RGD Reference Report - Beta2-Adrenergic agonists suppress rat autoimmune myocarditis: potential role of beta2-adrenergic stimulants as new therapeutic agents for myocarditis. - Rat Genome Database

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Beta2-Adrenergic agonists suppress rat autoimmune myocarditis: potential role of beta2-adrenergic stimulants as new therapeutic agents for myocarditis.

Authors: Nishii, M  Inomata, T  Niwano, H  Takehana, H  Takeuchi, I  Nakano, H  Shinagawa, H  Naruke, T  Koitabashi, T  Nakahata, J  Izumi, T 
Citation: Nishii M, etal., Circulation. 2006 Aug 29;114(9):936-44. Epub 2006 Aug 14.
RGD ID: 5129151
Pubmed: PMID:16908771   (View Abstract at PubMed)
DOI: DOI:10.1161/CIRCULATIONAHA.105.607903   (Journal Full-text)

BACKGROUND: The therapeutic potential of beta2-adrenergic receptor (AR) agonists in the treatment of autoimmune diseases has been reported. However, the role of these drugs in the myocardial structure-induced autoimmune process, which is thought to play a crucial role in the progression of myocarditis to subsequent complications, has not been elucidated. METHODS AND RESULTS: Experimental autoimmune myocarditis (EAM) was induced in rats by immunization with cardiac myosin. On daily administration from day 0 after immunization, the beta2-selective AR agonists formoterol or salbutamol ameliorated EAM on day 21 and increased myocardial interleukin-10/interferon-gamma mRNA levels. Propranolol, a nonselective beta-AR antagonist, aggravated EAM on day 21 and decreased mRNA levels, whereas metoprolol, a beta1-selective AR antagonist, showed no effect. These results were reflected in vivo by the proliferation of cardiac myosin-primed lymph node cells from drug-treated rats. In vitro addition of beta2-selective AR agonists inhibited the activation of cardiac myosin fragment-specific myocarditogenic T lymphocytes, and this effect was reversed by ICI118,551, a beta2-selective AR antagonist. Furthermore, treatment with 2 different beta2-selective AR agonists starting on day 14 also ameliorated EAM on day 21. CONCLUSIONS: beta2-AR stimulation suppressed the development of EAM by inhibiting cardiac myosin-specific T-lymphocyte activation in lymphoid organs and by shifting the imbalance in Th1/Th2 cytokine toward Th2 cytokine. Furthermore, it also ameliorated established myocardial inflammation. beta2-AR-stimulating agents may represent important immunomodulators of the cardiac myosin-induced autoimmune process and have potential as a new therapy for myocarditis.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
myocarditis  ISOAdrb2 (Rattus norvegicus)5129151; 5129151 RGD 
myocarditis  IMP 5129151 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Adrb2  (adrenoceptor beta 2)

Genes (Mus musculus)
Adrb2  (adrenergic receptor, beta 2)

Genes (Homo sapiens)
ADRB2  (adrenoceptor beta 2)


Additional Information