Disease relevance of IL6

• We used canine transmissible venereal tumor (CTVT), which produces TGF-beta1, as a model to determine whether IL-6 restores lymphokine-activated killer (LAK) activity [1].
• Our findings suggest that IL-6 is a good marker of active disease during leishmaniasis, and that other cytokines may be involved in the hypergammaglobulinemia characteristic of canine visceral leishmaniasis [2].
• In addition to its production by inflammatory cells, we demonstrate that IL-6 mRNA is induced in myocytes in the viable border zone of a myocardial infarct [3].
• We then investigated the expression of IL-6 mRNA in our canine model of ischemia and reperfusion [3].
• The decrease in nonsplenic interleukin-6 (IL-6) production after splenectomy indicates the existence of a positive feedback loop of IL-6 production during endotoxemia in dogs [4].

High impact information on IL6

• However, investigation of interleukin 6 (IL-6) revealed that recombinant IL-6 stimulated myocyte adhesiveness for ZAS-stimulated neutrophils (ED50 = 0.002 U/ml) and expression of ICAM-1 by isolated myocytes [5].
• These results indicate that cytokines capable of promoting neutrophil-myocyte adhesion occur in extracellular fluid during reperfusion of ischemic myocardium, and that one of these cytokines is IL-6 [5].
• Myocytes stimulated with preischemic lymph showed minimal or no IL-6 mRNA expression, whereas myocytes stimulated with tumor necrosis factor-alpha, IL-1beta, lipopolysaccharide, or postischemic lymph showed a strong IL-6 mRNA induction [3].
• Unstimulated myocytes showed no significant IL-6 mRNA expression [3].
• We have previously demonstrated the induction of IL-6 in the ischemic myocardium, and the current study addresses the cells of origin of IL-6 [3].

Chemical compound and disease context of IL6

• To test the hypothesis that cytokines play a role in ischemic or reperfusion injury, we measured tumor necrosis factor (TNF) and interleukin-6 (IL-6) in pentobarbital-anesthetized dogs before, during, and after coronary occlusion lasting 60 min [6].
• Because the origin of endotoxemia may affect the reactions to endotoxin, we compared the induction of tumor necrosis factor (TNF), interleukin-6 (IL-6), hormones, and glucose production after endotoxin (1.0 microg/kg Escherichia coli 0111:B4) administration into a peripheral (n = 8) versus the portal (n = 8) vein in anesthetized dogs [7].
• These data support the hypothesis that sepsis initiates a cascade of mediators with the cytokines TNF and IL-6 being proximal events which in turn stimulate the next level, with ibuprofen probably exerting its inhibitory effect distal to this point in the cascade [8].
• The brain-dead group treated with LPS (n = 6) responded with a significant elevation in IL-6-like and TNF-like activities compared with the vehicle-treated group [9].

Biological context of IL6

• IL-6 is a multifunctional cytokine that regulates cell growth, differentiation, and cell survival [1].
• METHODS AND RESULTS--In the present study, we combined Northern blot analysis and in situ hybridization to demonstrate IL-6 gene expression in cardiac myocytes [3].
• The data show that, in addition to augmenting the platelet count in normal dogs, IL-6 enhances the sensitivity of platelets to activation in response to thrombin and PAF [10].
• To determine if interleukin-6 (IL-6) administration influences platelet function, platelet activation was analyzed sequentially in IL-6-treated (80 micrograms/kg/d) and control dogs [10].
• CONCLUSIONS: IL-6 treatment decreases bacterial translocation to MLN and may be beneficial in reducing septic complications in acute pancreatitis [11].

Anatomical context of IL6

• METHODS: Synovial fluid activities of proinflammatory cytokines (IL-1beta, IL-6, and TNF-alpha) were determined by bioassay [12].
• Tumor-infiltrating lymphocyte secretion of IL-6 antagonizes tumor-derived TGF-beta 1 and restores the lymphokine-activated killing activity [1].
• The expressions of IL-2 and IL-6 genes were extremely low compared with the positive control (ConA-stimulated canine peripheral blood leukocytes) [13].
• Furthermore, we found that induction of IL-6 mRNA occurred very early on reperfusion of the infarcted myocardium [14].
• The potential roles of IL-6 in cardiac myocytes in an infarct border are discussed [3].

Associations of IL6 with chemical compounds

• The plasma was analysed with respect to roxithromycin, tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) [15].
• As measured by P-selectin expression, enhanced responsiveness to the strong agonist platelet activating factor (PAF) was also observed in the IL-6-treated dogs [10].
• The EC50 of thiazole orange-positive platelets from IL-6-treated dogs decreased dramatically by day 5 to 46.5% +/- 13.1% (n = 4) of control values (P < 0.001), whereas TPO-treated dogs did not significantly change [16].
• Blood for analysis of tumor necrosis factor (TNF) and IL-6 was sampled from the femoral artery and the portal, hepatic, and splenic (only in controls) veins [4].
• CONCLUSIONS: DHEA decreased the IL-6 concentration in the supernatant of LPS-stimulated DH82 cells by inhibiting the sequestration of IkappaBalpha, which is necessary for the activation of nuclear factor-kappa B [17].

Other interactions of IL6

• The objective of this study was to quantify the expression of mRNA encoding Th(1)-like [interferon (IFN)-gamma, interleukin (IL)-2 and IL-12], Th(2)-like [IL-4 and IL-6] and immunomodulatory cytokines [IL-10 and transforming growth factor (TGF)-beta] in lesional ImR-LPP, nonlesional ImR-LPP and healthy control pedal skin [18].

Analytical, diagnostic and therapeutic context of IL6

• This new mechanism, in which TIL manufacture high concentrations of IL-6 to block tumor TGF-beta1 anti-LAK activity, has potential applications in cancer immunotherapy and tumor prognosis [1].
• This study analyzed temporal expression levels of IL-1beta, IL-2, IL-6, IL-8, IFN-gamma, and TNF-alpha mRNA by peripheral blood leukocytes from dogs experimentally infected with a new virulent strain of E. canis by using real-time RT-PCR [13].
• Northern blot with ICAM-1 probe revealed ICAM-1 expression under every condition that demonstrated IL-6 induction [3].
• Supernatant IL-6 levels were measured by enzyme-linked immunosorbent assay, and cellular cytoplasmic IkappaBalpha protein expression measured by Western blot analysis [17].

References