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

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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.
RGD ID: 8549607
Pubmed: PMID:15902684   (View Abstract at PubMed)
DOI: DOI:10.1002/eji.200425776   (Journal Full-text)

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.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
IL13HumanExperimental Autoimmune Myocarditis treatmentISOIl13 (Rattus norvegicus) RGD 
Il13RatExperimental Autoimmune Myocarditis treatmentIMP  RGD 
Il13MouseExperimental Autoimmune Myocarditis treatmentISOIl13 (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Il13  (interleukin 13)

Genes (Mus musculus)
Il13  (interleukin 13)

Genes (Homo sapiens)
IL13  (interleukin 13)


Additional Information