The effect of hydrodynamics-based delivery of an IL-13-Ig fusion gene for experimental autoimmune myocarditis in rats and its possible mechanism.

Authors: Elnaggar, R  Hanawa, H  Liu, H  Yoshida, T  Hayashi, M  Watanabe, R  Abe, S  Toba, K  Yoshida, K  Chang, H  Minagawa, S  Okura, Y  Kato, K  Kodama, M  Maruyama, H  Miyazaki, J  Aizawa, Y 
Citation: Elnaggar R, etal., Eur J Immunol. 2005 Jun;35(6):1995-2005.
Pubmed: (View Article at PubMed) PMID:15902684
DOI: Full-text: DOI:10.1002/eji.200425776

Interleukin (IL)-13 is a pleiotropic cytokine secreted by activated Th2 T lymphocytes. Th1 cytokines are assumed to exacerbate and Th2 cytokines to ameliorate rat experimental autoimmune myocarditis (EAM). Here, we examined the effect of IL-13 on EAM, using a hydrodynamics-based delivery of an IL-13-Ig fusion gene, as well as 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, the IL-13-Ig gene therapy was effective in controlling EAM as monitored by a decreased heart weight/body weight ratio, by reduced myocarditis and by reduced atrial natriuretic peptide mRNA in the 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 target cells were CD11b(+) cells and non-cardiomyocytic noninflammatory (NCNI) cells, such as fibroblasts, smooth muscle or endothelial cells. IL-13-Ig inhibited expression of the genes for prostaglandin E synthase, cyclooxygenase-2, inducible nitric oxide synthase, IL-1beta and TNF-alpha in cultivated cells from EAM hearts, while it enhanced expression of the IL-1 receptor antagonist gene. We conclude that IL-13-Ig ameliorates EAM and suppose that its effectiveness may be due to the influence on these immunologic molecules in CD11b(+) and NCNI cells.

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RGD ID: 8549607
Created: 2014-04-01
Species: All species
Last Modified: 2014-04-01
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.