and IL-6 mRNA expression and ET-1 protein levels were significantly lower in the therapy group as compared with the control group [6].

High impact information on IL6

• Induction of interleukin-6 synthesis in the myocardium. Potential role in postreperfusion inflammatory injury [7].
• Preceding the increase in the number of megakaryocytes, the serum interleukin-6 levels were found to be approximately 5 times greater than those in control animals [8].
• Fibroblasts responded to the addition of dermatan sulfate, heparan sulfate and heparin with a decrease in fibronectin, collagenase and interleukin-6 mRNA [9].
• Fibroblasts readily contracted collagen gels, and mRNA levels for fibronectin, collagenase and interleukin-6 were stimulated [9].
• Time course of interleukin-6 and tumor necrosis factor-alpha increase in serum following inhalation of swine dust [10].

Chemical compound and disease context of IL6

• Regulation of cathelicidin gene expression: induction by lipopolysaccharide, interleukin-6, retinoic acid, and Salmonella enterica serovar typhimurium infection [5].
• Before acute lung injury and after 24 h the number of inflammatory cells and the levels of IL-6, leukotriene B4, and tumor necrosis factor-alpha were measured in the bronchoalveolar lavage fluid [11].
• MEASUREMENTS AND MAIN RESULTS: Measurements/calculations of standard global hemodynamics, gut and femoral blood flows/vascular resistance, metabolism, arterial plasma lactate, portal venous endotoxin, interleukin-6, and tumor necrosis factor-alpha were made before and after hemorrhage, before and after reinfusion, and at 30-min intervals for 3 hrs [12].
• Hemodynamics, coagulation parameters, tumor necrosis factor (TNF) alpha, and interleukin 6 levels were measured in pigs submitted to a bolus infusion of Escherichia coli endotoxin (lipopolysaccharide) [13].
• Inhibition of either ERK1/2, PKC, or the inhibitory G protein (Gi) with U-0126, bisindolylmaleimide HCl, and pertussis toxin, respectively, blocked (P < 0.05) the increase in IL-6 expression caused by LPS [14].

Biological context of IL6

• The presence of IL-6 mRNA in elongating preimplantation ovine (days 13-25), porcine (days 13-21), and bovine (days 16-20) conceptuses was also demonstrated by PCR after reverse transcription of total ribonucleic acid with reverse transcriptase and by solution hybridization with a pIL-6 cRNA probe [15].
• It shares 61% and 43% amino acid sequence identity with human and mouse IL-6, respectively [15].
• PCR procedures with primers designed from regions of sequence conserved between human and pig have been used to identify IL-6 cDNA in lambda gt11 libraries constructed from day 15-16 (sheep), day 17 (cattle), and day 13-17 (pig) conceptus mRNA [15].
• A porcine interleukin-6 (pIL-6) cDNA has been cloned from pig spleen cDNA library to provide information that would allow us to study IL-6 mRNA expression during pregnancy of several domestic Artiodactyla [15].
• Expression of mRNAs for interleukin-4, interleukin-6 and their receptors in porcine corpus luteum during the estrous cycle [16].

Anatomical context of IL6

• Interleukin-2 and interleukin-6 can stimulate the growth and proliferation of T lymphocytes and the differentiation of activated B lymphocytes respectively, and in turn enhance cellular and humoral immune responses [17].
• This study examined how PNF is affected by Kupffer cell activation (beta-galactosidase), the generation of cytokines tumor necrosis factor alpha and interleukin 6, antioxidant mechanisms (ascorbic acid, alpha-tocopherol, reduced glutathione), circulating redox-active iron, and sinusoidal endothelial cell function (hyaluronic acid clearance) [18].
• Kupffer cells were more activated in PNF recipients, as suggested by higher beta-galactosidase levels (15 minutes after reperfusion), and secondarily, by higher production of tumor necrosis factor alpha and interleukin 6 (180 minutes after reperfusion) [18].
• Blood leukocytes produced large quantities of IL6 by 1-2 weeks after birth and IL2 by 2-3 weeks [19].
• Treatment of low-responder alveolar macrophages with conditioned medium containing IFN-gamma did not significantly alter the capacity of these macrophages to synthesize IL-6 mRNA in response to LPS [2].

Associations of IL6 with chemical compounds

• Pretreatment with Zn2+ prior to lipopolysaccharide (LPS) infusion induced an increased heat shock protein 70 (HSP70) expression in the lungs, liver, and kidneys and significantly increased plasma levels of interleukin 6, 6-keto-PGF1 alpha, and thromboxane-B2, compared with untreated controls [20].
• RESULTS: Reperfusion levels of malondialdehyde, TNF-alpha, and interleukin 6 were significantly lower in group 1 at both 40 and 60 minutes [21].
• Neither IL-4 nor IL-6 had any effect on PGF2alpha secretion by the cells [16].
• These results suggest that IL-4 and IL-6 are locally produced in the porcine CL, and that they inhibit steroid production from luteal cells via their specific receptors [16].
• In addition, the amount of ammonia, aromatic amino acids, IL6, TNFalpha and C3a removed during the 6-h treatment in the present study was higher by 34% to 175% than the total plasma content of those substances at the start of therapy [22].

Physical interactions of IL6

• In control cells, treatment with linoleic acid reduced intracellular glutathione levels and induced the DNA binding activity of nuclear factor-kappaB (NF-kappaB) leading to the upregulation of interleukin-6 (IL-6) [23].

Other interactions of IL6

• Expression of IL-6 mRNA increased at 2 hours after reperfusion and HSP70 at 3 hours after reperfusion [1].
• Cytokine analysis showed increased IL-6, G-CSF, and TNF-alpha gene transcription in resuscitated swine compared with NF swine [24].
• WB cultures exhibited peak IL-2, IL-6, IL-8 and IL-10 mRNA levels at 24, 12, 6 and 24h, respectively [25].
• The inhibitory effect of PCV2 DNA was more diversified than if it had simply targeted CpG-ODN-induced cytokines (IFN-alpha, TNF-alpha, interleukin-6, IL-12) [26].
• At six hours post infection, a clear enhancement of mRNA expression of TNFalpha, IL6, IL12 and IL15 was observed in macrophages infected with the low virulent ASFV/NH/P68 (NHV) when compared to those infected with the highly virulent ASFV/L60 (L60) [27].

Analytical, diagnostic and therapeutic context of IL6

• Circulating concentrations of tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were measured by use of specific bioassays [28].
• Intra-arterial (i.a.) or intraperitoneal injections of double-stranded RNA induced pronounced fevers and strong elevations of circulating TNF-alpha and IL-6 [28].
• Linkage mapping of porcine interleukin 6 (IL6) [29].
• After cloning and sequencing of porcine IL-6, the expression pattern of porcine IL-6 mRNA was evaluated through real-time RT-PCR using porcine immune cells (spleen cells and alveolar macrophages) following stimulation with LPS [3].
• The levels of bioactive IL-1 and IL-6 in lavage fluids increased approximately 1,000-fold following A. pleuropneumoniae inoculation, but TNF bioactivity was not detected [30].

References