@article{oai:niigata-u.repo.nii.ac.jp:00001646,
 author = {Elnaggar, Raafat and Hanawa, Haruo and Liu, Hui and Yoshida, Tsuyoshi and Hayashi, Manabu and Watanabe, Ritsuo and Abe, Satoru and Toba, Ken and Yoshida, Kaori and Chang, He and Minagawa, Shiro and Okura, Yuji and Kato, Kiminori and Kodama, Makoto and Maruyama, Hiroki and Miyazaki, Junichi and Aizawa, Yoshifusa},
 issue = {6},
 journal = {European journal of immunology, European journal of immunology},
 month = {Jun},
 note = {Interleukin (IL)-13 is a pleiotropic cytokine secreted by activated Th2-T lymphocytes. Th1 cytokines are assumed to exacerbate while Th2 cytokines to ameliorate rat experimental autoimmune myocarditis (EAM). Here, we examined the effect of IL-13 on EAM using a hydrodynamic-based delivery of an IL-13-Ig and the possible mechanism of its effect. Rats were immunized on day 0 and IL-13-Ig treated rats were injected with pCAGGS-IL-13-Ig and control rats with pCAGGS-Ig on day 1 or 7. On day 17, IL-13-Ig gene therapy was effective in controlling EAM as monitored by the decreased heart weight/body weight ratio, reduced myocarditis and atrial natriuretic peptide mRNA in heart as a heart failure marker. On the basis of IL-13 receptor mRNA expression in separated cells from EAM hearts, we proposed that IL-13-Ig targeting cells were CD11b+ cells and non-cardiomyocytic non-inflammatory (NCNI) cells such as fibroblasts, smooth muscle or endothelial cells. IL-13-Ig inhibited expressing the genes of prostaglandin E synthase, cyclooxygenase-2, inducible nitric oxide synthase, IL-1β and TNFα of cultivated cells from EAM hearts in contrast, while it enhanced IL-1 receptor antagonist. We concluded that IL-13-Ig ameliorates EAM and supposed that its effectiveness may be due to the influence on these immunologic molecules in CD11b+ and NCNI cells.},
 pages = {1995--2005},
 title = {The effect of hydrodynamic-based delivery of an interleukin-13-Ig fusion gene for experimental autoimmune myocarditis in rats and its possible mechanism},
 volume = {35},
 year = {2005}
}