2024-03-28T09:32:24Z
https://niigata-u.repo.nii.ac.jp/oai
oai:niigata-u.repo.nii.ac.jp:00001646
2022-12-15T04:14:16Z
453:454
471:472:473
The effect of hydrodynamic-based delivery of an interleukin-13-Ig fusion gene for experimental autoimmune myocarditis in rats and its possible mechanism
Elnaggar, Raafat
4769
Hanawa, Haruo
4770
Liu, Hui
4771
Yoshida, Tsuyoshi
4772
Hayashi, Manabu
4773
Watanabe, Ritsuo
4774
Abe, Satoru
4775
Toba, Ken
4776
Yoshida, Kaori
4777
Chang, He
4778
Minagawa, Shiro
4779
Okura, Yuji
4780
Kato, Kiminori
4781
Kodama, Makoto
4782
Maruyama, Hiroki
4783
Miyazaki, Junichi
4784
Aizawa, Yoshifusa
4785
myocarditis
autoimmune
dilated cardiomyopathy
immune system
interleukin-13
gene therapy
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.
journal article
2005-06
application/pdf
European journal of immunology
6
35
1995
2005
European journal of immunology
AA00639610
00142980
https://niigata-u.repo.nii.ac.jp/record/1646/files/22_0003.pdf
eng
15902684
info:doi/10.1002/eji.200425776
WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim