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Synergistic activation of serum amyloid a (saa) by il - 6 and il - 1 in combination on human hep 3 b hepatoma cell line. Role of pge2 and il-1 receptor antagonist
No full text-Serum amyloid A (SAA) protein is a major acute phase reactant in human and many other species. Infections and traumatic inflammation are characterized by a rapid increase of SAA; its concentration in the plasma may augment many-fold. Cytokines such as IL-1 and IL-6 are considered mediators of acute phase protein synthesis. The most accredited mechanism of action of IL-1 in inflammatory diseases is the stimulation of PGE2 release, which is highly dependent on the concentration of IL-1. In this study we found that human Hep 3B hepatoma cells treated with the combination of hrIL-6 (10ng/ml) plus hrIL-1 (1ng/ml) produced an augmentation in steady-state levels of SAA mRNA (87%) compared to hrIL-6 (10ng/ml) plus PGE2 (5 microM), which induced an increase of only 33%, compared to IL-6 alone, while cells treated with hrIL-6 plus PGE2 (0.5 microM) had a similar effect as hrIL-6 did alone. Moreover, the addition of exogenous PGE2 (5 microM) to the cell cultures produced no significant increase in concentration of SAA mRNA compared to the control. In addition, according to the data obtained by the blot analysis we also found, by ELISA method, that hrIL-6 acts in synergism with hrIL-1 on SAA protein secretion in human Hep 3B hepatoma cell cultures after 48 h incubation. In fact, the cell cultures treated with hrIL-6 plus hrIL-1 caused a higher release approximately 1.5-4-fold of SAA protein than the cells treated with IL-6 plus PGE2 5 microM or IL-1 + PGE2 5 microM, respectively. The synergistic effect of hrIL-6 plus hrIL-1 beta was inhibited by hrIL-1 receptor antagonist (hrIL-1ra) 50 micrograms/ml, a protein which specifically binds to the IL-1 receptor and is structurally similar to IL-1 beta but with no IL-1-like activity; while indomethacin (5 microM) was ineffective. These results strongly suggest that the synergism between hrIL-6 plus hrIL-1 on the transcription and the protein release of SAA release is not due to a PGE2-dependent process in human Hep 3B hepatoma cells. This finding highlights a specific biological effect of IL-1 not in relation to PGE2, suggesting a specific mechanism of action for IL-1 in regulating acute phase protein synthesis
The down-regulation of il-6-stimulated fibrinogen steadu state mrna and protein levels by human recombinant il-1 is not pge2-dependent:effects of il-1 receptor antagonist (il-1ra)
No full text-Infections, trauma and inflammatory processes induce a host response with increases in a large group of structurally and functionally diverse plasma proteins. Parental administration of foreign proteins also induce an increase in plasma fibrinogen. Interleukin-6 (IL-6) is a monocyte-derived mediator and has regulatory effects on acute phase protein genes which result in the induction of fibrinogen synthesis in primary hepatocytes, while the addition of interleukin-1 (IL-1) exerts a negative modulating influence on the IL-6-stimulated fibrinogen. In order to understand the mechanisms by which IL-1 inhibits IL-6-stimulated fibrinogen transcription and translation, and since IL-1 is believed to act through PGE2 stimulation, we have studied the influence of PGE2 in IL-6 or IL-1, alone and in combination, on Fg mRNA expression (by Northern blot analysis) and the influence of PGE2, indomethacin, and arachidonic acid on Fg secretion. Moreover, since human recombinant interleukin-1 receptor antagonist (hrIL-1ra) is a strong inhibitor of IL-1 induced IL-1 transcription and translation and has an inhibitory effect on PGE2, we have studied the effects of IL-1ra on the down-regulation of IL-6 stimulated fibrinogen by IL-1, using an Fg ELISA metho
Mast cell recruitment after subcutaneous injection of RANTES in the sole of the rat paw.
No full text-The effect of hrRANTES was studied after the injection in the sole of the rat paw, an area particularly rich in mast cells. Subcutaneous injections of RANTES 50 ng/10 microl produced an erythematous reaction which was inhibited by anti-RANTES antibody 50 microg/rat injected in the tail vein 30 min before hrRANTES 50 ng/10 microl was injected. In another set of experiments the animals were injected subcutaneously in the sole of the paw with PBS 10 microl (control), LPS (100 ng/10 microl) hrRANTES 50 ng/10 microl or anti-RANTES 50 microl/rat injected in the tail vein 30 min before hrRANTES 50 ng/10 microl was injected. The biopsies were analysed after 4 h and counted in an optic field. hrRANTES produced a strong recruitment of mast cells selectively coloured with 0.1% toluidine blue and inhibited by anti-RANTES antibody. In addition to the optical and electron microscope study, in some of the excised tissue Northern blot analysis for histidine decarboxylase (HDC) mRNA was performed to estimate the amount of histamine generation in the tissue of the injection sites. We found that subcutaneous injections of hrRANTES 50 ng/10 microl in the sole of the rat paw produced an accumulation of a great number of mast cells compared to PBS 10 microl (negative control) or LPS 100 ng/10 microl (positive control) after 4 h. The hrRANTES effect was inhibited by anti-RANTES antibody injected in the tail vein 30 min before hrRANTES exposure. Moreover, hrRANTES increased HDC mRNA and histamine generation
Effect of interleukin-1 receptor antagonist (IL-1RA) on vascular smooth muscle cell proliferation (VSMC).
No full textModulation of rat vascular smooth muscle cell (VSMC) proliferation by cysteinyl leukotriene D4: a role for mediation of interleukin 1
No full text5-HT and histamine release from rat basophilic leukemia cells treated or non with IL-1RA
No full textHuman recombinant interleukin-1 receptor antagonist (hrIL-1RA) inhibits prostaglandin E2(PGE) generation but not alkaline phosphatase activity in in vivo chronic granulomatous tissue induced by KMnO4
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