| Autor: |
Elnaggar, Raafat, Hanawa, Haruo, Liu, Hui, Yoshida, Tsuyoshi, Hayashi, Manabu, Watanabe, Ritsuo, Abe, Satoru, Toba, Ken, Yoshida, Kaori, Chang, He, Minagawa, Shiro, Okura, Yuji, Kato, Kiminori, Kodama, Makoto, Maruyama, Hiroki, Miyazaki, Junichi, Aizawa, Yoshifusa |
| Jazyk: |
angličtina |
| Rok vydání: |
2005 |
| Předmět: |
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| Zdroj: |
European journal of immunology. 35(6):1995-2005 |
| ISSN: |
0014-2980 |
| Popis: |
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. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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