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      Plasma Interleukin-18 Levels in Chronic Renal Failure and Continuous Ambulatory Peritoneal Dialysis

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          Background/Aims: Based on associations of interleukin (IL)-18 with chronic inflammation, we investigated IL-18, IL-6, and tumor necrosis factor-α (TNF-α) in patients with chronic renal failure (CRF) and patients undergoing continuous ambulatory peritoneal dialysis (CAPD). Methods: Plasma was evaluated by ELISA methodology in 15 healthy controls, 27 CRF and 15 CAPD patients. Results: Plasma IL-18 levels in CRF (572.5 ± 41.9 pg/ml) or CAPD (479.2 ± 47.4 pg/ml) were significantly higher than normal (263.6 ± 20.0 pg/ml), but there was no difference in IL-18 between CRF and CAPD patients. The IL-18 concentration negatively correlated with creatinine clearance (Ccr). However, the duration of dialysis, normalized protein nitrogen appearance, weekly Ccr, and K<sub>t</sub>/V<sub>urea</sub> were not correlated with plasma IL-18 in CAPD. The plasma IL-18 concentration was positively correlated with TNF-α but not with IL-6 in renal failure patients with or without CAPD. Conclusion: Uremia is the principal origin of increased plasma IL-18 in these patients. Increased IL-18 levels may be associated with Th1 differentiation and elevated TNF-α.

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          Most cited references 17

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          A proinflammatory role for IL-18 in rheumatoid arthritis.

           Foo Liew,  X Wei,  Max Field (1999)
          IL-18 is a novel cytokine with pleiotropic activities critical to the development of T-helper 1 (Th1) responses. We detected IL-18 mRNA and protein within rheumatoid arthritis (RA) synovial tissues in significantly higher levels than in osteoarthritis controls. Similarly, IL-18 receptor expression was detected on synovial lymphocytes and macrophages. Together with IL-12 or IL-15, IL-18 induced significant IFN-gamma production by synovial tissues in vitro. IL-18 independently promoted GM-CSF and nitric oxide production, and it induced significant TNF-alpha synthesis by CD14(+) macrophages in synovial cultures; the latter effect was potentiated by IL-12 or IL-15. TNF-alpha and IFN-gamma synthesis was suppressed by IL-10 and TGF-beta. IL-18 production in primary synovial cultures and purified synovial fibroblasts was, in turn, upregulated by TNF-alpha and IL-1beta, suggesting that monokine expression can feed back to promote Th1 cell development in synovial membrane. Finally, IL-18 administration to collagen/incomplete Freund's adjuvant-immunized DBA/1 mice facilitated the development of an erosive, inflammatory arthritis, suggesting that IL-18 can be proinflammatory in vivo. Together, these data indicate that synergistic combinations of IL-18, IL-12, and IL-15 may be of importance in sustaining both Th1 responses and monokine production in RA.
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            Expression of interleukin-18 in human atherosclerotic plaques and relation to plaque instability.

            Interleukin (IL)-18 is a potent proinflammatory cytokine with potential atherogenic properties. Its expression and role in atherosclerosis, however, are unknown. In the present study, we examined stable and unstable human carotid atherosclerotic plaques retrieved by endarterectomy for the presence of IL-18 using reverse transcription-polymerase chain reaction (PCR), Western blot, and immunohistochemical techniques. IL-18 was highly expressed in the atherosclerotic plaques compared with control normal arteries and was localized mainly in plaque macrophages. IL-18 receptor was also upregulated in plaque macrophages and endothelial cells, suggesting potential biological effects. To examine the role of IL-18 in atherosclerosis, we determined the relation between IL-18 mRNA expression and signs of plaque instability using real-time quantitative PCR. Interestingly, significantly higher levels of IL-18 mRNA were found in symptomatic (unstable) plaques than asymptomatic (stable) plaques (P<0.01). These results suggest, for the first time, a major role for IL-18 in atherosclerotic plaque destabilization leading to acute ischemic syndromes.
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              Interleukin-18 (IFNgamma-inducing factor) induces IL-8 and IL-1beta via TNFalpha production from non-CD14+ human blood mononuclear cells.

              IL-18 is synthesized as a precursor molecule without a signal peptide but requires the IL-1beta converting enzyme (ICE, caspase-1) for cleavage into a mature peptide. Human precursor IL-18 was expressed, purified, and cleaved by ICE into a 18-kD mature form. Mature IL-18 induced IL-8, macrophage inflammatory protein-1alpha, and monocyte chemotactic protein-1 in human peripheral blood mononuclear cells in the absence of any co-stimuli. Blocking IL-1 with IL-1 receptor antagonist resulted in a 50% reduction in IL-8. Neutralization of TNF with TNF binding protein resulted in a 66% reduction in IL-1beta, an 80% reduction of IL-8, and an 88% reduction in mean TNFalpha mRNA. In purified CD14+ cells but not CD3+/CD4+, IL-18 induced gene expression and synthesis of IL-8 and IL-1beta. TNFalpha production was induced in the non-CD14+ population and there was no induction of TNFbeta by IL-18. In purified natural killer cells, IL-18 induced IL-8 that was also inhibited by TNF binding protein. IL-18 did not induce antiinflammatory cytokines, IL-1Ra, or IL-10, although IL-18 induction of TNFalpha was inhibited by IL-10. In the presence of IFNgamma, IL-18-induced TNFalpha was enhanced and there was an increase in the mature form of IL-1beta. We conclude that IL-18 possesses proinflammatory properties by direct stimulation of gene expression and synthesis of TNFalpha from CD3+/CD4+ and natural killer cells with subsequent production of IL-1beta and IL-8 from the CD14+ population.

                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                March 2005
                28 February 2005
                : 23
                : 2
                : 144-148
                Department of Internal Medicine, aFar Eastern Memorial Hospital and bNational Taiwan University Hospital, and cInstitute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan
                83620 Blood Purif 2005;23:144–148
                © 2005 S. Karger AG, Basel

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                Figures: 2, Tables: 2, References: 24, Pages: 5
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