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* Division of Cardiology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan;
Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan; and
Division of Stem Cell Regulation Research, G6, Osaka University Medical School, Suita, Japan
IL-22 is one of several cytokines with limited homology to IL-10. However, the biological activities of IL-22 are mostly unknown. The purpose of this study was to evaluate the effect of IL-22 on rat experimental autoimmune myocarditis (EAM) and elucidate an aspect of the biological activities of IL-22. Rats were immunized on day 0; IL-22-Ig-treated rats were injected with pCAGGS-IL-22-Ig and control rats with pCAGGS-Ig using hydrodynamics-based gene delivery on day 1 or day 6. IL-22-Ig gene therapy administered on day 1 or day 6 after immunization was effective in controlling EAM as monitored by the heart weight to body weight ratio, and the myocarditis area in rats was sacrificed on day 17. Examination of the expression of IL-22-related genes in purified cells from EAM hearts suggested that IL-22-Ig acting target cells were noncardiomyocytic (NC) noninflammatory cells such as fibroblasts, smooth muscle cells, and endothelial cells. Therefore, we examined the effect of rIL-22 or serum containing IL-22-Ig on the expression of immune-relevant genes in IL-1-stimulated NC cells cultured from EAM hearts. Results showed that the expression of immunologic molecules (PGE synthase, cyclooxygenase-2, MIP-2, MCP-1, IL-6, and cytokine-induced neutrophil chemoattractant-2) in IL-1-stimulated NC cells was significantly decreased by rIL-22 or serum containing IL-22-Ig. EAM was suppressed by hydrodynamics-based delivery of plasmid DNA encoding IL-22-Ig, and the reason for this effectiveness may be that IL-22 suppressed gene expression of PG synthases, IL-6, and chemokines in activated NC noninflammatory cells.
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1 This work was supported in part by Ministry of Health, Labor, and Welfare in Japan Grant "Research on Regulatory Science of Pharmaceutical and Medical Devices."
2 Address correspondence and reprint requests to Dr. Haruo Hanawa, Division of Cardiology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Niigata 951-8120, Japan. E-mail address: hanawa{at}med.niigata-u.ac.jp
3 Abbreviations used in this paper: EAM, experimental autoimmune myocarditis; CINC-2, cytokine-induced neutrophil chemoattractant-2; COX-2, cyclooxygenase-2; GLU, glucagon; NC, noncardiomyocytic; NCNI, NC noninflammatory; PGES, PGE synthase; SP, signal peptide; WBC, white blood cell.
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  D. Luger, P. B. Silver, J. Tang, D. Cua, Z. Chen, Y. Iwakura, E. P. Bowman, N. M. Sgambellone, C.-C. Chan, and R. R. Caspi Either a Th17 or a Th1 effector response can drive autoimmunity: conditions of disease induction affect dominant effector category J. Exp. Med., April 14, 2008; 205(4): 799 - 810. [Abstract] [Full Text] [PDF]
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